title: Nitric oxide decreases [Ca2+]i in vascular smooth muscle by inhibition of the calcium current.
abstract: Endothelium derived relaxing factor (nitric oxide, or NO) activates cytoplasmic guanylate cyclase in vascular smooth muscle and decreases vascular tone through cGMP-dependent mechanisms that are not yet understood fully. In cultured vascular smooth muscle cells (A7r5 cell line) sodium nitroprusside (NP), a vasodilator that decomposes into nitric oxide, lowered [Ca2+]i in cells in which [Ca2+]i was elevated after depolarization. NP decreased current through voltage-gated calcium channels, but did not affect release of calcium from intracellular stores. Hemoglobin, a scavenger of NO, reversed the effect of NP on [Ca2+]i and 8-Br-cGMP, a membrane permeant form of cGMP, mimicked the effect of NP on [Ca2+]i and on calcium currents. Thus, the signal transduction mechanism of endothelium dependent relaxation of vascular smooth muscle involves a decrease in [Ca2+]i by inhibition of Ca2+ entry. Relaxation or vasodilation would then result from decreased activity of myosin light chain kinase, in addition to myosin light chain dephosphorylation.
authors.affiliation: Department of Physiology, University of Maryland School of Medicine, Baltimore.
authors.forename: L A
authors.initials: LA
authors.lastname: Blatter
authors.forename: W G
authors.initials: WG
authors.lastname: Wier
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002460:Cell Line; D006152:Cyclic GMP / Q000494:pharmacology*; D006454:Hemoglobins / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D009569:Nitric Oxide / Q000502:physiology*; D009599:Nitroprusside / Q000494:pharmacology*; D051381:Rats; D015398:Signal Transduction
chemical_list: D006454:Hemoglobins; D009599:Nitroprusside; D009569:Nitric Oxide; D006152:Cyclic GMP; D002118:Calcium