Modulation by β-adrenoceptors and angiotensin II receptors of splanchnic nerve evoked catecholamine release from the adrenal medulla

In the present study, we have evaluated the effect of both facilitatory β2-adrenoceptor and angiotensin II receptor on the release of adrenal catecholamines induced by electrical stimulation of the splanchnic nerve in anaesthetized and vagotomized dog. In these experiments, individual or combined treatments with the β2-adrenoceptor antagonist ICI 118551 (0.3 mg/kg i.v.), the converting enzyme inhibitor captopril (2 mg/kg i.v.), or the angiotensin II receptor antagonist saralasin (2 μg∙kg−1∙min−1 i.v.) were found to significantly decrease the release of adrenal catecholamines during splanchnic nerve stimulation (5-V pulses of 2 ms duration for 3 min at 1 Hz) whatever the order of administration of the drugs. On the other hand, the infusion of angiotensin II (20 ng∙kg−1∙min−1) was shown to potentiate the release of adrenal catecholamines in response to electrical stimulation, and this effect was totally blocked by treatment with saralasin (4 μg kg−1∙min−1 i.v.). This facilitating angiotensin mechanism differed from β-adrenoceptor facilitating mechanism, since following β-blockade with ICI 118551, angiotensin II infusion still significantly potentiated the release of catecholamines during splanchnic nerve stimulation. These observations thus suggest that both facilitating β2-adrenoceptors and angiotensin II receptors can independently modulate the release of adrenal catecholamines.Key words: adrenal catecholamines, β2-adrenoceptors, angiotensin II receptors, adrenal medulla, facilitating sympathetic mechanisms, receptor interactions.