ENDOTHELIUM-DERIVED NITRIC-OXIDE LIMITS SYMPATHETIC NEUROGENIC CONSTRICTION IN INTESTINAL MICROCIRCULATION

We have recently shown that endogenous nitric oxide (NO) activity can attenuate the sympathetic neurogenic constriction of intestinal arteri oles. The purpose of this study war; to determine whether the microvas cular endothelium is an important site of NO production under these co nditions. In the superfused small intestine of the rat, intravital mic roscopy was used to study the responses of first-order arterioles (IA) to perivascular sympathetic nerve stimulation and directly applied no repinephrine before and then after passage of a CO2 embolus through th e 1A lumen to inhibit endothelial function. CO2 embolization did not s ignificantly alter resting arteriolar diameter (50 +/- 4 mu m before v s. 51 +/- 4 mu m after embolization) but abolished the dilator respons e to acetylcholine without altering the dilator response to sodium nit roprusside. Stimulation at 3, 8, and 16 Hz caused respective constrict ions of 4 +/- 1, 11 +/- 1, and 18 +/- 2 mu m, and after CO2 these resp onses were significantly increased to 9 +/- 1, 18 +/- 1, and 29 +/- 3 mu m, respectively. Exposure to the nitric oxide synthase inhibitor N- G-monomethyl-L-arginine(10(-4) M io superfusate) after CO2 embolizatio n had no further effect on the magnitude of neurogenic constriction. S imilar results were seen when embolization was achieved with N-2, and CO2 embolization had the same effect on norepinephrine-induced constri ction as it did on neurogenic constriction. These results suggest that nitric oxide of endothelial origin can attenuate sympathetic neurogen ic constriction in the intestinal microvasculature.