Influence of dietary protein on glomerular angiotensin II-receptor binding in normotensive and spontaneously hypertensive rats

1. The binding of angiotensin II to glomerular receptors was studied in spontaneously hypertensive and normotensive Wistar-Kyoto rats in response to 7, 16 and 32% isocaloric, isonatraemic protein diets. 2. Increased dietary protein elevated the systemic angiotensin II levels of both spontaneously hypertensive and Wistar-Kyoto rats [F0.05(2,26)=4.758, P<0.05; n=36], and this was not associated with changes in either systemic blood pressure or cortical renin activity. 3. Furthermore, no significant changes in the affinity or density of angiotensin II receptors were associated with changes of dietary protein intake in either strain. 4. These results indicate a dissociation between the systemic renin-angiotensin system and the tissue renin -angiotensin system in response to protein intake.

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Involvement of vasopressin and renin-angiotensin system in the vasopressor response to physostigmine in spontaneously hypertensive and Wistar Kyoto rats

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)62490-x ◽

1984 ◽

Vol 36 ◽

pp. 141

Author(s):

Koichiro Kawashima ◽

Yuko Miwa ◽

Kazuko Fujimoto ◽

Atsuko Koike

Keyword(s):

Renin Angiotensin System ◽

Angiotensin System ◽

Spontaneously Hypertensive ◽

Renin Angiotensin ◽

Wistar Kyoto Rats ◽

Wistar Kyoto

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Role of angiotensin II and catecholamines in blood pressure variability responses to stress in SHR

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1996.270.6.r1265 ◽

1996 ◽

Vol 270 (6) ◽

pp. R1265-R1272 ◽

Cited By ~ 6

Author(s):

E. Gaudet ◽

J. Blanc ◽

J. L. Elghozi

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Renin Angiotensin System ◽

Acute Administration ◽

Angiotensin Ii Receptor ◽

Angiotensin System ◽

Spontaneously Hypertensive ◽

Air Jet ◽

Wistar Kyoto

The contribution of the renin-angiotensin system (RAS) and the sympathetic nervous system (SNS) to blood pressure (BP) and heart rate (HR) variability responses to air-jet stress was assessed in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. Activity of the encogenous RAS was suppressed by chronic treatment by a nonpeptide angiotensin II receptor antagonist (Iosartan). The role of alpha 1-adrenoceptor activity was evaluated in rats by acute administration of prazosin. In untreated animals, an air jet induced an increase in systolic BP (SBP; 9 +/- 2 mmHg for WKY and 8 +/- 2 mmHg for SHR) and in HR (56 +/- 19 beats/min for WKY and 76 +/- 8 beats/min for SHR), followed by an increase of the midfrequency (MF; 0.2-0.6 Hz) component of HR in WKY (183%) and by an increase of the MF component of SBP and diastolic BP in SHR (65%). Prazosin prevented BP rises as well as the MF component of BP and HR increases associated with air-jet stress. Chronic suppression of the RAS by losartan did not alter the BP response to the air jet in WKY and slightly reduced it in SHR but abolished all the BP and HR variability changes in both strains. These results indicate that the SNS but not RAS is essential for the BP rise induced by stress and demonstrate that RAS in conjunction with SNS is involved in BP and HR variability changes associated with stress.

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The Intrinsic Brain Iso-Renin-Angiotensin System in the Rat: Its Possible Role in Central Mechanisms of Blood Pressure Regulation

Clinical Science ◽

10.1042/cs048265s ◽

1974 ◽

Vol 48 (s2) ◽

pp. 265s-268s ◽

Cited By ~ 15

Author(s):

D. Ganten ◽

J. S. Hutchinson ◽

P. Schelling

Keyword(s):

Blood Pressure ◽

Cerebrospinal Fluid ◽

Angiotensin Ii ◽

Spontaneously Hypertensive Rats ◽

Renin Angiotensin System ◽

Angiotensin Ii Receptor ◽

Hypertensive Rats ◽

Angiotensin System ◽

Spontaneously Hypertensive ◽

Renin Angiotensin

1. Angiotensin is produced by the intrinsic iso-renin-angiotensin system. 2. Angiotensin is secreted into the cerebrospinal fluid of nephrectomized rats. 3. Angiotensin in cerebrospinal fluid elevates systemic blood pressure. 4. Rats with hereditary diabetes insipidus are virtually non-responsive to intraventricular angiotensin. 5. Angiotensin II is elevated in the cerebrospinal fluid of spontaneously hypertensive rats. 6. An intraventricular perfusion of the angiotensin II receptor-blocking agent P 113 decreases blood pressure in spontaneously hypertensive rats.

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