Details

Autor(en) / Beteiligte

• Castelo-Branco, Regiane Cardoso
• Leite-Dellova, Deise C A
• Fernandes, Fernanda Barrinha
• Malnic, Gerhard
• de Mello-Aires, Margarida

Titel

The effects of angiotensin-(1-7) on the exchanger NHE3 and on [Ca 2+ ] i in the proximal tubules of spontaneously hypertensive rats

Ist Teil von

• American journal of physiology. Renal physiology, 2017-08, Vol.313 (2), p.F450-F460

Ort / Verlag

United States

Erscheinungsjahr

2017

Link zum Volltext

Quelle

Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals

Beschreibungen/Notizen

• 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 ·s ( = 120); losartan (10 M) or A779 (10 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 M, it inhibited, and at 10 , it stimulated the flow. S3226 [10 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 ·s ( = 56), and A779 and/or losartan reduced the flow. ANG-(1-7) at 10 M increased J[Formula: see text], and ANG-(1-7) at 10 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 or 10 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.