Página 1 dos resultados de 569 itens digitais encontrados em 0.004 segundos

NATRIURESIS, NOT SEIZURES, INDUCED BY CHOLINERGIC STIMULATION OF THE LOCUS-CERULEUS IS AFFECTED BY FOREBRAIN LESIONS AND WATER-DEPRIVATION

Deluca, L. A.; Franci, C. R.; Saad, W. A.; Camargo, LAA; Antunesrodrigues, J.
Fonte: Elsevier B.V. Publicador: Elsevier B.V.
Tipo: Artigo de Revista Científica Formato: 203-210
ENG
Relevância na Pesquisa
37.31%
Two groups of rats with electrolytic lesions of the medial and upper septal area (MUL) or, alternatively, of the anteroventral portion of the third ventricle (AV3V) and a third group of sham-operated rats were water loaded and received three carbachol injections into the locus coeruleus according to the following schedule: 1) prelesion, 2) on the second postlesion day and 3) on the seventh postlesion day. Both MUL and AV3V lesions inhibited the carbachol-induced natriuresis on the second postlesion day. Recovery was almost complete after MUL but not after AV3V lesion on the seventh day. Water deprivation also reduced the carbachol-induced natriuresis but passive hydration of AV3V animals did not avoid the impairment induced by the lesion. Transient seizure phenomena such as clonic convulsions, salivation and analgesia subsequent to carbachol injection were not altered by the lesions.

A1 Noradrenergic Neurons Lesions Reduce Natriuresis and Hypertensive Responses to Hypernatremia in Rats

da Silva, Elaine Fernanda; Freiria-Oliveira, André Henrique; Custódio, Carlos Henrique Xavier; Ghedini, Paulo César; Bataus, Luiz Artur Mendes; Colombari, Eduardo; de Castro, Carlos Henrique; Colugnati, Diego Basile; Rosa, Daniel Alves; Cravo, Sergio L
Fonte: Universidade Estadual Paulista Publicador: Universidade Estadual Paulista
Tipo: Artigo de Revista Científica
ENG
Relevância na Pesquisa
37.14%
Noradrenergic neurons in the caudal ventrolateral medulla (CVLM; A1 group) contribute to cardiovascular regulation. The present study assessed whether specific lesions in the A1 group altered the cardiovascular responses that were evoked by hypertonic saline (HS) infusion in non-anesthetized rats. Male Wistar rats (280-340 g) received nanoinjections of antidopamine-β-hydroxylase-saporin (A1 lesion, 0.105 ng.nL-1) or free saporin (sham, 0.021 ng.nL-1) into their CVLMs. Two weeks later, the rats were anesthetized (2% halothane in O2) and their femoral artery and vein were catheterized and led to exit subcutaneously between the scapulae. On the following day, the animals were submitted to HS infusion (3 M NaCl, 1.8 ml • kg-1, b.wt., for longer than 1 min). In the sham-group (n = 8), HS induced a sustained pressor response (ΔMAP: 35±3.6 and 11±1.8 mmHg, for 10 and 90 min after HS infusion, respectively; P<0.05 vs. baseline). Ten min after HS infusion, the pressor responses of the anti-DβH-saporin-treated rats (n = 11)were significantly smaller(ΔMAP: 18±1.4 mmHg; P<0.05 vs. baseline and vs. sham group), and at 90 min, their blood pressures reached baseline values (2±1.6 mmHg). Compared to the sham group, the natriuresis that was induced by HS was reduced in the lesioned group 60 min after the challenge (196±5.5 mM vs. 262±7.6 mM...

Does plasma ANP participate in natriuresis induced by a-MSH?

Fonte: Associação Brasileira de Divulgação Científica Publicador: Associação Brasileira de Divulgação Científica
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/04/1997 EN
Relevância na Pesquisa
37.31%
a-Melanocyte-stimulating hormone (a-MSH; 0.6 and 3 nmol) microinjected into the anteroventral region of the third ventricle (AV3V) induced a significant increase in diuresis without modifying natriuresis or kaliuresis. Intraperitoneal (ip) injection of a-MSH (3 and 9.6 nmol) induced a significant increase in urinary sodium, potassium and water excretion. Intraperitoneal (3 and 4.8 nmol) or iv (3 and 9.6 nmol) administration of a-MSH did not induce any significant changes in plasma atrial natriuretic peptide (ANP), suggesting that the natriuresis, kaliuresis and diuresis induced by the systemic action of a-MSH can be dissociated from the increase in plasma ANP. These preliminary results suggest that a-MSH may be involved in a g-MSH-independent mechanism of regulation of hydromineral metabolism

