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SKELETAL MUSCLE ARTERIOLAR CONSTRICTION TO VASOPRESSIN AND ANGIOTENSIN II IS DEPENDENT ON PROTEIN KINASE C ACTIVATION
Author(s) -
Fleming John T,
Kulenovic Elvedin,
Falcone Jeff C,
Dholakia Jaydev N
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.20.5.lb10-c
Subject(s) - protein kinase c , vasopressin , calphostin c , skeletal muscle , endocrinology , cremaster muscle , medicine , staurosporine , vasoconstriction , calphostin , constriction , angiotensin ii , vascular smooth muscle , chemistry , arteriole , microcirculation , biology , phosphorylation , biochemistry , receptor , smooth muscle
Arginine vasopressin (AVP) and angiotensin II (ANG II) regulate systemic vascular resistance and regional blood flow by virtue of their potent constrictor effects. In skeletal muscle, ANG II elicits a significant, but brief constriction of arterioles, whereas AVP causes a long‐lasting contraction. PKC is known to mediate the effects of both agonists in cultured smooth muscle cells and isolated, pressurized skeletal muscle arterioles. We investigated the role of PKC to mediate constriction of in vivo skeletal muscle arterioles in response to both agonists. Male Sprague Dawley rats were anesthetized and the intact cremaster muscle was exteriorized and outstretched in a pH‐ and temperature‐controlled bath for visualization of the microcirculation using in vivo television microscopy. The constriction of third‐order arterioles to Ang II or AVP was quantified before and after treatment with PKC inhibitors (Calphostin C, staurosporine or bisindolylmaleimide I). Cremaster muscle PKC activity was measured. Staurosporine and bisindolylmaleimide I (BIM) inhibited PKC activity by >75% and inhibited arteriolar constriction to both agonists. Calphostin C failed to inhibit PKC activity or arteriolar constriction to either agonist. Thus PKC activation plays a significant role in the transient constriction elicted by Ang II and the sustained response to AVP in intact skeletal muscle arterioles.