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Regulation of a1‐adrenoceptor‐mediated contractions of the uterine artery by PKC in pregnant sheep
Author(s) -
Zhang Hongying,
Zhang Lubo
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.a1173-c
Subject(s) - phenylephrine , medicine , protein kinase c , endocrinology , uterine artery , contraction (grammar) , activator (genetics) , phorbol , pregnancy , uterine contraction , circulatory system , gestation , vasoconstriction , uterus , receptor , biology , blood pressure , signal transduction , microbiology and biotechnology , genetics
Little is known about the adaptation of contractile mechanisms of uterine arterial smooth muscle to pregnancy. We hypothesize that PKC plays an important role in the regulation of α 1 ‐adrenoceptor‐mediated contractions of the uterine artery and their adaptation to pregnancy. Uterine arteries were isolated from pregnant ewes (~140 days gestation). α 1 ‐adrenoceptor‐mediated contractions were measured with increasing concentrations of phenylephrine (PE) in half‐log increments in the absence or presence of the PKC activator phorbol 12, 13‐dibutyrate (PDBu) and/or PKC inhibitor GF‐109203X (GF). PE produced dose‐dependent contractions of uterine arteries. PDBu (0.3 and 1 μM) significantly decreased pD 2 value and maximum contraction (E max ) induced by PE. GF itself (0.1, 0.3, 1 μM) markedly decreased pD 2 value and E max induced by PE in a dose dependent pattern. However, treatment with PDBu and 1 μM GF significantly increased pD 2 and E max as compared with PDBu treatment alone without GF. These results suggest that activation of PKC plays an inhibitory role in the regulation of α 1 ‐adrenoceptor‐mediated contraction of the uterine arteries during late pregnancy, which is likely to be important in the adaptation of α 1 ‐adrenoceptor‐mediated contractions to pregnancy. (Supported in part by NIH grants HL57787 and HD 31226)