Atrial natriuretic peptide and oxytocin induce natriuresis by release of cGMP

Soares, T. J.; Coimbra, T. M.; Martins, A. R.; Pereira, A. G. F.; Carnio, E. C.; Branco, L. G. S.; Albuquerque-Araujo, W. I. C.; de Nucci, G.; Favaretto, A. L. V.; Gutkowska, J.; McCann, S. M.; Antunes-Rodrigues, J.
Fonte: The National Academy of Sciences Publicador: The National Academy of Sciences
Tipo: Artigo de Revista Científica
Publicado em 05/01/1999 EN
Relevância na Pesquisa
27.65%
Our hypothesis is that oxytocin (OT) causes natriuresis by activation of renal NO synthase that releases NO followed by cGMP that mediates the natriuresis. To test this hypothesis, an inhibitor of NO synthase, l-nitroarginine methyl ester (NAME), was injected into male rats. Blockade of NO release by NAME had no effect on natriuresis induced by atrial natriuretic peptide (ANP). This natriuresis presumably is caused by cGMP because ANP also activates guanylyl cyclase, which synthesizes cGMP from GTP. The 18-fold increase in sodium (Na+) excretion induced by OT (1 μg) was accompanied by an increase in urinary cGMP and preceded by 20 min a 20-fold increase in NO3− excretion. NAME almost completely inhibited OT-induced natriuresis and increased NO3− excretion; however, when the dose of OT was increased 10-fold, a dose that markedly increases plasma ANP concentrations, NAME only partly inhibited the natriuresis. We conclude that the natriuretic action of OT is caused by a dual action: generation of NO leading to increased cGMP and at higher doses release of ANP that also releases cGMP. OT-induced natriuresis is caused mainly by decreased tubular Na+ reabsorption mediated by cGMP. In contrast to ANP that releases cGMP in the renal vessels and the tubules...

Paradoxical relationship between atriopeptin plasma levels and diuresis-natriuresis induced by acute volume expansion.

Sakata, M; Greenwald, J E; Needleman, P
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /05/1988 EN
Relevância na Pesquisa
27.56%
Surgical removal of one or both atrial appendages was employed in rats to reduce the intrinsic stores of atriopeptin (AP). In conscious rats (with intact baroreceptor reflexes), bilateral or unilateral atrial appendectomy suppressed the diuresis and natriuresis produced by acute volume expansion. Surprisingly, volume expansion (with 4% bovine serum albumin in saline at 1.5 ml/kg per min for 15 min) did not result in an increase in plasma AP immunoreactivity (APir) in control or atrial-appendectomized conscious rats. Previous studies demonstrated that acute volume expansion in anesthetized animals caused increased plasma APir. Indeed, we found that volume expansion causes comparable diuresis-natriuresis in conscious and chloral hydrate-anesthetized rats, but only the latter group exhibits an increase in plasma APir. Brattleboro rats, which are deficient in vasopressin, exhibit the same response as Long-Evans controls in that acute volume expansion in conscious animals produces a pronounced diuresis and natriuresis but no APir release, but when these same animals are anesthetized, there is a simultaneous induction of diuresis-natriuresis and APir release by volume expansion. Plasma AP does not increase in conscious rats despite a large volume load...

Subtype 2 of angiotensin II receptors controls pressure-natriuresis in rats.

Lo, M; Liu, K L; Lantelme, P; Sassard, J
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /03/1995 EN
Relevância na Pesquisa
27.42%
Angiotensin II recognizes two receptor subtypes, AT1 and AT2, both of them having been recently cloned. Although AT2 receptors represent 5-10% of angiotensin II receptors in the kidneys of adult rats, their function remains unknown. In the present work, we examined the possible contribution of AT2 receptors to the regulation of pressure-natriuresis in anesthetized rats infused either with the specific AT2 antagonist PD 123319, or with CGP 42112B, an AT2 ligand with agonistic properties. The effects of PD 123319 were examined in a preparation with stable levels of angiotensin II, and in which AT1 receptors were blocked by the specific antagonist losartan. The effects of CGP 42112B were studied in rats deprived of endogenous angiotensin II. AT2 receptor blockade with PD 123319 did not change the renal blood flow while it increased the diuresis and natriuresis. These effects persisted even after full AT1 receptor blockade with losarfan. CGP 42112B did not modify the renal blood flow, but dose-dependently decreased urine flow and natriuresis. These results show that, contrary to AT1 receptors, renal AT2 receptors have no effect on total renal blood flow, but blunt the pressure-natriuresis, thus demonstrating that this receptor subtype is involved in a function of importance for body fluid and blood pressure regulation.

