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Differential roles of rho‐kinase and protein kinase C (PKC) in contractile responses of rat aorta and mesenteric artery
Author(s) -
Budzyn Klaudia,
Paull Michelle,
Marley Philip D,
Sobey Christopher G
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a662-b
Subject(s) - protein kinase c , rho associated protein kinase , vasoconstriction , contraction (grammar) , phenylephrine , endocrinology , medicine , mesenteric arteries , stimulation , kinase , biology , artery , microbiology and biotechnology , blood pressure
Rho‐kinase and protein kinase C (PKC) have each been shown to mediate vasoconstriction via calcium sensitization in response to G protein‐coupled receptor (GPCR) stimulation. However, the relative contributions of rho‐kinase and PKC to vascular contraction, and whether their roles vary between large and small blood vessels, are not well understood. We therefore assessed the relative roles of rho‐kinase and PKC in mediating vascular contraction in isolated rings of aorta (Ao), superior mesenteric artery (MA) and second order branches of the superior mesenteric artery (BMA), from male Sprague‐Dawley rats. We tested the effects of the rho‐kinase inhibitor, Y‐27632 (1μM), and the PKC inhibitor, Ro 31‐8220 (5μM) either alone or in combination, on contractile responses to phenylephrine (PE). Maximum responses of Ao and MA to PE were reduced by Y‐27632 ( n =3‐10; P <0.05), whereas responses of BMA were unaffected. Ro 31‐8220 partly reduced contractile responses to PE in Ao and MA ( n =3‐10; P <0.05). Responses of BMA were completely abolished by Ro 31‐8220 ( n =6‐7; P <0.05), and endothelial removal did not alter this effect. Co‐treatment with Y‐27632 and Ro 31‐8220 abolished contractile responses in all arteries. Thus, contractile responses of Ao and MA to PE can involve both rho‐kinase and PKC, to varying degrees. In BMA, PKC appears to exclusively mediate these contractile responses, with no apparent role for rho‐kinase.