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Inhibition of basal nitric oxide synthesis increases aortic augmentation index and pulse wave velocity in vivo
Author(s) -
Wilkinson Ian B.,
MacCallum Helen,
Cockcroft John R.,
Webb David J.
Publication year - 2002
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1046/j.1365-2125.2002.1528adoc.x
Subject(s) - arterial stiffness , pulse wave velocity , medicine , pulse pressure , blood pressure , mean arterial pressure , cardiology , in vivo , vascular resistance , heart rate , artery , nitric oxide , placebo , ex vivo , anesthesia , biology , pathology , microbiology and biotechnology , alternative medicine
Aims To investigate the role of basal nitric oxide (NO) production in regulating large artery stiffness in vivo . Methods Incremental doses of the NO synthase inhibitor L‐N G ‐monomethyl arginine (LNMMA: 0.1, 0.3, 1.0 and 3.0 mg kg −1 min −1 ) or placebo were infused in eight healthy men. Arterial stiffness was assessed noninvasively by pulse wave analysis. Results Compared with placebo, infusion of LNMMA led to a dose‐dependent increase in mean arterial pressure, peripheral vascular resistance, and aortic and systemic arterial stiffness. There was an accompanying reduction in heart rate and cardiac index. The highest dose of LNMMA resulted in an increase of 25% in AIx (95% confidence limits; 12, 38) and of 16 mmHg in mean arterial pressure (9, 23) compared with infusion of saline. Conclusions These data indicate functional regulation of large artery stiffness in vivo by NO, and may provide new therapeutic strategies for cardiovascular risk reduction.