Abstract
The potent vasodilator nitric oxide (NO), produced mainly by the endothelium, acts through a BKCa-dependent mechanism to increase the frequency of calcium sparks (Ca2+ sparks) in myocyte isolated from rat cerebral arteries. Our present aim has been to assess the role of endogenous and exogenous NO on the Ca2+ 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 Ca2+ sparks in the intact artery. However, inhibition of nitric oxide synthase with N-ω-nitro-l-arginine or removal of endothelium reduced Ca2+ sparks frequency by about 50%. Under these conditions (i.e., absence of endogenous NO production), DEA-NONOate, increased Ca2+ spark frequency 3- to 4-fold. These results suggest that endothelial NO modulates local Ca2+ release events in the arterial smooth muscle and that this mechanism may contribute to the actions of nitrovasodilators. © 2006 Elsevier Inc. All rights reserved.
Original language | English |
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Pages (from-to) | 104-109 |
Number of pages | 5 |
Journal | Nitric Oxide - Biology and Chemistry |
Volume | 16 |
Issue number | 1 |
DOIs | |
Publication status | Published - Feb 2007 |
Keywords
- Calcium sparks
- Cerebral arteries
- Nitric oxide