scholarly journals Effects of voluntary exercise on blood pressure, angiotensin II, aldosterone, and renal function in two-kidney, one-clip hypertensive rats

2017 ◽  
Vol Volume 10 ◽  
pp. 41-51 ◽  
Author(s):  
Brian M Waldman ◽  
Robert A Augustyniak ◽  
Haiping Chen ◽  
Noreen F Rossi
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Angiotensin Ii ◽  
Voluntary Exercise ◽  
Hypertensive Rats

Antihypertensive and renal effects of cilazapril and their reversal by angiotensin in renovascular hypertensive rats

1988 ◽  
Vol 74 (4) ◽  
pp. 365-372 ◽  
Author(s):  
Yu-An Ding ◽  
Shin-Tsu Chang ◽  
Shyh-Ming Shieh ◽  
Wann-Chu Huang
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Fractional Excretion ◽  
Hypotensive Effect ◽  
Hypertensive Rats ◽  
Renal Effects ◽  
Angiotensin Iii ◽  
Excretion Rates

1. The antihypertensive and renal effects of cilazapril, a new angiotensin converting enzyme inhibitor, were evaluated in both two-kidney, one-clip Goldblatt hypertensive rats (n = 11) and normotensive rats (n = 6). 2. Intravenous infusion of cilazapril (1 mg/kg followed by 25 μg min−1 kg−1) caused significant reductions of blood pressure from 163 ± 3 to 122 ± 4 mmHg and from 157 ± 2 to 113 ± 3 mmHg in two separate groups of hypertensive rats and from 124 ± 1 to 105 ± 2 mmHg in normotensive rats. The hypotensive effect in terms of absolute value or percentage change was greater in hypertensive rats than in normotensive rats (41 ± 6 vs 20 ± 3 mmHg or 25 ± 4% vs 16 ± 2%, respectively). 3. Cilazapril increased glomerular filtration rate, urine flow, and absolute and fractional excretion rates of sodium and potassium in the non-clipped kidney of hypertensive rats. In contrast, the clipped kidney exhibited a depressed renal function during cilazapril infusion. 4. In normotensive rats, the hypotensive and enhanced renal function responses to cilazapril were much less than those of the non-clipped kidney of hypertensive rats. 5. Superimposed administration of either angiotensin II or angiotensin III during cilazapril infusion completely reversed the blood pressure and bilateral renal responses of cilazapril in both hypertensive and normotensive rats. 6. These results indicate that cilazapril reduces arterial pressure and enhances renal excretion mainly via inhibition of angiotensin II and angiotensin III formation.

Effect of chronic NG-nitro-L-arginine methyl ester (L-NAME) on blood pressure and renal function in conscious uninephrectomized spontaneously hypertensive rats

1998 ◽  
Vol 76 (1) ◽  
pp. 63-67 ◽  
Author(s):  
María Reverte ◽  
Olga Flores ◽  
Belén Gallego ◽  
Antonio Lestón ◽  
José Miguel López-Novoa
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Renal Function ◽  
Methyl Ester ◽  
Spontaneously Hypertensive Rats ◽  
Low Dose ◽  
Potassium Excretion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Sodium And Potassium

We have studied during 30 days the effect of a low dose of NG-nitro-L-arginine methyl ester (1 mg ·kg-1 ·day-1 in drinking water) in the presence of D- or L-arginine (1 mg ·kg-1 ·day-1 in drinking water) in comparison with D- or L-arginine alone on blood pressure and renal function in conscious uninephrectomized female spontaneously hypertensive rats. At the end of the study, there was a significant increase in systolic blood pressure in the NG-nitro-L-arginine methyl ester + D-arginine group (307 ± 6 mmHg (1 mmHg = 133.3 Pa), n = 14, p << 0.05) in comparison with NG-nitro-L-arginine methyl ester + L-arginine (281 ± 6 mmHg, n = 14), L-arginine (262 ± 5 mmHg, n = 13), and D-arginine (258 ± 7 mmHg, n = 12) groups. There were no changes in diuresis, proteinuria, or sodium and potassium excretion between differently treated animals during this study. These results suggest that in uninephrectomized female spontaneously hypertensive rats, after 1 month blockade of NO synthesis with a low dose of NG-nitro-L-arginine methyl ester, vasculature is under tonic control by NO and it is not correlated with renal dysfunction.Key words: Key words: NG -nitro-L-arginine methyl ester (L-NAME), kidney, hypertension, spontaneously hypertensive rats, renaldysfunction, uninephrectomy.

Abstract 7: Angiotensin II Type 2 Receptor Deficiency Increases Renal ACE/ACE2 Ratio-Ang II-AT1R Expression In Male but not in Female Mice

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Quaisar Ali ◽  
Yonnie Wu ◽  
Tadashi Inagami ◽  
Tahir Hussain
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Angiotensin Ii ◽  
Renin Activity ◽  
Ang Ii ◽  
Male And Female ◽  
Female Mice ◽  
Gender Specific

