Different receptors for angiotensin II at pre- and postjunctional level of the canine mesenteric and pulmonary arteries

1 This investigation was undertaken to compare pre- and postjunctional receptors involved in the responses of the canine mesenteric and pulmonary arteries to angiotensin II. 2 In the mesenteric artery, angiotensin II caused an enhancement of tritium overflow evoked by electrical stimulation (EC30% = 5 nM), the maximal effect representing an increase by about 45%. Postjunctionally, angiotensin II caused concentration-dependent contractions (pD(2) = 8.57). Saralasin antagonized both pre- and postjunctional effects of angiotensin II, but it was more potent at post- than at prejunctional level (pA(2) of 9.51 and 8.15, respectively), while losartan antagonized exclusively the postjunctional effects of angiotensin II (pA(2) = 8.15). PD123319 had no antagonist effect either pre- or postjunctionally. 3 In the pulmonary artery, angiotensin II also caused an enhancement of the electrically-evoked tritium overflow (EC30% = 1.54 nM), its maximal effect increasing tritium overflow by about 80%. Postjunctionally, angiotensin II caused contractile responses (pD(2) = 8.52). As in the mesenteric artery, saralasin antagonized angiotensin II effects at both pre- and postjunctional level and it was more potent postjunctionally (pA(2) of 9.58 and 8.10, respectively). Losartan antagonized only the postjunctional effects of angiotensin II (pA(2) = 7.96) and PD123319 was ineffective. 4 It is concluded that in both vessels: (1) pre- and postjunctional receptors belong to a different subtype, since they are differently antagonized by the same antagonists; (2) postjunctional receptors belong to AT(1) subtype. since they are blocked by losartan but not by AT(2) antagonists; (3) prejunctional receptors apparently belong to neither AT(1) or AT(2) subtype since they are blocked by neither AT(1) nor AT(2) antagonists.