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Volume and vasoconstriction in experimental renovascular hypertension
Federation Proceedings
|June 1, 1982
Summary
Chronic renovascular hypertension can develop without volume expansion or the renin-angiotensin system. However, its pathogenesis requires either salt/fluid retention or the renin-angiotensin vasoconstrictor mechanism.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Hypertension Research
Background:
- Renovascular hypertension involves complex interactions between volume and vasoconstrictor factors.
- Previous theories suggested whole-body autoregulation plays a key role in hypertension development.
Purpose of the Study:
- To analyze the roles of volume expansion and vasoconstrictor factors in experimental renovascular hypertension.
- To determine the essential components for the development and maintenance of chronic renovascular hypertension.
Main Methods:
- Experimental models of one-kidney and two-kidney renovascular hypertension in rats and dogs.
- Manipulation of volume status (salt/water retention) and renin-angiotensin system activity (SQ 14225).
Main Results:
- Volume expansion and increased cardiac output are not essential for chronic one-kidney renovascular hypertension.
- The renin-angiotensin system is not essential for chronic one-kidney renovascular hypertension in dogs or rats.
- In two-kidney hypertension, the angiotensin system's role varies by species and duration.
- Deleting both volume and angiotensin components prevented hypertension in one-kidney rats.
Conclusions:
- Chronic renovascular hypertension pathogenesis requires either volume expansion via renal salt/fluid retention or the renin-angiotensin vasoconstrictor mechanism.
- The relative importance of these factors differs between one-kidney and two-kidney models and across species.