Exogenous No-derived No Regulation Of Vascular Smooth Muscle Cell Ion Channels And Intracellular Ca (2 +) Concentration

Vascular function is controlled by vasoactive agents synthesized and released by the vascular endothelium. NO has been identified as an endothelium-dericed relaxing factor(EDRF)which, in vascular smooth muscle, stimulates the soluble enzyme guanylate cyclase and increase cGMP.There are several mechanisms hypothesized to account for NO-mediated relaxation of vascular smooth muscle and cGMP exists in key position. Howerver, based on the free radical charicteristic of NO and the effect on different targets; the vasodilative mechanism of NO should be a compicted physiological question. Also, there are differently functional characteristie and different responses to some vascular activities on different vascular segment, it is important to study the electric-physiological basis of vascular individulization. Using single channel and whole-cell recording techniques, combined with Fura-2/AM techniques, we studied on the effects of exogenous NO and induced relaxing NO on K⁺ ,Ca²⁺ channels, Ca²⁺-releasing channels and [Ca²⁺], and a possible non-NO-cGMP pathway is hypothesized.We also report that a spontaneous inward cation chammel in vascular smooth muscle cells.1. Single channel K_ca currents were recorded in cell-attached mode in dispersed single smooth muscle cells of the rat tail artery. Under asymmetric K⁺ condition (126/5.6mmol/l), K_ca currents with two kinds of conductances were recorded at a series of testing voltages.The single channel conductance were 151.0±13.7ps(n=5)and 73.1±11.9pS(n=9), respectively, and their reversal potential were near 5mV.2. In cell-attached patches, a: K_cawas activated by exgenous N0(n=8). b: NP_owas increased by NO from (4.53±0.71)% to (40.9±5.09)% (p<0.01; HP=-60mV). c: In addition, K_ca was activated transiently by NO, the...