NITRIC OXIDE-DEPENDENT AND NITRIC OXIDE-INDEPENDENT NOREPINEPHRINE RELEASE IN RAT MESENTERIC-ARTERIES

The role of nitric oxide (NO) in endogenous norepinephrine (NE) releas e in the perfused isolated rat mesenteric vasculature was examined. NE overflow elicited by electrical field stimulation (EFS) at various fr equencies was significantly smaller at 24 than at 37 degrees C. The pr esser 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 stimulati on was diminished by 50% at 37 degrees C but remained unchanged at 24 degrees C, whereas the presser 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 do nor, increased EFS-elicited NE overflow at 24 degrees C but had no eff ect at 37 degrees C. These results demonstrate that NE release is NO d ependent and NO independent. The NO-dependent mechanism is more sensit ive 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.