Bradykinin caused graded contractions of rings of rabbit aorta and jugular vein with EC M values of 13 /xM and 2.2 nM. In denuded preparations, responses of bradykinin in jugular vein but not in aorta were potentiated 1,000-fold. Both preparations bathed in calcium-free solution showed markedly depressed responses to bradykinin, but addition of 1 mM EGTA further inhibited bradykinin responses only in aorta. Time-course experiments carried out in calciumfree solution plus EGTA revealed that

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... kinin contractions in rabbit aorta were very sensitive to extracellular calcium, whereas responses of the jugular vein depended on both extracellular and intracellular calcium sources. Responses to bradykinin in both tissues were unaffected by nicardipine (1 /AM) but were partially antagonized by NiCl 2 (0.1-0.3 mM) . Ryanodine (30 /AM) incubated in calcium-free medium markedly inhibited jugular vein responses to bradykinin but had no effect on aortic responses. Phorbol ester (1 /iM) caused a slow tonic contraction in jugular vein but not in aorta and inhibited bradykinin responses in the former preparation. Staurosporine (1-100 nM) and l-(5-isoquinolinesulfonyl)-2-methylpiperizine (H-7, 3 and 10 fiM) caused a dose-dependent inhibition of bradykinin-induced contractions in jugular vein but were less effective in aorta. We concluded that 1) contractions of rabbit aorta and jugular vein are largely dependent on external calcium and are insensitive to nicardipine but inhibited by NiCl 2 , a T-type calcium channel antagonist; 2) responses of jugular vein to bradykinin appear to require mobilization of an intracellular calcium source rather than calcium influx, as this response is very sensitive to ryanodine; and 3) responses of jugular vein but not rabbit aorta to bradykinin appear to involve activation of protein kinase C. {Hypertension 1992;19[suppl n]:II-87-II-93)