NITRIC-OXIDE MODULATES ARTERIOLAR RESPONSES TO INCREASED SYMPATHETIC-NERVE ACTIVITY

The purpose of this study was to determine whether arteriolar response s to increased sympathetic nerve activity are limited by the actions o f endogenous nitric oxide. Intravital microscopy was used to examine d iameter responses of small feed arteries (SFA), first-order arterioles (1A) and second-order arterioles (2A) to perivascular sympathetic ner ve stimulation in the superfused rat small intestine. Stimulation indu ced a frequency-dependent constriction in all vessel types that was co mpletely abolished by the a-adrenoceptor antagonist phentolamine (10(- 6) M). In SFA and 1A, the magnitude of sympathetic constriction was in creased significantly in the presence of the nitric oxide synthase inh ibitor NG-monomethyl-L-arginine (L-NMMA, 10(-4) M). In SFA (n = 7), st imulation at 3, 8, and 16 Hz induced constrictions of 11 +/- 1, 28 +/- 4, and 42 +/- 3%, respectively, under the normal superfusate vs. 28 /- 3, 46 +/- 5, and 76 +/- 3% in the presence of L-NMR?A. For 1A (n = 7), stimulation induced constrictions of 10 +/- 1, 27 +/- 4, and 37 +/ - 3% under the normal superfusate vs. 24 +/- 2, 47 +/- 3, and 72 +/- 4 % in the presence of L-NMMA. The effect of L-NMMA on sympathetic const riction in SFA (n = 7) was completely reversed by the additional prese nce of 5 x 10(-3) M L-arginine in the superfusate. These results sugge st that endogenous nitric oxide activity can attenuate sympathetic neu rogenic constriction in the intestinal microvasculature.