The potent vasodilator nitric oxide (NO), produced mainly by the endothelium, acts through a BK(Ca)-dependent mechanism to increase the frequency of calcium sparks (Ca(2+) sparks) in myocyte isolated from rat cerebral arteries. Our present aim has been to assess the role of endogenous and exogenous NO on the Ca(2+) sparks through ryanodine-sensitive channels in the sarcoplasmic reticulum of an intact artery. Calcium sparks, detected with fluo-4 and laser scanning confocal microscopy, were examined in isolated pressurized rat posterior cerebral arteries with (intact) and without endothelium (denuded). Addition of the NO donor, DEA-NONOate (N-(2-aminoethyl)-N-(2-hydroxy-2-nitrosohydrazino)-1,2-ethylenediamine), did not change the amplitude and frequency of Ca(2+) sparks in the intact artery. However, inhibition of nitric oxide synthase with N-omega-nitro-L-arginine or removal of endothelium reduced Ca(2+) sparks frequency by about 50%. Under these conditions (i.e., absence of endogenous NO production), DEA-NONOate, increased Ca(2+) spark frequency 3- to 4-fold. These results suggest that endothelial NO modulates local Ca(2+) release events in the arterial smooth muscle and that this mechanism may contribute to the actions of nitrovasodilators.

Effect of endogenous and exogenous nitric oxide on calcium sparks as targets for vasodilation in rat cerebral artery

MANDALA', Maurizio;
2007

Abstract

The potent vasodilator nitric oxide (NO), produced mainly by the endothelium, acts through a BK(Ca)-dependent mechanism to increase the frequency of calcium sparks (Ca(2+) sparks) in myocyte isolated from rat cerebral arteries. Our present aim has been to assess the role of endogenous and exogenous NO on the Ca(2+) sparks through ryanodine-sensitive channels in the sarcoplasmic reticulum of an intact artery. Calcium sparks, detected with fluo-4 and laser scanning confocal microscopy, were examined in isolated pressurized rat posterior cerebral arteries with (intact) and without endothelium (denuded). Addition of the NO donor, DEA-NONOate (N-(2-aminoethyl)-N-(2-hydroxy-2-nitrosohydrazino)-1,2-ethylenediamine), did not change the amplitude and frequency of Ca(2+) sparks in the intact artery. However, inhibition of nitric oxide synthase with N-omega-nitro-L-arginine or removal of endothelium reduced Ca(2+) sparks frequency by about 50%. Under these conditions (i.e., absence of endogenous NO production), DEA-NONOate, increased Ca(2+) spark frequency 3- to 4-fold. These results suggest that endothelial NO modulates local Ca(2+) release events in the arterial smooth muscle and that this mechanism may contribute to the actions of nitrovasodilators.
artery; calcium signals; Nitric oxide
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11770/129999
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