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 loaed with the calcium-sensitive dye, fura-2 and treated or not with PTX (30 ± 1000 ng ml 71 ). Arteries were stimulated with noradrenaline (NA, 0.1 ± 100 mM) 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 71 ) had no e ect 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 ia and anti-G oa antibodies in membranes prepared from de-endothelialized tail arteries. [a 32 P]-ADP-ribosylation of G-proteins by PTX (1000 ng ml 71 ) 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 ampli®es [Ca 2+ ] i sensitivity of contraction in the presence of agonists such as NA.

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