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(Hypertension. 2002;40:491.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Exogenous Angiotensin II Does Not Facilitate Norepinephrine Release in the Heart

Thomas W. Lameris; Sandra de Zeeuw; Dirk J. Duncker; Gooitzen Alberts; Frans Boomsma; Pieter D. Verdouw; Anton H. van den Meiracker

From the Department of Internal Medicine (T.W.L., G.A., F.B., A.H.v.d.M.) and Experimental Cardiology, Thoraxcenter (S.d.Z., K.J.D., P.D.V.), Erasmus MC, Rotterdam, The Netherlands.

Correspondence to Thomas W. Lameris, Dept. Internal Medicine I, Room L 264, University Hospital Dijkzigt, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. E-mail Lameris{at}twl.myweb.nl

Studies on the effect of angiotensin II on norepinephrine release from sympathetic nerve terminals through stimulation of presynaptic angiotensin II type 1 receptors are equivocal. Furthermore, evidence that angiotensin II activates the cardiac sympathetic nervous system in vivo is scarce or indirect. In the intact porcine heart, we investigated whether angiotensin II increases norepinephrine concentrations in the myocardial interstitial fluid (NE_MIF) under basal conditions and during sympathetic activation and whether it enhances exocytotic and nonexocytotic ischemia-induced norepinephrine release. In 27 anesthetized pigs, NE_MIF was measured in the left ventricular myocardium using the microdialysis technique. Local infusion of angiotensin II into the left anterior descending coronary artery (LAD) at consecutive rates of 0.05, 0.5, and 5 ng/kg per minute did not affect NE_MIF, LAD flow, left ventricular dP/dt_max, and arterial pressure despite large increments in coronary arterial and venous angiotensin II concentrations. In the presence of neuronal reuptake inhibition and -adrenergic receptor blockade, left stellate ganglion stimulation increased NE_MIF from 2.7±0.3 to 7.3±1.2 before, and from 2.3±0.4 to 6.9±1.3 nmol/L during, infusion of 0.5 ng/kg per minute angiotensin II. Sixty minutes of 70% LAD flow reduction caused a progressive increase in NE_MIF from 0.9±0.1 to 16±6 nmol/L, which was not enhanced by concomitant infusion of 0.5 ng/kg per minute angiotensin II. In conclusion, we did not observe any facilitation of cardiac norepinephrine release by angiotensin II under basal conditions and during either physiological (ganglion stimulation) or pathophysiological (acute ischemia) sympathetic activation. Hence, angiotensin II is not a local mediator of cardiac sympathetic activity in the in vivo porcine heart.

Key Words: norepinephrine • angiotensin II • renin-angiotensin system • sympathetic nervous system

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