Mechanisms in human renovascular hypertension.
To clarify the pathophysiology of renovascular hypertension, we monitored intraarterial pressure continuously and measured hourly hormone levels for 24 hours under carefully controlled conditions in two hypertensive patients with unilateral renal artery occlusion. Comparison of the results with those obtained when the patients were normotensive 3 months after uninephrectomy indicated that, while the renin-angiotensin system played a central role in maintaining the hypertension, the sympathetic nervous system also contributed and, in addition, modulated short-term arterial pressure fluctuations. In the untreated state, the sympathetic regulation of renin secretion was heightened, and angiotensin II/aldosterone dose-responsiveness was augmented. It is suggested that these adaptive changes might serve to offset the tendency to severe sodium depletion and thence exacerbation of the hypertension.
D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D001794:Blood Pressure; D005260:Female; D006801:Humans; D006977:Hypertension, Renal / Q000503:physiopathology*; D006978:Hypertension, Renovascular / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology; D009392:Nephrectomy; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System; D013564:Sympathetic Nervous System / Q000503:physiopathology
D000804:Angiotensin II; D000450:Aldosterone; D012083:Renin