1. We studied the involvement of pertussis toxin (PTX)-sensitive G-proteins in the sensitivity of arterial constriction to intracellular calcium ([Ca(2+)](i)) mobilization. 2. Vasoconstriction was measured in vitro in perfused, de-endothelialized rat tail arteries loaded with the calcium-sensitive dye, fura-2 and treated or not with PTX (30 - 1000 ng ml(-1)). Arteries were stimulated with noradrenaline (NA, 0.1 - 100 microM) or KCl (15 - 120 mM). 3. KCl elicited a smaller vasoconstrictor response (E(max)=94+/-8 mmHg) than NA (E(max)=198+/-9 mmHg) although [Ca(2+)](i) mobilization was similar (E(max)=123+/-8 and 135+/-7 nM for KCl and NA, respectively). PTX (1000 ng ml(-1)) had no effect on [Ca(2+)](i) mobilization but lowered NA- (but not KCl-) induced vasoconstriction (E(max)=118+/-7 mmHg). 4. G(i/o)-proteins were revealed by immunoblotting with anti-G(i alpha) and anti-G(o alpha) antibodies in membranes prepared from de-endothelialized tail arteries. [alpha(32)P]-ADP-ribosylation of G-proteins by PTX (1000 ng ml(-1)) was demonstrated in the intact rat tail artery (pixels in the absence of PTX: 3150, presence: 25053). 5. In conclusion, we suggest that smooth muscle cells possess a PTX-sensitive G(i)-protein-mediated intracellular pathway which amplifies [Ca(2+)](i) sensitivity of contraction in the presence of agonists such as NA.