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

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.

Salt loading produces severe renal hemodynamic dysfunction independent of arterial pressure in spontaneously hypertensive rats

2007 ◽  
Vol 292 (2) ◽  
pp. H814-H819 ◽  
Author(s):  
Luis C. Matavelli ◽  
Xiaoyan Zhou ◽  
Jasmina Varagic ◽  
Dinko Susic ◽  
Edward D. Frohlich
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Plasma Flow ◽  
Spontaneously Hypertensive Rats ◽  
Renal Plasma Flow ◽  
Renal Hemodynamics ◽  
Dietary Salt ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive

We have previously shown that salt excess has adverse cardiac effects in spontaneously hypertensive rats (SHR), independent of its increased arterial pressure; however, the renal effects have not been reported. In the present study we evaluated the role of three levels of salt loading in SHR on renal function, systemic and renal hemodynamics, and glomerular dynamics. At 8 wk of age, rats were given a 4% ( n = 11), 6% ( n = 9), or 8% ( n = 11) salt-load diet for the ensuing 8 wk; control rats ( n = 11) received standard chow (0.6% NaCl). Rats had weekly 24-h proteinuria and albuminuria quantified. At the end of salt loading, all rats had systemic and renal hemodynamics measured; glomerular dynamics were specially studied by renal micropuncture in the control, 4% and 6% salt-loaded rats. Proteinuria and albuminuria progressively increased by the second week of salt loading in the 6% and 8% salt-loaded rats. Mean arterial pressure increased minimally, and glomerular filtration rate decreased in all salt-loaded rats. The 6% and 8% salt-loaded rats demonstrated decreased renal plasma flow and increased renal vascular resistance and serum creatinine concentration. Furthermore, 4% and 6% salt-loaded rats had diminished single-nephron plasma flow and increased afferent and efferent arteriolar resistances; glomerular hydrostatic pressure also increased in the 6% salt-loaded rats. In conclusion, dietary salt loading as low as 4% dramatically deteriorated renal function, renal hemodynamics, and glomerular dynamics in SHR independent of a minimal further increase in arterial pressure. These findings support the concept of a strong independent causal relationship between salt excess and cardiovascular and renal injury.

Renal Hemodynamics during Development of Hypertension in Young Spontaneously Hypertensive Rats

2002 ◽  
Vol 25 (5) ◽  
pp. 322-328 ◽  
Author(s):  
Rolf E.F. Christiansen ◽  
Anca B. Roald ◽  
Olav Tenstad ◽  
Bjarne M. Iversen
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renal Hemodynamics ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Effect of acute unilateral renal denervation on renal hemodynamics in spontaneously hypertensive rats

2008 ◽  
Vol 28 (2-3) ◽  
pp. 87-94 ◽  
Author(s):  
M. H. Abdulla ◽  
M. A. Sattar ◽  
I. M. Salman ◽  
N. A. Abdullah ◽  
O. Z. Ameer ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renal Denervation ◽  
Renal Hemodynamics ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

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.

Sign in / Sign up

Export Citation Format

Share Document