Neuropeptide Y-enhanced diuresis and natriuresis in anaesthetized rats is independent of renal blood flow reduction.

Bischoff, A; Erdbrügger, W; Smits, J; Michel, M C
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 01/09/1996 EN
Relevância na Pesquisa
27.42%
1. Neuropeptide Y (NPY) has been reported to enhance diuresis and natriuresis in anaesthetized rats although it is a potent renal vasoconstrictor in vitro in vivo in several species. Therefore, we have investigated anaesthetized rats to see whether reduction in renal blood flow (RBF) and enhancement of diuresis and natriuresis can occur concomitantly, and how diuresis and natriuresis might be enhanced despite reduced RBF. 2. Systemic or intrarenal NPY infusion (0.03-3 micrograms kg-1 min-1) had only a small effect on mean arterial pressure (maximal increase 15-20 mmHg) and heart rate (maximal decrease 30 beats min-1) but dose-dependently reduced RBF (maximal peak reduction 3 ml min-1) Endogenous creatinine clearance was not significantly altered. 3. In anaesthetized rats systemic infusion of 1 or 3 micrograms kg-1 min-1 NPY enhanced urine formation and sodium and calcium excretion by a maximum of 110, 110 and 45%, respectively, but did not alter potassium excretion. Enhancement of diuresis was also detectable in conscious rats. 4. The diuretic and natriuretic effects of systemically infused NPY were at least partly maintained in rats with decapsulated kidneys and in rats where NPY-induced increase of renal perfusion pressure was excluded mechanically by an adjustable clamp placed on the abdominal aorta. 5. Intrarenal infusion of 0.3 or 1 microgram kg-1 min-1 NPY reduced RBF to a greater extent than systemic infusion (maximal peak reduction 4 ml min-1) but caused a smaller enhancement or even a reduction of urine formation and sodium excretion. 6. We conclude that systemic infusion of NPY reduces RBF by a direct effect on the renal vasculature. Systemic NPY infusion enhances urine formation and sodium and calcium excretion. This occurs independently (at least in part) of pressure natriuresis by formation and/or release of an extrarenal factor which might act on distal tubules and/or collecting ducts.

Elevated renal perfusion pressure does not contribute to natriuresis induced by isotonic saline infusion in freely moving dogs

Seeliger, Erdmann; Andersen, Jens Lundbæk; Bie, Peter; Reinhardt, H Wolfgang
Fonte: Blackwell Science Inc Publicador: Blackwell Science Inc
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
27.5%
The study was designed to determine to what extent moderate elevation of renal perfusion pressure (RPP) via the mechanism of ‘pressure natriuresis’ contributes to the natriuresis induced by acute i.v. saline loading. Nine Beagle dogs maintained on ample sodium intake (5.5 mmol (kg body mass)−1 day−1) were chronically equipped with an aortic occluder to servocontrol RPP, a bladder catheter to measure renal function, and catheters for measurement of RPP and mean arterial blood pressure (MABP). A swivel system allowed free movement in the kennel during experiments. Isotonic saline loading (500 ml in 100 min) was studied as follows: with and without servocontrol of RPP, and these two protocols repeated in the presence of angiotensin-converting enzyme inhibition (ACEI, Enalapril, 2 mg (kg body mass)−1). Saline loading increased MABP by about 12 mmHg and sodium excretion from about 28 μmol min−1 up to about 350 μmol min−1. Without ACEI, servocontrol of RPP at 10% below control 24 h MABP slightly delayed the onset of the saline-induced natriuresis, but did not reduce peak sodium excretion or cumulative sodium excretion. The slight delay most probably resulted from pressure-controlled renin release because, with ACEI, servocontrol of RPP did not delay or reduce the saline-induced natriuresis. In conclusion...

