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This Article Full Text Full Text (PDF) All Versions of this Article: 290/5/H1826    most recent 00938.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Hataishi, R. Articles by Ichinose, F. Search for Related Content PubMed PubMed Citation Articles by Hataishi, R. Articles by Ichinose, F.

Inhaled nitric oxide does not reduce systemic vascular resistance in mice

¹Department of Anesthesia and Critical Care and ²Cardiovascular Research Center, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts

Submitted 1 September 2005 ; accepted in final form 11 November 2005

Inhaled nitric oxide (NO) is a highly selective pulmonary vasodilator. It was recently reported that inhaled NO causes peripheral vasodilatation after treatment with a NO synthase (NOS) inhibitor. These findings suggested the possibility that inhibition of endogenous NOS uncovered the systemic vasodilating effect of NO or NO adducts absorbed via the lungs during NO inhalation. To learn whether inhaled NO reduces systemic vascular resistance in the absence of endothelial NOS, we studied the systemic vascular effects of NO breathing in wild-type mice treated without and with the NOS inhibitor N-nitro-L-arginine methyl ester and in NOS3-deficient (NOS3^–/–) mice. During general anesthesia, the cardiac output, left ventricular function, and systemic vascular resistance were not altered by NO breathing at 80 parts/million in both genotypes. Breathing NO in air did not alter blood pressure and heart rate, as measured by tail-cuff and telemetric methods, in either awake wild-type mice (whether or not they were treated with N-nitro-L-arginine methyl ester), or in awake NOS3^–/– mice. Our findings suggest that absorption of NO or adducts during NO breathing is insufficient to cause systemic vasodilation in mice, even when endogenous endothelial NO production is congenitally absent.

peripheral vasodilation; endothelial nitric oxide synthase; telemetry; tail cuff

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