Angiotensin-(1-7) modulates vascular resistance and sympathetic neurotransmission in kidneys of spontaneously hypertensive rats

doi:10.1016/j.cardiores.2003.11.017

Cardiovascular Research 2004 61(2):352-359; doi:10.1016/j.cardiores.2003.11.017
© 2004 by European Society of Cardiology

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Angiotensin-(1–7) modulates vascular resistance and sympathetic neurotransmission in kidneys of spontaneously hypertensive rats

Johannes Stegbauer, Vitus Oberhauser, Oliver Vonend and Lars Christian Rump^*

Department of Internal Medicine I, Marienhospital Herne, Ruhr-University Bochum, Hölkeskampring 40, D-44625 Herne, Germany

^* Corresponding author. Tel.: +49-2323-499-1671; fax: +49-2323-499-302. christian.rump{at}ruhr-uni-bochum.de

Objective: Angiotensin (Ang)-(1–7) generated from AngI and II is reported to act as an endogenous angiotensin-convertingenzyme (ACE) inhibitor and angiotensin type 1 (AT1)-receptorantagonist in vitro and in vivo. Ang-(1–7) has been suggestedto play an important role in hypertension. Methods and results:Therefore, we tested whether Ang-(1–7) differentiallymodulates vascular resistance and neurotransmission in isolatedkidneys of spontaneously hypertensive rats stroke prone (SHR-SP)and Wistar–Kyoto rats (WKY). Ang-(1–7) was administeredin three concentrations (0.1, 1 and 10 µmol/l) to preventAng I- and Ang II-induced pressor responses and facilitationof noradrenaline release. There were indeed concentration-dependentstrain differences. Ang-(1–7) prevented Ang I- and AngII-mediated changes in vascular resistance more potently inSHR-SP than in WKY by inhibiting ACE and by blocking AT1-receptors.Ang-(1–7) by itself had no influence on renal vasculartone in both strains. Ang-(1–7) inhibited Ang I-mediatedfacilitation of noradrenaline release more potently than AngII-mediated facilitation of noradrenaline release. Ang-(1–7)by itself enhanced noradrenaline release from SHR-SP, but notfrom WKY kidneys. Conclusion: Ang-(1–7) had a greaterimpact on Ang I and Ang II modulation of renal vascular resistancein SHR-SP than in normotensive rats. Furthermore, Ang-(1–7)by itself has facilitatory presynaptic effects on noradrenalinerelease but no postsynaptic effects on renal vascular resistancein SHR-SP. Since plasma levels of Ang-(1–7) accumulateduring ACE-inhibitor or AT1-receptor antagonist therapy, Ang-(1–7)could contribute to antihypertensive effects of these agents.

KEYWORDS Angiotensin-(1–7); Renin-angiotensin-system; Noradrenaline release; Vascular resistance; Experimental hypertension

Time for primary review 21 days

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