The effects of angiotensin-(1-7) on the exchanger NHE3 and on [Ca²⁺]_i in the proximal tubules of spontaneously hypertensive rats.

The acute effects of angiotensin-1-7 [ANG-(1-7)] on the reabsorptive bicarbonate flow (J[Formula: see text]) were evaluated using stationary microperfusion in vivo in the proximal tubules of spontaneously hypertensive rats (SHR) and their normotensive controls, Wistar-Kyoto (WKY) rats, using a microelectrode sensitive to H⁺ In WKY rats, the control J[Formula: see text] was 2.40 ± 0.10 nmol·cm^-2·s^-1 (n = 120); losartan (10^-7 M) or A779 (10^-6 M, a specific Mas antagonist), alone or in combination with losartan, decreased the J[Formula: see text] ANG-(1-7) had biphasic effects on J[Formula: see text]: at 10^-9 M, it inhibited, and at 10^-6, it stimulated the flow. S3226 [10^-6 M, a specific Na⁺-H⁺ exchanger 3 (NHE3) antagonist] decreased J[Formula: see text] and changed the stimulatory effect of ANG-(1-7) to an inhibitory one but did not alter the inhibitory action of ANG-(1-7). In SHR, the control J[Formula: see text] was 2.04 ± 0.13 nmol·cm^-2·s^-1 (n = 56), and A779 and/or losartan reduced the flow. ANG-(1-7) at 10^-9 M increased J[Formula: see text], and ANG-(1-7) at 10^-6 M reduced it. The effects of A779, losartan, and S3226 on the J[Formula: see text] were similar to those found in WKY rats, which indicated that in SHR, the ANG-(1-7) action on the NHE3 was via Mas and ANG II type 1. The cytosolic calcium in the WKY or SHR rats was ~100 nM and was increased by ANG-(1-7) at 10^-9 or 10^-6 M. In hypertensive animals, a high plasma level of ANG-(1-7) inhibited NHE3 in the proximal tubule, which mitigated the hypertension caused by the high plasma level of ANG II. Copyright © 2017 the American Physiological Society.

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