Effect of calcitonin on mechanisms of urine formation and sodium excretion in hormotensive and spontaneously hypertensive rats

1991 ◽  
Vol 111 (2) ◽  
pp. 128-130 ◽  
Author(s):  
V. B. Brin ◽  
Z. T. Tsabolova
Keyword(s):  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Urine Formation

Stimulating effects of atenolol on vasodepressor prostaglandin generation in spontaneously hypertensive rats

1991 ◽  
Vol 81 (s25) ◽  
pp. 499-507 ◽  
Author(s):  
Nobuhito Hirawa ◽  
Yoshio Uehara ◽  
Atsushi Numabe ◽  
Satoru Takada ◽  
Hiroaki Matsuoka ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Blood Pressure Reduction ◽  
Vascular Wall ◽  
Urinary Sodium Excretion ◽  
Prostaglandin Synthesis ◽  
Dependent Manner ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

1. To assess the role of the vasodepressor prostaglandin system in the antihypertensive properties of β-adrenoceptor antagonist, we investigated the alterations of prostaglandin generation in the kidney and in the aorta when spontaneously hypertensive rats were treated with atenolol for 2 weeks. 2. The blood pressure reduction was associated with an increase in urinary sodium excretion and urinary prostaglandin E2 excretion. The sodium excretion was positively related to the prostaglandin E2 excretion. 3. Basal release of prostaglandin E2 from the sliced renal cortex was enhanced by the atenolol treatment. Prostacyclin-generating capacity in the aortic wall was also significantly increased. 4. Atenolol treatment stimulated prostaglandin synthesis in the kidney and vascular wall in a dose-dependent manner. However, atenolol per se did not directly stimulate prostaglandin synthesis in the vascular wall. 5. Inhibition of prostaglandin generation by a cyclo-oxygenase inhibitor, indomethacin, was associated with attenuation of the antihypertensive effects of atenolol. 6. Thus these data indicate that sub-chronic atenolol treatment stimulates vasodepressor prostaglandin generation in the kidney and in the aortic vessels, and this shares the antihypertensive effects of this drug with the mechanism of β-adrenergic antagonism probably mediated through vasorelaxation and natriuresis.

scholarly journals Effects of Renal Sympathectomy on Renal Hemodynamics and Sodium Excretion in Spontaneously Hypertensive Rats

1988 ◽  
Vol 29 (4) ◽  
pp. 563-563
Author(s):  
Jiro Kubota ◽  
Shinichiro Kubo ◽  
Hikaru Nishimura ◽  
Masakuni Ueyama ◽  
Keishiro Kawamura
Keyword(s):  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Renal Hemodynamics ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Effects of dopamine on urinary sodium excretion in spontaneously hypertensive rats

1989 ◽  
Vol 30 (4) ◽  
pp. 593-593
Author(s):  
Yoko Jo ◽  
Takuzo Hano ◽  
Hideki Nishio ◽  
Kenji Ueshima ◽  
Masahiko Shiotani ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Renal hemodynamics and sodium excretion in stroke-prone spontaneously hypertensive rats

1981 ◽  
Vol 241 (3) ◽  
pp. F244-F249 ◽  
Author(s):  
A. Nagaoka ◽  
M. Kakihana ◽  
M. Suno ◽  
K. Hamajo
Keyword(s):  
Arterial Pressure ◽  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Renal Perfusion ◽  
Renal Hemodynamics ◽  
Hypertensive Rats ◽  
Water Excretion ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Renal Vascular

Renal blood flow (RBF), renal vascular resistance (RVR), glomerular filtration rate (GFR), and sodium and water excretion were measured in anesthetized stroke-prone spontaneously hypertensive rats (SHRSP), spontaneously hypertensive rats (SHR), and control Wistar-Kyoto rats (WKY) at 9 wk of age. Mean arterial pressure in SHRSP and SHR was significantly higher than that in WKY. RBF was slightly increased in SHR and decreased in SHRSP. RVR was markedly elevated only in SHRSP. In both strains of SHR, GFR was significantly increased but water and sodium excretion were similar. When renal perfusion pressure in both strains of SHR was reduced to a level similar to that of WKY by aortic constriction, RBF was slightly but significantly reduced in both SHRSP and SHR, and GFR only in SHRSP. RVR in SHRSP was still higher. Sodium and water excretion were markedly decreased in both SHR and SHRSP. The data suggest that SHRSP are characterized by an alteration in renal hemodynamics at a young age and support the hypothesis that kidneys of SHR require a higher arterial pressure than kidneys of WKY to excrete a given amount of salt and water.

