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Characterization of Local Vascular Effects of the Nitric Oxide Inhibitor NG‐Monomethyl‐L‐Arginine on Dorsal Hand Veins
Author(s) -
Schindler Christoph,
Leuschner Sven,
Schwanebeck Uta,
Kirch Wilhelm
Publication year - 2012
Publication title -
the journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.92
H-Index - 116
eISSN - 1552-4604
pISSN - 0091-2700
DOI - 10.1177/0091270011406277
Subject(s) - omega n methylarginine , nitric oxide , phenylephrine , medicine , vein , endothelium , nitric oxide synthase , anesthesia , pharmacology , blood pressure
Infusion of NG‐monomethyl‐L‐arginine (L‐NMMA; 6.4 μmol/min) into hand veins can cause a 20% increase in vein size in specific subjects. This study explored potential underlying mechanisms in healthy male participants. Ten healthy male participants received in phenylephrine (PE)‐preconstricted veins a dose‐response curve (DRC) to L‐NMMA (0.2–6.4 μmol/min) without and with coinfusion of the endothelium‐dependent dilator histamine, a DRC to L‐arginine with and without coinfusion of L‐NMMA, a DRC to NG‐monomethyl‐D‐arginine (D‐NMMA), and a DRC to L‐NMMA in prostaglandin F 2α ‐(PGF 2α )–preconstricted veins. Participants were classified as L‐NMMA responders (R) and nonresponders (NR). Infusion of L‐NMMA resulted in a maximum venodilation of 38% ± 11% (R) versus 10% ± 5% (NR; P = .005). In PGF 2α ‐preconstricted veins, L‐NMMA caused venodilation to 26% ± 34% (NS) in responders. Results suggest that endothelial nitric oxide synthase‐mediated formation of nitric oxide (NO) from L‐NMMA in doses >3.2 μmol/min and continuous PE‐induced α‐adrenergic stimulation resulting in release of very small amounts of NO from L‐NMMA contribute to the observed L‐NMMA‐induced increase in vein size. Venous reactivity to L‐NMMA resulting in a phenotype as R or NR is most likely genetically predetermined, which requires further study.

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