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Angiotensin II Increases Catecholamine Release from Bovine Adrenal Medulla but Does Not Enhance That Evoked by K + Depolarization or by Carbachol
Author(s) -
Powis D. A.,
O'Brien K. J.
Publication year - 1991
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1991.tb06339.x
Subject(s) - adrenal medulla , catecholamine , medicine , endocrinology , saralasin , angiotensin ii , carbachol , chromaffin cell , depolarization , chemistry , angiotensin receptor , biology , receptor , stimulation
: The effect of angiotensin II on catecholamine release from bovine adrenal medulla has been investigated. In retrogradely perfused, isolated bovine adrenal glands, angiotensin II increased basal efflux of catecholamines, but the presence of angiotensin II did not increase the release of catecholamines evoked either by bolus injections of the secretogogue carbachol or by depolarization with a perfusing solution containing a raised concentration of K + . In chromaffin cells maintained in primary tissue culture, angiotensin II increased 3 H release from cells preloaded with [ 3 H]‐noradrenaline but did not enhance the release evoked by carbachol or by depolarization with K + . The increase in 3 H release evoked by angiotensin II from chromaffin cells in tissue culture was inhibited by its analogue antagonist Sar 1 ,Ala 8 ‐angiotensin II (saralasin) and was entirely dependent on the presence of Ca 2+ in the experimental medium. These findings suggest that, in the chromaffin cells of the bovine adrenal medulla, angiotensin II acts on specific receptors to cause a calcium‐dependent catecholamine release but triggers no additional response that acts synergistically with depolarizing or nicotinic stimuli to augment catecholamine release.