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Reduced renovascular resistance by clonidine.
Clinical Pharmacology and Therapeutics
|November 1, 1979
Summary
Long-term clonidine therapy lowers blood pressure by affecting the renin-angiotensin system, specifically suppressing plasma renin activity (PRA) in supine positions. This impacts renal vascular resistance (RVR) and mean arterial pressure (MAP).
Area of Science:
- Nephrology
- Cardiovascular Pharmacology
- Hypertension Research
Background:
- The acute antihypertensive effect of clonidine is linked to central sympathetic inhibition.
- The long-term mechanisms, particularly concerning renal hemodynamics, remain less understood.
- Antihypertensive treatments can influence renal function and systemic blood pressure.
Purpose of the Study:
- To investigate the impact of long-term clonidine therapy on intrarenal hemodynamics.
- To assess effects on the renin-angiotensin system and sympathetic nervous system activity.
- To elucidate the mechanism of sustained blood pressure reduction by clonidine.
Main Methods:
- Studied 13 patients with essential hypertension undergoing long-term clonidine therapy.
- Monitored mean arterial pressure (MAP) and renal vascular resistance (RVR).
- Assessed plasma renin activity (PRA), renal plasma flow (RPF), renal blood flow (RBF), filtration fraction (FF), and urinary kallikrein excretion (UKA).
Main Results:
- Long-term clonidine therapy decreased MAP and RVR.
- Supine PRA was suppressed, while upright PRA showed no significant change.
- RPF, RBF, FF, and WBV remained unchanged; UKA was also unaffected.
Conclusions:
- Long-term clonidine therapy influences intrarenal hemodynamics and the renin-angiotensin system.
- Suppressed supine PRA appears to play a role in modulating RVR during chronic clonidine treatment.
- These changes are associated with the observed reduction in MAP.