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To investigate the endothelial dependence of angiotensin II(A II)-induced responses in the systemic and pulmonary arterial system of acute renal hypertensive rats of 2-kidney, 1-ligation type (RHRs), A II-induced vasocontractile and pressor effects were evaluated in isolated arteries and in vivo, respectively. A II dose-dependently contracted intact thoracic aorta and pulmonary artery (Emax: 40% at 10-7M and 80% at 3 X 10-8M, respectively) from normotensive rats(NRs), which was significantly increased by removal of endothelial cells or pretreatment with EDRF inhibitors. In NRs, A II increased mean systemic and pulmonary arterial pressure(33 and 5.6mmHg at 0.1mcg/kg, respectively), the effect being significantly increased (P<0.01) by L-NAME(30mg/kg, i.v.). However, A II-induced contraction of intact thoracic aorta and pulmonary artery(Emax : 33% at 10-7M and 93% at 3 X 10-8M, respectively) from RHRs were not changed after endothelial function was disrupted as above; similarly, pressor effects of A II on the systemic and pulmonary arterial pressure in RHRs did not altered by L-NAME. A II tachyphylactic responses for intact thoracic aorta from NRs and RHRs(65 and 87% at 10-8M, respectively) were greater than those for pulmonary artery(19 and 19% at 10-8M, respectively). Distruption of endothelial function significantly (P<0.01) depressed A II tachyphylaxis for thoracic aorta, but not for pulmonary artery. These results suggest that vascular reactivity to A II is not altered in RHRS, and it is greater for pulmonary arterial system than for systemic arterial system. A II reactivity is EDRF-dependent in both arterial systems of NRs, but EDRF-independent for RHRS. Finally, EDRF is one of the major factors underlying A II tachyphylaxis for thoracic aorta, but not for pulmonary artery.
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