In pig renal arteries, angiotensin II enhances neuronal noradrenaline release and contraction, while dopamine exerts a subsequent inhibitory effect mediated by DA2-receptors.
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May inform renal sympathetic modulation studies; leaves open translational relevance in human renovascular disease.
Electrical stimulation of pig renal arteries causes contractions which are potentiated in the presence of angiotensin II (5 x 10(-8) M). 2. The potentiation is followed by a long-lasting inhibitory phase which is mimicked by dopamine and 2-amino-6,7,dihydroxy-1,2,3,4,-tetrahydronaphthalene (ADTN), but blocked by sulpiride (5 x 10(-8) M). 3. Release of noradrenaline from renal artery rings by 25 mM K+ was measured by h.p.l.c. and found to be increased by 5 x 10(-8) M angiotensin II. As this was done in the presence of 1 x 10(-6) M desmethylimipramine it was concluded that the increase was due to increase neuronal release of noradrenaline, not inhibition of neuronal uptake. 4. The experiments indicate that dopamine is present in the artery wall and produces its effects through DA2-receptors.
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Ferguson et al. (1989) studied this question.
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