Role of sulfhydryl groups in aortic responses using N-ethylmaleimide.

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This study examines the effects of N-ethylmaleimide (NEM) 10(-7) M on agonist-induced contraction, and the relaxation following drug washout of vascular smooth muscle (VSM) segments. 45Ca flux, cyclic 3':5'-adenosine-monophosphate (cAMP), and cyclic 3':5'-guanosine-monophosphate (cGMP) were analyzed in an attempt to understand the observed physiological modifications with NEM. Cyclic nucleotides were measured by 125I-radioimmunoassay. Contractile responses to norepinephrine (NE) 5.9 x 10(-7) M, angiotensin II (AT) 9.8 x 10(-8) M, and potassium chloride (KCl) 2.2 x 10(-2) M were significantly depressed when VSM segments were exposed to NEM prior to agonist challenge. An inhibition of relaxation occurred when NEM was added after the development of a maximal contractile response to NE, AT, or KCl. VSM relaxation was significantly inhibited when compared to controls. Altered 45Ca efflux, increased cGMP, and decreased cAMP levels were all associated with an inhibition of relaxation of VSM. These results suggest a regulatory role of sulfhydryl (SH) groups in contraction and relaxation of VSM involving both the control of Ca2+ flux and cAMP and cGMP metabolism.