Contribution of pressure natriuresis to control of total body sodium: balance studies in freely moving dogs

Seeliger, Erdmann; Safak, Erdal; Persson, Pontus B; Reinhardt, H Wolfgang
Fonte: Blackwell Science Inc Publicador: Blackwell Science Inc
Tipo: Artigo de Revista Científica
Publicado em 15/12/2001 EN
Relevância na Pesquisa
27.56%
This study aims at determining whether elevation of renal perfusion pressure (RPP) may correct for increased total body sodium (TBS), via pressure natriuresis.Freely moving dogs were studied on four consecutive days. During day 1, low-dose angiotensin II and aldosterone were infused. Pressure natriuresis was prevented by servo-controlling RPP to 20% below the control level. Sodium and water retention increased TBS and total body water. Mean arterial blood pressure rose by ∼25 mmHg.In protocol 1, infusions and control of RPP were maintained over three more days. Sodium was retained on all days, resulting in a continuous increase in TBS.In protocol 2, control of RPP was stopped after day 1. Thus, pressure natriuresis could exert its effect beginning with day 2. Angiotensin II and aldosterone infusions were continued. This prevented the effects of endogenous suppression of the renin-angiotensin-aldosterone system (RAAS), which is caused by increased TBS. No further sodium retention occurred, i.e. TBS remained at the elevated level gained on day 1.In protocol 3, control of RPP and the infusions were stopped. Thus, pressure natriuresis and RAAS suppression could exert their combined effects. Sodium excretion exceeded sodium intake on day 2. Control level of TBS was regained within 24 h.It was concluded that when RPP is considerably elevated...

INTRARENAL ANGIOTENSIN III INFUSION INDUCES NATRIURESIS AND AT2R TRANSLOCATION IN WKY BUT NOT IN SHR

Padia, Shetal H.; Kemp, Brandon A.; Howell, Nancy L.; Gildea, John J.; Keller, Susanna R.; Carey, Robert M.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
27.56%
In Sprague-Dawley rats, renal AT2Rs mediate natriuresis in response to renal interstitial (RI) D1-like receptor (D1R) stimulation or RI Ang III infusion. After D1R activation, apical membrane (AM) but not total renal proximal tubule cell (RPTC) AT2R expression is increased, suggesting that AM AT2R translocation may be important for natriuresis. The onset of hypertension in spontaneously hypertensive rats (SHR) is preceded by defects in renal sodium excretion. The present study examines AT2R-mediated natriuresis in response to RI Ang III infusion in Wistar-Kyoto rats (WKY) and SHR. WKY and SHR received RI Ang III infusion after 24 h of systemic AT1R blockade with candesartan (CAND). In WKY, urine sodium excretion rate (UNaV) increased from 0.043±0.01 to 0.191±0.06 μmol/min (P<0.05) in response to Ang III infusion, but identical conditions failed to increase UNaV in SHR. The increase in UNaV was blocked by co-infusion of PD-123319, a selective AT2R antagonist. On confocal microscopy images, Ang III-infused WKY demonstrated greater RPTC AM AT2R fluorescence intensity compared to SHR (5385±725 vs. 919±35, P<.0001), and Western blot analysis demonstrated increased AM (0.050±0.003 vs. 0.038±0.003, P<0.01) but not total cell AT2R expression in WKY. In SHR...

ROLE OF Src-FAMILY KINASE IN EXTRACELLULAR RENAL CYCLIC GMP- AND PRESSURE-INDUCED NATRIURESIS

Nascimento, Nilberto RF; Kemp, Brandon A.; Howell, Nancy L.; Gildea, John J.; Santos, Cláudia F.; Harris, Thurl E.; Carey, Robert M.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
27.61%
Cyclic guanosine 3’,5’-monophosphate (cGMP) functions as an extracellular (paracrine) messenger acting at the renal proximal tubule and is an important modulator of pressure-natriuresis (P-N). The signaling pathway activated by cGMP in the tubule cell basolateral membrane remains unknown. We hypothesized that renal interstitial (RI) micro-infusion of cGMP (50 nmol/kg/min) or P-N would be accompanied by increased renal protein levels of phospho-Src (Tyr 416) and that the natriuresis would be decreased by Src inhibition. RI cGMP induced natriuresis, which was blocked by Src inhibitor PP2 (2.0±0.4 vs. 0.5±0.01 µEq/g/min; P<0.001). The inactive analogue of PP2, PP3, had no effect on cGMP-induced natriuresis. SU6656, another Src inhibitor, also inhibited cGMP-induced natriuresis (2.0±0.4 vs 1.02±0.01 µEq/g/min; P<0.001). RI cGMP infusion increased phospho-Src protein levels 5.6-fold at 15 min and 6.8-fold at 30 min compared to vehicle (VEH) infusion, but returned towards basal levels after 60 min. PP2 also blunted P-N (3.1±0.1 vs. 1.1±0.3 µEq/g/min; P<0.01) despite a similar increase in blood pressure (BP). PP3 had no effect on P-N. Phospho-Src protein levels increased during P-N in VEH- (1.8-fold) and PP3-treated (2.1-fold) groups compared to the SHAM-operated group. PP2 blocked the pressure-induced increase in renal phospho-Src protein levels. PP2 had no effect on renal hemodynamics...

