The acute effects of Ang-(1-7) on the reabsorptive bicarbonate flow (JHCO3-) 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 JHCO3- was 2.40 ± 0.10 nmol.cm-2.s-1 (28); Losartan (10-7 M) or A779 (10-6 M, a specific Mas antagonist), alone or in combination with Losartan, decreased the JHCO3-. Ang-(1-7) had biphasic effects on JHCO3-: at 10-9 M, it inhibited and at 10-6, it stimulated the flow. S3226 (10-6 M, a specific NHE3 antagonist) decreased JHCO3- 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 JHCO3- was 2.04 ± 0.13 nmol.cm-2.s-1 (14), and A779 and/or Losartan reduced the flow. Ang-(1-7) at 10-9 M increased JHCO3-, and Ang-(1-7) at 10-6 M reduced it. The effects of A779, Losartan and S3226 on the JHCO3- 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 AT1. The cytosolic calcium ([Ca2+]i), 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.