{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T22:17:35Z","timestamp":1773958655414,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,5,15]]},"abstract":"<jats:p>The acute direct action of angiotensin-(1\u20137) [ANG-(1\u20137)] on bicarbonate reabsorption ( JHCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>) was evaluated by stationary microperfusions on in vivo middle proximal tubules in rats using H ion-sensitive microelectrodes. The control JHCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>is 2.82 \u00b1 0.078 nmol\u00b7cm<jats:sup>\u22122<\/jats:sup>\u00b7s<jats:sup>\u22121<\/jats:sup>(50). ANG-(1\u20137) (10<jats:sup>\u221212<\/jats:sup>or 10<jats:sup>\u22129<\/jats:sup>M) in luminally perfused tubules decreases JHCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>(36 or 60%, respectively), but ANG-(1\u20137) (10<jats:sup>\u22126<\/jats:sup>M) increases it (80%). A779 increases JHCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>(30%) and prevents both the inhibitory and the stimulatory effects of ANG-(1\u20137) on it. S3226 decreases JHCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>(45%) and changes the stimulatory effect of ANG-(1\u20137) to an inhibitory effect (30%) but does not affect the inhibitory effect of ANG-(1\u20137). Our results indicate that in the basal condition endogenous ANG-(1\u20137) inhibits JHCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>and that the biphasic dose-dependent effect of ANG-(1\u20137) on JHCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>is mediated by the Mas receptors via the Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchanger 3 (NHE3). The control value of intracellular Ca<jats:sup>2+<\/jats:sup>concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>), as monitored using fura-2 AM, is 101 \u00b1 2 nM ( 6 ), and ANG-(1\u20137) (10<jats:sup>\u221212<\/jats:sup>, 10<jats:sup>\u22129<\/jats:sup>, or 10<jats:sup>\u22126<\/jats:sup>M) transiently (3 min) increases it (by 151, 102, or 52%, respectively). A779 increases the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>(25%) but impairs the stimulatory effect of all doses of ANG-(1\u20137) on it. The use of BAPTA or thapsigargin suggests a correlation between the ANG-(1\u20137) dose-dependent effects on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>and JHCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>. Therefore, the interaction of the opposing dose-dependent effects of ANG II and ANG-(1\u20137) on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>and JHCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>may represent an physiological regulatory mechanism of extracellular volume and\/or pH changes. However, whether [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>modification is an important direct mechanism for NHE3 activation by these peptides or is a side effect of other signaling pathways will require additional studies.<\/jats:p>","DOI":"10.1152\/ajprenal.00401.2012","type":"journal-article","created":{"date-parts":[[2013,3,21]],"date-time":"2013-03-21T03:49:21Z","timestamp":1363837761000},"page":"F1258-F1265","source":"Crossref","is-referenced-by-count":24,"title":["Dose-dependent effects of angiotensin-(1\u20137) on the NHE3 exchanger and [Ca<sup>2+<\/sup>]<sub>i<\/sub>in in vivo proximal tubules"],"prefix":"10.1152","volume":"304","author":[{"given":"Regiane C.","family":"Castelo-Branco","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Biomedical Sciences Institute, University of S\u00e3o Paulo, S\u00e3o Paulo, Brazil; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Deise C. 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