Atriopeptin II caused endothelium-independent relaxation and cGMP accumulation in bovine intrapulmonary artery but not vein, without involving soluble guanylate cyclase.
Atriopeptin II selectively relaxes arterial smooth muscle and stimulates cGMP accumulation independently of endothelial cells and soluble guanylate cyclase.
Atriopeptin II, a 23-amino acid synthetic peptide fragment of atrial natriuretic factor, caused an endothelium-independent relaxation of isolated precontracted rings of bovine intrapulmonary artery that was accompanied by the concomitant accumulation of guanosine 3',5'-cyclic monophosphate (cGMP) but not adenosine 3',5'-cyclic monophosphate. In contrast, rings of intrapulmonary vein were unaffected by atriopeptin II whether or not endothelium was present. Whereas methylene blue, an inhibitor of soluble guanylate cyclase, abolishes endothelium-dependent and independent arterial relaxation and cGMP accumulation in response to acetylcholine and glyceryl trinitrate, respectively, methylene blue failed to alter these responses to atriopeptin II. Similarly, the effects of atriopeptin II were unaltered by propranolol, indomethacin, or atropine. These results indicate that relaxation elicited by atriopeptin II may be selective for arterial smooth muscle receptors, does not require endothelial cells, and does not involve the soluble form of guanylate cyclase, although cGMP accumulation is stimulated.
Ignarro et al. (1986) studied this question. Atriopeptin II was evaluated on Arterial relaxation and cGMP accumulation. Atriopeptin II caused endothelium-independent relaxation and cGMP accumulation in bovine intrapulmonary artery but not vein, without involving soluble guanylate cyclase.