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Ca(2+)-insensitive vascular protein kinase C during pregnancy and NOS inhibition.
Stimulated mechanisms of Ca2+ entry into vascular smooth muscle during NO synthesis inhibition in pregnant rats.
Interleukin-6 impairs endothelium-dependent NO-cGMP-mediated relaxation and enhances contraction in systemic vessels of pregnant rats.
[Ca(2+)](i) signaling in renal arterial smooth muscle cells of pregnant rat is enhanced during inhibition of NOS.
Pregnancy-associated reduction in vascular protein kinase C activity rebounds during inhibition of NO synthesis.
Low-salt diet enhances vascular reactivity and Ca(2+) entry in pregnant rats with normal and reduced uterine perfusion pressure.
TNF-alpha enhances contraction and inhibits endothelial NO-cGMP relaxation in systemic vessels of pregnant rats.
Enhanced [Ca2+]i in renal arterial smooth muscle cells of pregnant rats with reduced uterine perfusion pressure.
Enhanced vascular reactivity during inhibition of nitric oxide synthesis in pregnant rats.
EMMPRIN-mediated induction of uterine and vascular matrix metalloproteinases during pregnancy and in response to estrogen and progesterone.
Downregulation of microvascular endothelial type B endothelin receptor is a central vascular mechanism in hypertensive pregnancy.