Angiotensin II acting via Angiotensin II type 2 receptors (AT2Rs) is believed to be protective against blood pressure increase and affects renal function under pathophysiological condition. Recently we have observed that stimulation of AT2Rs in male obese Zucker rats has shifted the two opposing arms of renin angiotensin system (RAS) i.e. ACE-Ang II-AT1 vs ACE2/Ang-(1-7)-Mas. Evidence suggests that estrogen regulates RAS, including AT2R in female mice. We hypothesized that AT2R has a gender specific regulation of RAS. In the present study, we investigated the role of AT2Rs in regulating RAS components in male and female mice. Kidney cortex from AT2R knockout (AT2RKO) male and female mice and wild type (WT) with similar background (C57BL/6) of 20 weeks of age were used in the study. The cortical ACE expression (ng ACE/μg tissue) was significantly increased in AT2RKO mice (3±0.02) compared to WT males (1.9±0.02). LC/MS analysis of cortical tissue revealed that Ang II was also significantly increased in AT2RKO mice (WT: 31±3, AT2RKO: 47±3 fmoles/mg tissue). Deletion of AT2R significantly increased AT1R (204%, 204 of 100) expression and had no effect on renin activity compared to WT males. The cortical expression of ACE2 activity (WT: 113±8, AT2RKO: 40±11, RFU/min), Ang-(1-7) levels (WT: 7.3±1.4, AT2RKO: 3±0.8 fmoles/mg tissue) and Mas receptor (AT2RKO: 54±15, % of WT) was significantly decreased in AT2RKO males compared to WT. The cortical expression of the AT2R and MasR was 2-fold greater in WT females compared to WT male. The renin activity (WT: 32±2, AT2RKO: 21±0.3, RFU/min) and MasR expression (WT: 187.5±55, AT2KO: 47±9) was significantly decreased in AT2RKO females compared to the female WT. Interestingly, Ang-(1-7) level (WT: 5.7±0.7, AT2RKO 2.6±0.7 fmoles/mg tissue) was decreased but no changes in ACE or ACE2 activity was observed in AT2KO females compared to their WT, suggesting a role of non-ACE2 pathway. This study suggests that AT2R regulates ACE/ACE2 ratio-Ang II-AT1R expression negatively only in males, whereas in females, it regulates Ang-(1-7) potentially via non-ACE2 pathway. Such changes indicate a gender specific mechanisms potentially associated with AT2R-mediated regulation of renal function and blood pressure control.

Renin content and excretory function of the kidney in rats with experimental hypertension

1962 ◽  
Vol 202 (4) ◽  
pp. 795-799 ◽  
Author(s):  
H. Brunner ◽  
P. A. Desaulles ◽  
D. Regoli ◽  
F. Gross
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Renal Hypertension ◽  
Experimental Hypertension ◽  
Elevated Blood ◽  
Hypertensive Rats ◽  
Excretory Function ◽  
Contralateral Kidney ◽  
Ligation Of The Ureter ◽  
Renin Content

To determine relationship between kidney renin content and excretory function, rats with renal hypertension induced by unilateral clamping of the renal artery were given an oral load of 3 ml of 0.9% saline/100 g body wt. Excretion of the saline load was accelerated in rats with renal hypertension as well as in animals with hypertension due to overdosage with cortexone and salt, provided that the loading experiment was made 3–4 weeks after hypertension was established, but not when animals had been hypertensive for 11–14 weeks. Renin concentration was markedly reduced in the unclamped kidney and also in the kidney of the rats overdosed with cortexone and salt. Excreting capacity of the clamped kidney was compared with that of the unclamped kidney, after removal or after functional elimination of the contralateral kidney, by ligation of the ureter, 3, 24, and 48 hr after the operation. In all experiments excretion of saline load by the unclamped kidney was more rapid than by the clamped kidney, but the highest values were reached in the presence of a functional clamped kidney. Only in rats with elevated blood pressure was the load more rapidly excreted than in normal rats, but hypertension alone cannot be the only factor responsible, the excretion not being accelerated in unilaterally nephrectomized hypertensive rats. Although these hint at a connection between the renin concentration and renal function the nature of this relationship remains uncertain.

High-potassium diet attenuates salt-induced acceleration of hypertension in SHR

1991 ◽  
Vol 260 (1) ◽  
pp. R21-R26 ◽  
Author(s):  
Y. Sato ◽  
K. Ando ◽  
E. Ogata ◽  
T. Fujita
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
High Potassium ◽  
Spontaneously Hypertensive ◽  
Antihypertensive Action ◽  
High K ◽  
Wistar Kyoto ◽  
Renal Vascular

We studied the effects of K supplementation (8% KCl) for 4 wk on blood pressure (BP), Na space, and renal hemodynamics in 5-wk-old, spontaneously hypertensive rats (SHR) or age-matched Wistar-Kyoto rats (WKY) eating normal-NaCl (0.66%) or high-NaCl (8%) diet. In WKY, high-Na and/or high-K diets had no effects on BP. In SHR, Na load accelerated the development of hypertension, whereas K supplementation did not affect BP of normal-Na SHR but attenuated the increase in BP with Na load. Correspondingly, Na load in SHR significantly increased renal vascular resistance (RVR), and K supplementation attenuated the increased RVR of Na-loaded SHR. Moreover, Na space of SHR was increased compared with that of WKY, and although Na load did not affect Na space, K supplementation tended to decrease Na space in SHR. These results indicate that 9-wk-old SHR is relatively volume-expanded compared with age-matched WKY, and K supplementation could improve the lowered slope of the pressure-Na excretion relationship in SHR, resulting in maintenance of Na balance. Thus the data suggest that changes in RVR, which might be intimately related to renal function for Na excretion, contribute to both salt sensitivity of SHR and antihypertensive action of K supplementation in Na-loaded SHR.

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