mPGES-1-derived PGE2 mediates dehydration natriuresis

Jia, Zhanjun; Liu, Gang; Sun, Ying; Kakizoe, Yutaka; Guan, Guangju; Zhang, Aihua; Zhou, Shu-Feng; Yang, Tianxin
Fonte: American Physiological Society Publicador: American Physiological Society
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
27.42%
PGE2 is a natriuretic factor whose production is elevated after water deprivation (WD) but its role in dehydration natriuresis is not well-defined. The goal of the present study was to investigate the role of microsomal prostaglandin E synthase-1 (mPGES-1) in dehydration natriuresis. After 24-h WD, wild-type (WT) mice exhibited a significant increase in 24-h urinary Na+ excretion accompanied with normal plasma Na+ concentration and osmolality. In contrast, WD-induced elevation of urinary Na+ excretion was completely abolished in mPGES-1 knockout (KO) mice in parallel with increased plasma Na+ concentration and a trend increase in plasma osmolality. WD induced a 1.8-fold increase in urinary PGE2 output and a 1.6-fold increase in PGE2 content in the renal medulla of WT mice, both of which were completely abolished by mPGES-1 deletion. Similar patterns of changes were observed for urinary nitrate/nitrite and cGMP. The natriuresis in dehydrated WT mice was associated with a significant downregulation of renal medullary epithelial Na channel-α mRNA and protein, contrasting to unaltered expressions in dehydrated KO mice. By quantitative RT-PCR, WD increased the endothelial nitric oxide synthase (eNOS), inducible NOS, and neuronal NOS expressions in the renal medulla of WT mice by 3.9-...

Impaired pressure natriuresis resulting in salt-sensitive hypertension is caused by tubulointerstitial immune cell infiltration in the kidney

Franco, Martha; Tapia, Edilia; Bautista, Rocio; Pacheco, Ursino; Santamaria, Jose; Quiroz, Yasmir; Johnson, Richard J.; Rodriguez-Iturbe, Bernardo
Fonte: American Physiological Society Publicador: American Physiological Society
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
27.5%
Immune cell infiltration of the kidney is a constant feature in salt-sensitive hypertension (SSHTN). We evaluated the relationship between the renal inflammation and pressure natriuresis in the model of SSHTN that results from transient oral administration of Nω-nitro-l-arginine methyl ester (l-NAME). Pressure natriuresis was determined in Wistar rats that received 4 wk of a high-salt (4% NaCl) diet, starting 1 wk after stopping l-NAME, which was administered alone (SSHTN group, n = 17) or in association with mycophenolate mofetil (MMF; MMF group, n = 15). The administration of MMF in association with l-NAME is known to prevent the subsequent development of SSHTN. Control groups received a high (n = 12)- and normal (0.4%)-salt diet (n = 20). Rats with SSHTN had increased expression of inflammatory cytokines and oxidative stress. The severity of hypertension correlated directly (P < 0.0001) with the number of tubulointerstitial immune cells and angiotensin II-expressing cells. Pressure natriuresis was studied at renal arterial pressures (RAPs) of 90, 110, 130, and 150 mmHg. Glomerular filtration rate was similar and stable in all groups, and renal blood flow was decreased in the SSHTN group. Significantly decreased natriuresis (P < 0.05) was found in the SSHTN group at RAPs of 130 and 150 mmHg...

