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The acute effects of angiotensin-1–7 [ANG-(1–7)] on the reabsorptive bicarbonate flow (JHCO-3 ) were evaluated using stationary microperfusion in vivo in the proximal tubules of spontaneously hypertensive rats (SHR) and their normotensive controls, WistarKyoto (WKY) rats, using a microelectrode sensitive to H. In WKY rats, the control JHCO-3 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 JHCO-3 . ANG-(1–7) had biphasic effects on JHCO-3 : 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 JHCO-3 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 JHCO-3 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 JJHCO-3 , and ANG-(1–7) at 10-6 M reduced it. The effects of A779, losartan, and S3226 on the JHCO-3were 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. [ABSTRACT FROM AUTHOR]