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Atriopeptin II‐induced relaxation of rabbit aorta is potentiated by M&B 22,948 but not blocked by haemoglobin
Author(s) -
Martin William,
Morgan Robert O.,
Smith Jerry A.,
White David G.
Publication year - 1986
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1986.tb11156.x
Subject(s) - vasodilation , endocrinology , medicine , chemistry , aorta , long term potentiation , stimulation , receptor , atrial natriuretic peptide , biochemistry , biology
1 We examined the effects of haemoglobin (which inhibits the vascular responses to stimulation of soluble guanylate cyclase) and of M&B 22,948 (which selectively inhibits cyclic GMP phosphodiesterase) on the relaxation induced in rabbit aorta by the atrial natriuretic peptide, atriopeptin II (which stimulates particulate guanylate cyclase). 2 Pretreatment with M&B 22,948 (100 μM) produced a 2.3 fold potentiation of atriopeptin II‐induced relaxation of endothelium‐denuded rings of rabbit aorta. 3 Pretreatment with haemoglobin (10 μM) had no effect on the relaxation or the 10.9 fold increase in cyclic GMP content induced by atriopeptin II in endothelium‐denuded rings of rabbit aorta. 4 The potentiation by M&B 22,948 suggests a causal role for cyclic GMP in mediating atriopeptin II‐induced vasodilatation of rabbit aorta. 5 The inability of haemoglobin to block the atriopeptin II‐induced rise in cyclic GMP suggests that it does not block stimulation of particulate guanylate cyclase. Thus, it is unlikely that a ferrous haem‐containing receptor site is involved in the activation of the particulate form of guanylate cyclase as it is with soluble guanylate cyclase.