AT2 receptor non-peptide agonist C21 promotes natriuresis in obese Zucker rats

Ali, Quaisar; Hussain, Tahir
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
27.56%
Previously, we demonstrated that angiotensin II type 2 (AT2) receptors have a role in natriuresis in obese Zucker rats (OZR). In the present study, we investigated the role of a novel, non-peptide agonist, C21, in natriuresis via AT2 receptor activation in OZR. Infusion of C21 (1 and 5 μg kg−1 min−1) into rats under anesthesia caused a dose-dependent increase in urine flow (UF) and urinary Na volume (UNaV). These effects of C21 were blocked by pre-infusion of the AT2 receptor antagonist, PD123319, (50 μg kg−1 min−1), suggesting involvement of the AT2 receptor. Infusion of C21 (5 μg kg−1 min−1) significantly increased the fractional excretion of sodium without changing the glomerular filtration rate or blood pressure, suggesting a tubular effect. Similarly, C21 infusion increased the fractional excretion of lithium, suggesting a proximal tubular effect. Furthermore, we tested the effect of C21 on natriuresis after blocking two main, distal-nephron Na transporters, the epithelial Na channels (ENaC), with amiloride (AM, 3 mg kg−1 body wt), and the NaCl cotransporters (NCC), with bendroflumethiazide (BFTZ, 7 mg kg−1 body wt). Infusion of AM + BFTZ caused significant increases in both diuresis and natriuresis, which were further increased by infusion of C21 (5 μg kg−1min−1). Natriuresis in response to C21 was associated with increases in urinary NO and cGMP levels. The data indicate that the AT2 receptor agonist...

ROLE OF ANGIOTENSIN AT2 RECEPTORS IN NATRIURESIS: INTRARENAL MECHANISMS AND THERAPEUTIC POTENTIAL

Carey, Robert M.; Padia, Shetal H.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /08/2013 EN
Relevância na Pesquisa
27.5%
The renin-angiotensin system is a coordinated hormonal cascade critical for the regulation of blood pressure (BP) and kidney function. Angiotensin II (Ang II), the major angiotensin effector peptide, binds to two major receptors, type-1 (AT1Rs) and type-2 (AT2Rs). AT1Rs engender antinatriuresis and raise BP, whereas AT2Rs oppose these effects, inducing natriuresis and reducing BPAT2Rs are highly expressed in the adult kidney, especially in the proximal tubule. In AT2R-null mice, long-term Ang II infusion results in pressor and antinatriuretic hypersensivivity compared to responses in wild-type animals.The major endogenous receptor ligand for AT2R-mediated natriuretic responses appears to be des-aspartyl1-Ang II (Ang III) instead of Ang II. Recent studies have demonstrated that Ang II requires metabolism to Ang III by aminopeptidase A in order to induce natriuresis and that inhibition of aminopeptidase N increases intrarenal Ang III and augments Ang III-induced natriuresis.The renal dopaminergic system is another important natriuretic pathway. Renal proximal tubule D1-like receptors (D1LIKERs) control approximately 50% of basal sodium (Na+) excretion. We have recently found that natriuresis induced by proximal tubule D1LIKERs requires AT2R activation and that D1LIKER stimulation induces recruitment of AT2Rs to the apical plasma membrane via a cyclic AMP-dependent mechanism.Initial studies employing potent AT2R non-peptide agonist Compound 21 demonstrate natriuresis in both the presence and absence of AT1R blockade indicating the therapeutic potential of this compound in fluid retaining states and hypertension.

Role of atrial natriuretic peptide in mediating the blood pressure-independent natriuresis elicited by systemic inhibition of nitric oxide

Dobrowolski, Leszek; Kuczeriszka, Marta; Castillo, Alexander; Majid, Dewan S.; Navar, L. Gabriel
Fonte: Springer Berlin Heidelberg Publicador: Springer Berlin Heidelberg
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
27.56%
While it is clearly recognized that increased intrarenal nitric oxide (NO) levels elicit natriuresis, confounding data showing that systemic nitric oxide synthase inhibition (NOSi) also increases sodium excretion (UNaV) poses a conundrum. This response has been attributed to the associated increases in arterial pressure (AP); however, the increases in AP and in UNaV are temporally dissociated. The changes in regional renal haemodynamics induced by NOSi could also contribute to the alterations of UNaV. To evaluate the roles of AP and non-AP mechanisms mediating the natriuresis, Nω-nitro-l-arginine methyl ester hydrochloride (L-NAME) was infused i.v. at doses ranging from 5 to 50 μg/kg/min in anaesthetized rats. UNaV, perfusion of the cortex (cortical blood flow, CBF) and medulla (medullary blood flow, MBF) with laser-Doppler flowmetry and glomerular filtration rate (GFR) were measured. UNaV increased from 0.6 ± 0.2 to 1.6 ± 0.1 μmol/kg/min (P < 0.05) with the lower nonpressor doses. With the higher doses, AP increased from 116 ± 4 to 122 ± 4 mmHg and UNaV increased from 1.1 ± 0.3 to 3.3 ± 0.7 μmol/min/g (P < 0.002). UNaV increased similarly in a group where renal AP was maintained at baseline levels. The associated reductions in CBF (17 ± 5 and 38 ± 5 %) and MBF (27 ± 6 and 52 ± 6 %) would be expected to attenuate rather than contribute to the natriuresis. Plasma atrial natriuretic peptide (ANP) concentrations increased significantly following NOSi. Anantin...

