The renin angiotensin system and nociception in spontaneously hypertensive rats

The development of malignant hypertension was studied in stroke-prone spontaneously hypertensive rats (SHR) kept on 1% NaCl as drinking water. Along with salt-loading, blood pressure gradually increased and reached a severe hypertensive level (greater than 230 mmHg), which was followed by increases in urinary protein (greater than 100 (mg/250 g body wt)/day) and plasma renin concentration (PRC, from 18.9 +/- 0.1 to 51.2 +/- 19.4 (ng/ml)/h, mean +/- SD). At this stage, renal small arteries and arterioles showed severe sclerosis and fibrinoid necrosis. Stroke was observed within a week after the onset of these renal abnormalities. The dose of exogenous angiotensin II (AII) producing 30 mmHg rise in blood pressure increased with the elevation of PRC, from 22 +/- 12 to 75 +/- 36 ng/kg, which was comparable to that in rats on water. The fall of blood pressure due to an AII inhibitor, [1-sarcosine, 8-alanine]AII (10(microgram/kg)/min for 40 min) became more prominent with the increase in PRC in salt-loaded rats, but was not detected in rats on water. These findings suggest that the activation of renin-angiotensin system participates in malignant hypertension of salt-loaded stroke-prone SHR rats that show stroke signs, proteinuria, hyperreninemia, and renovascular changes.

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OS 32-02 EFFECTS OF RENIN-ANGIOTENSIN SYSTEM INHIBITORS ON VAGINA AND CARDIAC EXPRESSION OF RAAS COMPONENTS IN FEMALE SPONTANEOUSLY HYPERTENSIVE RATS

Journal of Hypertension ◽

10.1097/01.hjh.0000500997.92798.5f ◽

2016 ◽

Vol 34 (Supplement 1) ◽

pp. e390

Author(s):

Zhao Yang ◽

Ma Ruixin ◽

Yu Jing

Keyword(s):

Spontaneously Hypertensive Rats ◽

Renin Angiotensin System ◽

Hypertensive Rats ◽

Angiotensin System ◽

Spontaneously Hypertensive ◽

Renin Angiotensin

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Effects of AT1 Receptor Blockade on Blood Pressure and the Renin-Angiotensin System in Spontaneously Hypertensive Rats of the Stroke Prone Strain

Clinical and Experimental Hypertension ◽

10.3109/10641969809053215 ◽

1998 ◽

Vol 20 (2) ◽

pp. 205-221 ◽

Cited By ~ 38

Author(s):

Jurgen Wagner ◽

Marek Drab ◽

JÜRgen Bohlender ◽

Kerstin Amann ◽

Wolfgang Wienen ◽

...

Keyword(s):

Blood Pressure ◽

Spontaneously Hypertensive Rats ◽

Renin Angiotensin System ◽

At1 Receptor ◽

Receptor Blockade ◽

Hypertensive Rats ◽

Angiotensin System ◽

Spontaneously Hypertensive ◽

Renin Angiotensin

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Cardiovascular hypertrophy in diabetic spontaneously hypertensive rats: optimizing blockade of the renin–angiotensin system

Clinical Science ◽

10.1042/cs1040341 ◽

2003 ◽

Vol 104 (4) ◽

pp. 341-347 ◽

Cited By ~ 1

Author(s):

Markus LASSILA ◽

Belinda J. DAVIS ◽

Terri J. ALLEN ◽

Louise M. BURRELL ◽

Mark E. COOPER ◽

...

Keyword(s):

Blood Pressure ◽

Systolic Blood Pressure ◽

Calcium Channel ◽

Spontaneously Hypertensive Rats ◽

Renin Angiotensin System ◽

At1 Receptor ◽

Hypertensive Rats ◽

Angiotensin System ◽

Spontaneously Hypertensive ◽

Renin Angiotensin

The aim of the present study was to compare the antihypertrophic effects of blockade of the renin–angiotensin system (RAS), vasopeptidase inhibition and calcium channel antagonism on cardiac and vascular hypertrophy in diabetic spontaneously hypertensive rats (SHR). SHR with streptozotocin-induced diabetes were treated with one of the following therapies for 32 weeks: the angiotensin-converting enzyme (ACE) inhibitor captopril (100mg/kg); the angiotensin AT1 receptor antagonist valsartan (30mg/kg); a combination of captopril with valsartan; the vasopeptidase inhibitor mixanpril (100mg/kg); or the calcium channel antagonist amlodipine (6mg/kg). Systolic blood pressure and cardiac and mesenteric artery hypertrophy were assessed. Mean systolic blood pressure in diabetic SHR (200±5mmHg) was reduced by captopril (162±5mmHg), valsartan (173±5mmHg), mixanpril (176±2mmHg) and amlodipine (159±4mmHg), and was further reduced by the combination of captopril with valsartan (131±5mmHg). Captopril, valsartan and mixanpril reduced heart and left ventricle weights by approx. 10%. The combination of captopril and valsartan further reduced heart weight (-24%) and left ventricular weight (-29%). Amlodipine did not affect cardiac hypertrophy. Only mixanpril and the combination of captopril and valsartan significantly reduced mesenteric weight. The mesenteric wall/lumen ratio was reduced by all drugs, and to a greater extent by the combination of captopril and valsartan. We conclude that optimizing the blockade of vasoconstrictive pathways such as the RAS, particularly with the combination of ACE inhibition and AT1 receptor antagonism, is associated with antitrophic effects in the context of diabetes and hypertension. In contrast, calcium channel blockade, despite similar effects on blood pressure, confers less antitrophic effects in the diabetic heart and blood vessels.

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