The major functional α1-adrenoceptor in the rat aorta is of the α1Dsubtype and that in the caudal artery is of the α1Asubtype. In the present study, the participation of protein kinase C (PKC) and Rho kinase (RhoK) in contractile responses to stimulation of the α1-adrenoceptors in these two arteries was investigated. Both the PKC inhibitor Ro-318220 and the RhoK inhibitor Y-27632 significantly blocked contractile responses of the aorta to phenylephrine (PE) and the selective α1A-adrenoceptor agonist A61603. When used in combination, the inhibitors had an additive blocking effect. In the caudal artery, Y-27632 but not Ro-318220 inhibited contractile responses to PE and A61603, and, in combination, the antagonism produced was no greater than that by Y-27632 alone. Contractile responses to direct activation of PKC with phorbol 12,13-dibutyrate were much smaller and levels of CPI-17 (PKC-activated protein phosphatase inhibitor of 17 kDa) were much lower in the caudal artery than the aorta. The results suggest that both PKC and RhoK contribute independently to contractile responses to stimulation of α1D-adrenoceptors in the aorta. However, RhoK, but not PKC, participates in contractile responses to stimulation of α1A-adrenoceptors in the caudal artery. This difference may largely be due to differences between the two arteries in the extent to which PKC participates in contraction.Key words: vascular smooth muscle, α1-adrenoceptors, protein kinase C, rho kinase, phenylephrine.
Differential roles of rho‐kinase and protein kinase C (PKC) in contractile responses of rat aorta and mesenteric artery
