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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.

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

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