Renin-angiotensin system in stroke-prone 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.
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004032:Diet; D006973:Hypertension / Q000235:genetics*; D006974:Hypertension, Malignant / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D051381:Rats; D012083:Renin / Q000097:blood*; D012504:Saralasin / Q000494:pharmacology; D012965:Sodium Chloride / Q000008:administration & dosage; D014655:Vascular Resistance
D000804:Angiotensin II; D012965:Sodium Chloride; D012083:Renin; D012504:Saralasin