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 (EC 30% = 5 n m ), 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 (EC 30% = 1.54 n m ), 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.British Journal of Pharmacology (1998) 124 , 1207–1212; doi: 10.1038/sj.bjp.0701959