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Angiotensin subtype 1 blockade selectively potentiates adenosine subtype 2-mediated vasodilation
G J Smits1, J M Kitzen, M H Perrone
1Rhône-Poulenc Rorer Central Research, Collegeville, Pa. 19426-0107.
Hypertension (Dallas, Tex. : 1979)
|August 1, 1993
Summary
Angiotensin II (AT1 receptor) selectively reduces the blood pressure lowering effects of adenosine A2 receptor activation. Blocking AT1 receptors enhances vasodilation in the kidneys and mesenteric arteries.
Area of Science:
- Cardiovascular Pharmacology
- Renal Physiology
- Vascular Biology
Background:
- Adenosine infusion increases local angiotensin II production.
- Angiotensin II may counteract adenosine's vasodilator effects via A2 receptors.
Purpose of the Study:
- To investigate if angiotensin II (AT1 receptor) attenuates A2 receptor-mediated vasodilation.
- To determine the role of endogenous angiotensin II in regulating adenosine A2 receptor responses.
Main Methods:
- Hemodynamic responses to an A2-selective agonist (DPMA) were measured in rats.
- Angiotensin subtype 1 (AT1) receptor blockade with losartan was employed.
- Responses to nitroglycerin and nifedipine were assessed for specificity.
Main Results:
- Losartan pretreatment potentiated DPMA-induced reductions in renal and mesenteric vascular resistance.
- A greater depressor response was observed with AT1 receptor blockade.
- Losartan did not affect nitroglycerin responses but attenuated nifedipine responses.
- Lowering blood pressure with nitroglycerin did not mimic losartan's potentiation of DPMA effects.
Conclusions:
- Endogenous angiotensin II selectively attenuates A2-mediated vasodilation in renal and mesenteric vasculature.
- This interaction is specific and not due to generalized blood pressure reduction.