Open AccessAtrial natriuretic factor elicits an endothelium-independent relaxation and activates particulate guanylate cyclase in vascular smooth muscle.
Author(s) -
Raymond J. Winquist,
Elizabeth P. Faison,
Scott A. Waldman,
Karen Schwartz,
Ferid Murad,
Robert M. Rapoport
Publication year - 1984
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.81.23.7661
Subject(s) - sodium nitroprusside , medicine , vasodilation , endocrinology , gucy1a3 , gucy1b3 , vascular smooth muscle , chemistry , atrial natriuretic peptide , npr1 , guanylate cyclase , nitric oxide , phosphodiesterase , phosphodiesterase 3 , npr2 , endothelium derived relaxing factor , natriuretic peptide , endothelium , guanylate cyclase 2c , enzyme , biochemistry , biology , smooth muscle , heart failure
A 26 amino acid synthetic peptide fragment of atrial natriuretic factor (ANF) relaxed isolated rabbit aortic segments in which the endothelium was either intact or functionally destroyed. The relaxations were temporally associated with increases in levels of cGMP with no change in the levels of cAMP. The ANF-induced increases in cGMP were also observed in aortic segments pretreated with calcium-free buffer or the cGMP phosphodiesterase inhibitor M&B 22,948. Qualitatively similar results were obtained for sodium nitroprusside. ANF selectively activated particulate guanylate cyclase, having no effect on the soluble form of the enzyme. Thus, the direct (endothelium-independent) vasodilator effect of ANF may be mediated via increased tissue levels of cGMP. ANF appears to increase vascular cGMP levels by activation of particulate guanylate cyclase.