C-PROTEINS IN RAT-BLOOD VESSELS .2. ASSESSMENT OF FUNCTIONAL INVOLVEMENT

1. In this study, we compared G-protein-mediated contractile responses of rat aorta and mesenteric artery rings induced by the alpha-adrenoc eptor agonist, norepinephrine (NE) and by the direct G-protein activat or, sodium fluoride, using various probes. 2. Activator of the stimula tory G-protein (G(s)), cholera toxin (CT), attenuated the sensitivity and maximum contractile response of both aorta and mesenteric artery t o NE and sodium fluoride. The effect of the toxin on the NE-sensitivit y was greater in mesenteric artery. 3. Pretreatment of tissues with th e inhibitor of G(i)-protein, pertussis toxin (PT), reduced the sensiti vity as well as maximum contraction of both the aorta and mesenteric a rtery to sodium fluoride, and of the mesenteric artery to NE. PT atten uated only the sensitivity but not the maximum contraction of the aort a to NE. The inhibitory effect of PT on sensitivity to NE or sodium fl uoride was greater in the aorta. 4. NE and sodium fluoride-induced con tractions were reduced by the sulfhydryl G-protein inhibitor, N-ethylm aleimide (NEM) in both blood vessels. NEM produced greater inhibitory effect on the sensitivity of the aorta to both contractile agents. 5. These data demonstrate that CT, PT and MEM-sensitive G-proteins are in volved in NE- and sodium fluoride-induced contractile responses of the rat aorta and mesenteric artery. The differential effects of the G-pr otein probes indicate that certain variations in G-protein-mediated co ntractile responses exist among the two blood vessels, suggesting that G-protein involvement in functional responses may vary with the type of blood vessel investigated.