Chronic hydralazine treatment alters the acute pressure–natriuresis curve in young spontaneously hypertensive rats

1991 ◽  
Vol 69 (2) ◽  
pp. 164-169 ◽  
Author(s):  
Robert L. Kline ◽  
Graham P. McLennan
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Renal Artery ◽  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Artery Pressure ◽  
Fractional Sodium Excretion ◽  
Pressure Natriuresis

The pressure–natriuresis relationship was studied in anesthetized, 7- to 9-week-old control spontaneously hypertensive rats (SHR) and in SHR that had been treated with hydralazine (20 mg∙kg−1∙day−1 in drinking water) starting at 4–5 weeks of age. To minimize reflex changes in kidney function during changes in renal artery pressure, neural and hormonal influences on the kidney were fixed by surgical renal denervation, adrenalectomy, and infusion of a hormone cocktail (330 μL∙kg−1∙min−1) containing high levels of aldosterone, arginine vasopressin, hydrocortisone, and norepinephrine dissolved in 0.9% NaCl containing 1% albumin. Changes in renal function were measured using standard clearance techniques, while renal artery pressure was varied between 136 ± 1 and 186 ± 2 mmHg (1 mmHg = 133.32 Pa) in control SHR (n = 10) and between 113 ± 1 and 162 ± 2 mmHg in treated SHR (n = 11). Mean arterial pressure (+SE) under Inactin anesthesia was 172 ± 3 mmHg in control SHR and 146 ± 3 mmHg in treated SHR (p < 0.05). Where renal artery pressure overlapped between groups, there were no significant differences in glomerular filtration rate. Renal blood flow was also similar in both groups, although at 160 mmHg blood flow was slightly but significantly reduced in treated SHR. Urine flow and total and fractional sodium excretion increased similarly with increases in renal artery pressure in both groups, but the pressure–natriuresis curve in hydralazine-treated SHR was displaced to the left along the pressure axis. The data indicate that chronic administration of hydralazine in young SHR enhances fractional sodium excretion, suggesting that tubular reabsorption of sodium is decreased by hydralazine.Key words: renal function, volume loading, sodium excretion.

Abnormal pressure-diuresis-natriuresis response in spontaneously hypertensive rats

1985 ◽  
Vol 248 (2) ◽  
pp. F199-F205 ◽  
Author(s):  
R. J. Roman ◽  
A. W. Cowley
Keyword(s):  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Fourfold Increase ◽  
Renal Perfusion Pressure ◽  
Wistar Kyoto

The renal responses to changes in perfusion pressure (RPP) were studied in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) to determine whether an abnormality in the pressure-diuresis phenomenon could be involved in the resetting of kidney function in hypertension. Differences in the neural and endocrine background to the kidneys were minimized by denervating the kidney and by holding plasma vasopressin, aldosterone, corticosterone, and norepinephrine levels constant by intravenous infusion. In WKY, increasing renal perfusion pressure 54 mmHg, from 103 to 157 mmHg, produced a ninefold increase in urine flow and sodium excretion with no measurable change in renal blood flow (RBF) or glomerular filtration rate (GFR). In SHR, increasing renal perfusion pressure 54 mmHg, from 133 to 187 mmHg, produced only a fourfold increase in urine flow and sodium excretion. GFR, RBF, and peritubular capillary pressures were well autoregulated and were similar in the SHR and WKY at pressures above 110 mmHg. These results indicate the presence of intrinsic changes in the kidney of SHR that enhance fractional tubular reabsorption and impair the pressure-diuresis response. This blunting of the renal pressure-diuresis phenomenon in SHR may represent the functional resetting of the kidney that is necessary for sustained hypertension.

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