Participation of prostaglandins and bradykinin in the effects of angiotensin II and converting enzyme-inhibition on sympathetic neurotransmission in vivo

Acta Physiologica Scandinavica
J SchwielerP Hjemdahl

Abstract

We investigated the mechanism(s) by which angiotensin converting enzyme (ACE)-inhibition and angiotensin (Ang) II influence peripheral sympathetic neurotransmission in canine gracilis muscle in situ, with alpha-adrenoceptors either intact or irreversibly blocked by phenoxybenzamine. ACE-inhibition by ramiprilat reduced, and subsequent infusion of Ang II (30 ng kg-1 min-1 i.v.) markedly increased arterial plasma Ang-(1-8)octapeptide levels, basal muscle perfusion pressures and mean arterial pressure. Local intra-arterial bolus injection of Ang II caused marked vasoconstriction followed by vasodilation. This vasoconstrictor response was enhanced and the ensuing vasodilation was abolished following prostaglandin synthesis inhibition by diclofenac. The vasoconstrictor response to low frequency (0.5 Hz) sympathetic nerve stimulation was also enhanced by diclofenac. The nerve stimulation-evoked noradrenaline (NA) overflow was reduced by ramiprilat when alpha-adrenoceptors were blocked (-11 +/- 3%, P < 0.05), but increased when alpha-adrenoceptors were intact (+28 +/- 14%, P < 0.05). During ACE-inhibition, effective bradykinin receptor antagonism by HOE 140 reduced stimulation-evoked NA overflow irrespective of alpha-adrenoceptor bloc...Continue Reading

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Citations

Feb 1, 1997·Acta Physiologica Scandinavica·T KahanP Hjemdahi
Jul 30, 1999·Journal of Clinical Neurophysiology : Official Publication of the American Electroencephalographic Society·C M MichelM Seeck
Jun 11, 1999·Japanese Journal of Pharmacology·A DendorferP Dominiak
Apr 3, 2013·European Journal of Pharmacology·Rakesh B PatelMukul R Jain
Nov 8, 2001·Canadian Journal of Physiology and Pharmacology·J L Lavoie, L Béliveau
Sep 2, 1998·The American Journal of Physiology·I D CallowJ M Arnold

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