Prostanoids, but not nitric oxide, counterregulate angiotensin II mediated vasoconstriction in vivo.

To evaluate the modulating effects of nitric oxide and prostanoids during angiotensin II-mediated vasoconstriction, male Wistar rats (n=25) were infused with increasing doses of angiotensin II following pretreatment with the cyclooxygenase inhibitor indomethacin, the nitric oxide-synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) plus sodium nitroprusside to restore mean arterial blood pressure, or saline. Hemodynamics were studied with the radioactive microsphere method. Indomethacin did not alter systemic or regional hemodynamics. L-NAME+sodium nitroprusside reduced cardiac output, as well as systemic and renal vascular conductance. Angiotensin II increased mean arterial blood pressure and heart rate, and decreased systemic vascular conductance as well as vascular conductance in gastrointestinal tract, kidney, skeletal muscle, skin, mesentery+pancreas, spleen and adrenal. Indomethacin enhanced the angiotensin II-mediated effects in all vascular beds, whereas L-NAME+sodium nitroprusside enhanced its effect in mesentery+pancreas only. In conclusion, vasodilator prostanoids, but not nitric oxide, counterregulate angiotensin II-mediated vasoconstriction in vivo.