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Nitric Oxide‐Mediated Vasodilatory Effect Of Atrial Natriuretic Peptide In Forearm Vessels Of Healthy Humans
Author(s) -
Sugamori Takashi,
Ishibashi Yutaka,
Shimada Toshio,
Sakane Takeshi,
Takahashi Nobuyuki,
Ohata Shuzo,
Kodani Nobuhiro,
Kunizawa Yoshitsugu,
Inoue Shinichi,
Ohta Yoko,
Nakamura Ko,
Shimizu Hiromi,
Katoh Harumi,
Murakami Yo
Publication year - 2002
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2002.03597.x
Subject(s) - atrial natriuretic peptide , medicine , nitric oxide , vasodilation , forearm , endocrinology , omega n methylarginine , plethysmograph , endothelium , arginine , natriuretic peptide , chemistry , nitric oxide synthase , heart failure , anatomy , biochemistry , amino acid
SUMMARY 1. The aim of the present study was to determine whether the vasorelaxant effect of atrial natriuretic peptide (ANP) is, in part, endothelium dependent in humans. 2. We used veno‐occlusive plethysmography to measure forearm blood flow (FBF) during intra‐arterial infusions of ANP (4, 8, 16, 32 pmol/min per dL forearm tissue volume) before and after the inhibition of nitric oxide (NO) synthesis by N G ‐monomethyl‐ L ‐arginine ( L ‐NMMA; 100 μ mol) in seven normal healthy subjects. 3. Atrial natriuretic peptide caused a dose‐dependent increase in FBF both before and after L ‐NMMA and significantly reduced the plasma concentration of angiotensin (Ang) II. Administration of L ‐NMMA significantly diminished the increase in FBF in response to ANP infusion ( P < 0.05). 4. These results suggest that the forearm vasodilatative response to ANP is modulated, in part, by an endothelium‐derived NO‐mediated mechanism associated with a decrease in AngII caused by ANP.