Enhancement of blood pressure response to dopamine by angiotensin II

The interaction of dopamine and angiotensin II (AII) on blood pressure and heart rate was studied in rats. The influence of reserpine pretreatment and vagotomy was also studied. Inbred rats anesthetized with urethane received intravenous (i.v.) doses of 50, 100, 200, or 400 micron g (per 100 g body weight) of dopamine HCI, before and after a single i.v. dose of 0.025 micron g of AII. The same doses of dopamine were tested in vagotomized rats and in rats pretreated with reserpine. The effect of dopamine alone on blood pressure was biphasic, since 16 of 38 rats showed an early fall followed by a later rise. The early fall decreased significantly with the dose and was absent with the highest dose tested (400 micron g). The late rise was observed in all experiments, and it increased significantly with the dose. Parallel to hypotension, a decrease of heart rate was observed, but both phenomena appeared not to be linked by a sauce-effect relationship. Vagotomy prevented both hypotension and bradycardia induced by dopamine. Angiotensin II inhibited the early fall and increased the late rise of blood pressure induced by dopamine but had no effect on the bradycardia. Reserpine retreatment prevented the hypotensive and enhanced the hypertensive response to dopamine, and in this situation dopamine induced cardiac arrhythmia. The interaction between dopamine and AII is inhibited by pretreatment with reserpine. The early hypotensive phase and bradycardia caused by dopamine appeared to be the consequence of a vagal reflex.