Receptor-operated Ca2+ channels were characterized by their ability to decrease steady-state ATP-dependent Ca2+ accumulation into pig aortic microsomes. The vasoconstrictor agents noradrenaline, angiotensin II and adenosine 5′-[alpha beta-methylene]triphosphate (pp[CH2]pA) all decreased Ca2+ accumulation only when sonicated into vesicles (to allow access to receptor sites) and in the presence of guanosine 5′-[beta gamma-imido]triphosphate to activate transducing G-proteins. The effect of noradrenaline was inhibited by the alpha 2 antagonist yohimbine, but not by the alpha 1 antagonist prazosin. The effect of none of the agonists was reversed by diltiazem. SK&F 96365 (an inhibitor of receptor-mediated Ca2+ influx into intact cells) reversed the effect of noradrenaline, but not that of pp[CH2]pA, which suggests that at least two receptor-operated channels may be present in this preparation.
Vasoconstrictor agonists activate G-protein-dependent receptor-operated calcium channels in pig aortic microsomes
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L M Blayney, P W Gapper, A C Newby; Vasoconstrictor agonists activate G-protein-dependent receptor-operated calcium channels in pig aortic microsomes. Biochem J 15 February 1992; 282 (1): 81–84. doi: https://doi.org/10.1042/bj2820081
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