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      Intrarenal Infusion of Angiotensin-(1–7) Modulates Renal Functional Responses to Exogenous Angiotensin II in the Rat

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          In the present study we investigated the possible role of angiotensin-(1–7) [Ang-(1–7)] in modulating renal functional responses to intrarenal (i.e.) infusion of angiotensin II (ANG II) in normotensive anesthetized rats. ANG II (6 ng/min, n = 14) decreased glomerular filtration rate (GFR), renal plasma flow (RPF), absolute and fractional sodium excretion by –24 ± 5, –25 ± 6, –44 ± 6 and –28 ± 7%, respectively (p < 0.05). i.r. infusion of Ang-(1–7) (50 ng/min, n = 13) did not significantly alter GFR (+6 ± 4%) but reduced RPF by –19 ± 7% (p < 0.05). Ang-(1–7) increased absolute and fractional sodium excretion by +36 ± 6 and +37 ± 8%, respectively (p < 0.05). Infusion of Ang-(1–7) did not prevent the decreases in GFR and RPF but completely blunted the decreases in absolute (–2 ± 2%) and fractional sodium excretion (–4 ± 4%) induced by ANG II (n = 11). Blockade of the Ang-(1–7) receptor by [7-D-Ala]-Ang-(1–7) (5 µg/min, n = 11) significantly decreased GFR, RPF, absolute and fractional sodium excretion by –28 ± 7, –20 ± 5, –32 ± 7 and –24 ± 4%, respectively (p < 0.05), suggesting that the action of endogenous ANG II is unopposed by compensatory effect of endogenous Ang-(1–7). i.r. infusion of Ang-(1–7) (n = 10) did not alter the effect of Ang-(1–7) receptor blockade on RPF (–21 ± 6%) but blunted its effects on GFR (+4 ± 3%) and absolute (+7 ± 5%) and fractional (+6 ± 4%) urinary sodium excretion probably by displacing the receptor blocker. While exogenous ANG II during blockade of the Ang-(1–7) receptor and the AT<sub>2</sub> receptor (by PD 123319; 1 µg/min i.r., n = 9) resulted in the same decreases in absolute and fractional sodium excretion (–39 ± 8 and –38 ± 6%, respectively, p < 0.05) as did ANG II in the absence of Ang-(1–7) receptor blockade. These results suggest that in normotensive rats high i.r. Ang-(1–7) concentration attenuates the tubular, i.e. sodium reabsorptive effect, but not the vascular effect of exogenous i.r. ANG II. Results obtained during blockade of Ang-(1–7) and of AT<sub>2</sub> receptors imply that AT<sub>2</sub> receptors play a role in tubular sodium reabsorption in the presence of high ANG II concentration

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          Characterization of a new angiotensin antagonist selective for angiotensin-(1–7): Evidence that the actions of angiotensin-(1–7) are mediated by specific angiotensin receptors

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            Cardiovascular actions of angiotensin(1–7)

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              Gender differences in the attenuation of salt-induced hypertension by angiotensin (1-7)


                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                08 November 2002
                : 25
                : 4
                : 202-210
                aTransplant Center, Department of Nephrology, Institute for Clinical and Experimental Medicine, Prague, Czech Republic; bSection of Nephrology, Medical Policlinic, Department of Medicine, University of Bonn, Germany; cDepartment of Experimental Medicine, Institute for Clinical and Experimental Medicine, dDepartment of Physiology, 2nd Medical Faculty Charles University, and eCenter for Experimental Cardiovascular Research, Prague, Czech Republic
                66340 Kidney Blood Press Res 2002;25:202–210
                © 2002 S. Karger AG, Basel

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                Figures: 2, Tables: 1, References: 37, Pages: 9
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