ArticleThe Journal of physiology1998
Nitric oxide lowers the calcium sensitivity of tension in the rat tail artery.
Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 26 citations in OpenAlex.
- Potassium channel-mediated NO-induced vasodilation during maturation: Dominance of Kv7 channels.FASEB bioAdvances · 2025Article
- Endothelial γ-glutamyltransferase contributes to the vasorelaxant effect of S-nitrosoglutathione in rat aorta.PloS one · 2012Article
- Cellular mechanisms of nitric oxide-induced relaxation of corporeal smooth muscle in the guinea-pig.The Journal of physiology · 2002Article
- Urocortin relaxes rat tail arteries by a PKA-mediated reduction of the sensitivity of the contractile apparatus for calcium.British journal of pharmacology · 2001Article
- Relaxation to authentic nitric oxide and SIN-1 in rat isolated mesenteric arteries: variable role for smooth muscle hyperpolarization.British journal of pharmacology · 2001Article
- Pertussis toxin-sensitive G(i)-proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery.British journal of pharmacology · 2000Article
- Effects of chronic and acute aminoguanidine treatment on tail artery vasomotion in ageing rats.British journal of pharmacology · 2000Article
- Action of a NO donor on the excitation-contraction pathway activated by noradrenaline in rat superior mesenteric artery.The Journal of physiology · 2000Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Controversy exists as to whether a fall in the intracellular Ca2+ concentration ([Ca2+]i) is a requisite element of the vasodilatory response to nitric oxide (NO). 2. We studied the effect of NO on the coupling between [Ca2+]i and vasoconstriction in arterial segments loaded with the [Ca2+]i-sensitive, intracellular dye fura-2. As data interpretation is equivocal when fura-2 is loaded into both endothelial and smooth muscle cells, we compared results from in vitro experiments on segments of the rat tail artery in which fura-2 and noradrenaline were applied on the luminal or adventitial side, and endothelium was removed 'physically' (rubbing or air) or 'functionally' (Nomega-nitro-L-arginine methyl ester). The use of air perfusion to remove endothelium is of considerable benefit since it allows paired observations in a single tissue. 3. Fura-2 loaded into endothelial cells but endothelial 'contamination' of the smooth muscle cell [Ca2+]i signal was minimal. 4. Endogenous NO decreased vasoconstrictor responses to noradrenaline but had no effect on [Ca2+]i. 5. Nitroglycerine decreased vasoconstrictor responses in a concentration-dependent fashion but had no effect on [Ca2+]i. 6. In conclusion, NO causes vasodilatation via a mechanism which is downstream of [Ca2+]i mobilization.
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