Beteiligung von Dopamin-D3-Rezeptoren an der Regulation der Nierenfunktion; Contribution of dopamine-D3-receptors to the regulation of renal function

Schäfer, Ralf
Fonte: Universidade de Tubinga Publicador: Universidade de Tubinga
Tipo: Dissertação
DE_DE
Relevância na Pesquisa
27.5%
In der vorliegenden Arbeit wurde die Beteiligung des Dopamin-D3-Rezeptors an der Regulation der Nierenfunktion untersucht. In 4 Versuchsgruppen wurden an narkotisierten männlichen Sprague Dawley Ratten unter physiologischen Bedingungen Clearance-Versuche durchgeführt. Die Nierenfunktion wurde durch die exogene Zufuhr einer 10%igen Aminosäurelösung, der Infusion von 7-OH-DPAT, einem selektiven D3-Agonisten sowie durch eine isotone Volumenexpansion und schließlich durch Verabreichung von Dopamin beeinflusst. Danach wurde untersucht, inwieweit die beobachteten Effekte durch D3-Antagonisten wie BSF 135170 und BSF 201640 moduliert werden. Es sollte somit die Beteiligung des D3-Rezeptors an der Veränderung der renalen Funktion nach Aminosäurenzufuhr und nach isotoner Volumenexpansion geklärt werden. Durch die Zufuhr von exogenem Dopamin sollte der funktionelle Stellenwert des D3-Rezeptors innerhalb der Dopaminrezeptor-Familie beurteilt werden. Die pharmakologische Aktivierung des D3-Rezeptors führte zu einer Steigerung der glomerulären Filtrationsrate und einer verstärkten Natiurese. Die Ergebnisse legen daher nahe, dass dieser Rezeptor seine Wirkung nicht nur am Glomerulum entfaltet. Der Anstieg der fraktionellen Natriumausscheidung spricht für eine verminderten Natriumrückresorption im Tubulus. Eine D3-Rezeptorblockade konnte diese Effekte fast vollständig unterdrücken. Die gleichen Beobachtungen wurden im Rahmen der Gabe einer Aminosäurelösung gemacht. Die aminosäurebedingte GFR-Steigerung war nach Rezeptorblockade wiederum aufgehoben. Die Diurese und die Natriurese waren jedoch nur im geringen Ausmaß abzuschwächen. Durch eine Volumenexpansion wurde erwartungsgemäß die GFR wenig beeinflusst. Im Gegensatz dazu ergab sich eine massive Steigerung der Salzausscheidung und ein ebenso erhöhtes Urinvolumen. Vermutlich ist der D3-Rezeptor auch hierbei involviert...

Evidence Linking Alterations in the Moment-to-Moment Pressure-Natriuresis Mechanism to Hypertension and Salt-Sensitivity in Rodents

Komolova, Marina
Fonte: Quens University Publicador: Quens University
Tipo: Tese de Doutorado
EN; EN
Relevância na Pesquisa
37.31%
Hypertension and salt-sensitivity are independent risk factors for cardiovascular disease. Although both conditions are idiopathic, they develop due to a complex interplay between susceptibility genes and environmental factors. Given that the kidney plays an important role in regulating blood pressure, in particular, by maintaining sodium and water balance via pressure-natriuresis, it is not surprising that disturbances in the proper functioning of this intrarenal mechanism have been linked to these conditions. Although direct coupling of changes in renal arterial pressure (RAP) to renal interstitial hydrostatic pressure (RIHP) and consequent sodium excretion is well established, few studies have characterized the moment-to-moment aspects of this process. Thus, the main focus of the research presented herein was to characterize the moment-to-moment RAP-RIHP relationship, and assess the functioning of this intrarenal mechanism in various animal models of genetic and environmentally-induced hypertension and/or salt-sensitivity. In adult normotensive rats, the response time of RIHP to acute changes in RAP was rapid (<2 seconds), and the moment-to-moment RAP-RIHP relationship was linear over a wide range of pressures. Additionally...

