Connexin expression is not altered in omental resistance vessels from women with preeclampsia.

OBJECTIVE: To compare connexin expression in omental resistance arteries from preeclamptic women and normal gravidas. METHODS: Small arteries (approximately 200-400 microm i.d.) were dissected from omental fat biopsies, taken at cesarean delivery from normotensive and preeclamptic women. Vessels were frozen and homogenized, then connexin-43 protein was detected by Western blot and quantitated by comparison with alpha-actin. RESULTS: Connexin-43 was detected in all specimens, primarily in its phosphorylated form. Abundance did not differ between vessels from preeclamptic and normotensive gravidas. CONCLUSIONS: Phasic activity in omental resistance vessels from preeclamptic women likely depends on abnormal genesis of an oscillatory signal rather than on more extensive gap junctional communication between vascular cells.

Possible role of P-450-derived metabolites in endothelium-dependent relaxation of rat small mesenteric arteries.

We reported previously that acetylcholine (ACh)-induced endothelium-dependent relaxation of rat mesenteric microvessels depended both on nitric oxide (NO) and on a charybdotoxin (CTX)-sensitive endothelium-derived hyperpolarizing vasodilator. Cytochrome P450 (CYP)-dependent arachidonic acid metabolites act in some systems as hyperpolarizing vasodilators. We sought to quantitate contributions of such metabolites to the CTX-sensitive component of ACh-induced vasodilation in isolated rat mesenteric resistance arteries. ACh relaxed these vessels nearly completely (93.3+/-1.2%, n = 71); cyclooxygenase inhibition with indomethacin did not diminish this response (94.3+/-11.4%, n = 9). NO synthase inhibition with Nitro-L-arginine (NNLA) reduced relaxation by 30% (n = 54, p<0.05). Pretreatment of vessels with CYP inhibitors, either clotrimazole (CTM) or 17-octadecynoic acid (17-ODYA), or with selective K+ channel inhibitors, either tetraethyammonium acetate (TEA) or CTX, each led to similar small reductions in maximal relaxation (17%, 22%, 16%, and 9% respectively, n = 3-6). Combined pretreatment with NNLA + either (CTM or 17-ODYA) or (TEA or CTX) each led to similar maximal relaxations (52.2+/-4.8%, 50.6+/-9.2, 37.6+/-8.6%, and 44.1+/-11.5%, respectively, n = 6-35; p<0.05 for NNLA+[CTM or TEA or CTX] vs NNLA alone). Combined pretreatment with NNLA+CTM+(CTX or TEA) led to similar maximal relaxations (43.0+/-7.3%, 43.7+/-15%, n = 6-11) that did not differ from values in vessels pretreated with either NNLA+CTM or NNLA+(CTX or TEA). We conclude that the ACh-induced vasodilation was insensitive to cyclooxygenase inhibition, partially sensitive to NO synthase inhibition, and that the K+ channel blockers TEA and CTX identified the same minor component of ACh relaxation as did the CYP inhibitor CTM.