Abstract

Interaction between the renin-angiotensin system and the sympathetic nervous system has been proposed to be like a physiological regulation mechanism. The present work was designed to study the cross talk between angiotensin II and adrenergic receptors on the smooth muscle contractile response and the endothelium influence in this phenomenon. Homologous and endothelium independent desensitization of angiotensin II-contractile response was observed. Treatment with noradrenaline between two cumulative doses response curves (CDRC) to angiotensin II caused a rightward shift of the second CDRC in unrubbed arteries and increased the maximal response in rubbed arteries. Prazosin blocked these effects. No homologous desensitization of noradrenaline contractile response was found. Treatment with angiotensin II between two CDRC to noradrenaline caused a loss of affinity in the second CDRC in unrubbed arteries. Losartan was able to avoid this phenomenon. Maximal response was enhanced both in arteries with and without endothelium treated or not with angiotensin II. Results demonstrate homologous and endothelium-independent desensitization of the contractile response to angiotensin II but not to noradrenaline. In addition, heterologous and endothelium-dependent desensitization induced by noradrenaline and angiotensin II on the contractile response to each other was found. Furthermore, results provided the first evidence that there is an endothelium-dependent cross talk between alpha1-adrenergic and angiotensin II receptors in smooth muscle of rabbit aorta.

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