Patterns of renal dopamine release to regulate diuresis and natriuresis during volume expansion: Role of renal monoamine-oxidase

de Luca Sarobe,Verónica; Di Ciano,Luis; Carranza,Andrea M.; Levin,Gloria; Arrizurieta,Elvira E.; Ibarra,Fernando R.
Fonte: Medicina (Buenos Aires) Publicador: Medicina (Buenos Aires)
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/02/2010 EN
Relevância na Pesquisa
37.31%
Diuretic and natriuretic effects of renal dopamine (DA) are well established. However, in volume expansion the pattern of renal DA release into urine (U DA V) and the role of enzymes involved in DA synthesis/degradation have not yet been defined. The objective was to determine the pattern of U DA V during volume expansion and to characterize the involvement of monoamine-oxidase (MAO) and aromatic amino-acid decarboxylase (AADC) in this response. In this study male Wistar rats were expanded with NaCl 0.9% at a rate of 5% BWt per hour. At the beginning of expansion three groups received a single drug injection as follows: C (vehicle, Control), IMAO (MAO inhibitor Pargyline, 20 mg/kg BWt, i.v.) and BNZ (AADC inhibitor Benserazide, 25 mg/kg BWt, i.v.). Results revealed that in C rats U DA V (ng/30 min/100g BWt) increased in the first 30 min expansion from 11.5 ± 1.20 to 21.8 ± 3.10 (p < 0.05) and decreased thereafter. IMAO showed a similar pattern but significantly higher than C at 30 min expansion (32.5 ± 2.20, p < 0.05). IMAO greatly reduced MAO activity from 8.29 ± 0.35 to 1.1 ± 0.03 nmol/mg tissue/hour and significantly increased diuresis and natriuresis over controls. BNZ abolished the early U DA V peak to 3.2±0.72 (p < 0.01) and though...

La Oxitocina media la natriuresis inducida por la Angiotensina II administrada centralmente

Arzola,J; Zavala,L; Díaz,E; Pastorello,M; Garrido,M del R; Israel,A
Fonte: Sociedad Venezolana de Farmacológia y Farmacológia Clínica y Terapéutica. Escuela de Medicina; José Maria Vargas. Cátedra de Farmacológia, piso 3, esquina san jacinto, San José Caracas Publicador: Sociedad Venezolana de Farmacológia y Farmacológia Clínica y Terapéutica. Escuela de Medicina; José Maria Vargas. Cátedra de Farmacológia, piso 3, esquina san jacinto, San José Caracas
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/01/2005 ES
Relevância na Pesquisa
37.42%
El sistema renina-angiotensina cerebral es uno de los sistemas más importantes que participan en la regulación del balance hidromineral. La administración central de renina o angiotensina II (Ang II) induce dipsogenia, apetito por la sal, aumento de presión arterial, natriuresis, liberación de oxitocina y vasopresina desde el núcleo paraventricular hipotalámico. La evidencia indica que la oxitocina es una hormona natriurética. Por ello, estudiamos el papel de la oxitocina como posible efector humoral de la natriuresis inducida por la administración intracerebroventricular (ICV) de Ang II en ratas euvolémicas, mediante el uso del atosiban (AT), un antagonista selectivo de los receptores de oxitocina. La administración central de renina o Ang II produjo un efecto antidiurético a la primera hora y un aumento en la excreción urinaria de sodio, de potasio y de GMPc a las 1, 3 y 6 horas. El AT potenció el efecto antidiurético e inhibió completamente la natriuresis, kaliuresis y aumento de la excreción de GMPc, inducidos por la Ang II. Los efectos renales de renina fueron independientes del óxido nítrico ya que el pretratamiento con L-NAME, un inhibidor de la sintasa del óxido nítrico, no alteró la respuesta renal inducida por la administración de renina-ICV. Nuestros resultados apoyan el papel de la oxitocina como efector de la acción natriurética mediada por el sistema renina angiotensina cerebral.