In spontaneously hypertensive rats, Angiotensin I and II enhance renal vascular resistance and sympathetic neurotransmission exclusively via the AT1 receptor, with no apparent AT2 receptor involvement.
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AT1 selectivity may guide renal sympathetic modulation in hypertension models; leaves open AT2 relevance and human translation.
BACKGROUND/AIMS: Angiotensin (Ang) II modulates vascular resistance and sympathetic neurotransmission through Ang II type 1 (AT1) receptors. Recent studies reported an involvement of AT2 receptors. We investigated whether AT2 receptors participate in modulation of vascular resistance and sympathetic neurotransmission in spontaneously hypertensive rats (SHR). METHODS: Kidneys of 6- and 16-week-old normotensive (WKY) and SHR were isolated and perfused. RESULTS: Noradrenaline release induced by renal nerve stimulation (RNS) was increased in SHR (WKY: 1,837 +/- 128, SHR: 2,310 +/- 192 pg/g). Ang I- and II-induced pressor responses and enhancement of noradrenaline release were greater in SHR than in WKY. Pressor responses to Ang I and II were greater in adult compared with young SHR. The AT1 receptor antagonist EXP3174 (0.1 microM) blocked Ang I- and II-induced renal vasoconstriction and noradrenaline release to RNS in both strains. In contrast, the selective AT2 receptor antagonist PD 123319 (1 microM) had no influence in young and adult WKY and SHR. CONCLUSION: Ang I and II had a greater impact on renal vascular resistance and neurotransmission in SHR, which was more pronounced in adult SHR. All effects are mediated by the AT1 receptor and no modulatory influence of the AT2 receptor could be found.
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Stegbauer et al. (2004) studied this question.
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