Objective: Angiotensin (Ang)-(1–7) generated from Ang I and II is reported to act as an endogenous angiotensin-converting enzyme (ACE) inhibitor and angiotensin type 1 (AT1)-receptor antagonist in vitro and in vivo. Ang-(1–7) has been suggested to play an important role in hypertension. Methods and results: Therefore, we tested whether Ang-(1–7) differentially modulates vascular resistance and neurotransmission in isolated kidneys of spontaneously hypertensive rats stroke prone (SHR-SP) and Wistar–Kyoto rats (WKY). Ang-(1–7) was administered in three concentrations (0.1, 1 and 10 µmol/l) to prevent Ang I- and Ang II-induced pressor responses and facilitation of noradrenaline release. There were indeed concentration-dependent strain differences. Ang-(1–7) prevented Ang I- and Ang II-mediated changes in vascular resistance more potently in SHR-SP than in WKY by inhibiting ACE and by blocking AT1-receptors. Ang-(1–7) by itself had no influence on renal vascular tone in both strains. Ang-(1–7) inhibited Ang I-mediated facilitation of noradrenaline release more potently than Ang II-mediated facilitation of noradrenaline release. Ang-(1–7) by itself enhanced noradrenaline release from SHR-SP, but not from WKY kidneys. Conclusion: Ang-(1–7) had a greater impact on Ang I and Ang II modulation of renal vascular resistance in SHR-SP than in normotensive rats. Furthermore, Ang-(1–7) by itself has facilitatory presynaptic effects on noradrenaline release but no postsynaptic effects on renal vascular resistance in SHR-SP. Since plasma levels of Ang-(1–7) accumulate during ACE-inhibitor or AT1-receptor antagonist therapy, Ang-(1–7) could contribute to antihypertensive effects of these agents.
Copyright (C) 2004, European Society of Cardiology
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