Nitric oxide-dependent and -independent norepinephrine release in rat mesenteric arteries

• Published in: The American journal of physiology Vol. 272; no. 1 Pt 2; p. H207
• Main Authors: Yamamoto, R, Wada, A, Asada, Y, Yanagita, T, Yuhi, T, Niina, H, Sumiyoshi, A, Kobayashi, H, Lee, T J
• Format: Journal Article
• Language: English
• Published: United States 01.01.1997
• Subjects: Animals; Arginine - pharmacology; Cold Temperature; Electric Stimulation; Enzyme Inhibitors - pharmacology; In Vitro Techniques; Male; Mesenteric Arteries - metabolism; Nitric Oxide - physiology; Nitroarginine - pharmacology; Nitroprusside - pharmacology; Norepinephrine - metabolism; Perfusion; Pressure; Rats; Rats, Sprague-Dawley
• ISSN: 0002-9513
• DOI: 10.1152/ajpheart.1997.272.1.H207

The role of nitric oxide (NO) in endogenous norepinephrine (NE) release in the perfused isolated rat mesenteric vasculature was examined. NE overflow elicited by electrical field stimulation (EFS) at various frequencies was significantly smaller at 24 than at 37 degrees C. The pressor response upon EFS at 8 and 10 Hz, however, was higher at 24 than at 37 degrees C. When production of NO was blocked by N omega-nitro-L-arginine (L-NNA), NE overflow upon EFS at each frequency of stimulation was diminished by 50% at 37 degrees C but remained unchanged at 24 degrees C, whereas the pressor response elicited by EFS became greater at 37 than at 24 degrees C. These effects of L-NNA were reversed by L-arginine, but not by its D-enantiomer. Sodium nitroprusside, an NO donor, increased EFS-elicited NE overflow at 24 degrees C but had no effect at 37 degrees C. These results demonstrate that NE release is NO dependent and NO independent. The NO-dependent mechanism is more sensitive to cooling than the NO-independent mechanism. The increase in EFS-elicited perfusion pressure at 24 degrees C may be due to reduction in synthesis of NO (a potent vasodilator), thus unmasking the effect of NE and other noncatecholamine vasoconstrictors.