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      AT 1 Receptor Expression in Glomeruli from NO-Deficient Rats


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          Chronic inhibition of nitric oxide synthase promotes renin-dependent hypertension and renal injury. The present study examines how renal angiotensin II receptors are expressed in this model. N<sup>G</sup>-nitro- L-arginine methyl ester ( L-NAME) was given orally to rats for 1 month and was associated or not with captopril during the 4 last days of the administration. <sup>125</sup>I-[Sar<sup>1</sup>, Ile<sup>8</sup>]-Ang II binding, AT<sub>1 </sub>mRNA and cytosolic calcium were studied in isolated glomeruli from L-NAME and control rats and in cultured mesangial cells from normal rats. Renal injury was marked in rats receiving L-NAME. Type I angiotensin II (AT<sub>1)</sub> receptor number and mRNA expression were decreased (p < 0.05) in glomeruli isolated from L-NAME-treated rats compared with controls, unless they received captopril in combination. The low level of AT<sub>1</sub> receptor expression was associated with an attenuated rise of cytosolic calcium in response to angiotensin II. Angiotensin-converting enzyme activity in glomeruli and angiotensin II concentration in renal cortex were increased (p < 0.05) in rats receiving L-NAME alone, whereas aminopeptidase A activity was not modified. To better discriminate between the direct and indirect effects of nitric oxide deficiency, rat mesangial cells were exposed or not for 24 h to S-nitroso-N-acetyl penicillamine, a nitric oxide donor. Angiotensin II binding, AT<sub>1</sub> mRNA expression and calcium response to angiotensin II were decreased in presence of the nitric oxide donor (p < 0.01). These results suggest that the decrease of AT<sub>1</sub> receptor expression after 1 month of L-NAME treatment does not depend on a direct effect of nitric oxide deficiency but results from the high local angiotensin II concentration due to the stimulated angiotensin-converting enzyme activity. They also show that the renin-angiotensin dependence of this model of hypertension does not result from the overexpression of AT<sub>1</sub> receptors.

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          Effects of angiotensin IV and angiotensin-(1-7) on basal and angiotensin II-stimulated cytosolic Ca2+ in mesangial cells.

          This study analyzed the influence of two main metabolites of angiotensin II, angiotensin IV and angiotensin-(1-7), on basal and angiotensin II-dependent [Ca2+](i) in rat mesangial cells. Angiotensin IV behaved as a weak agonist. Its effects were abolished by angiotensin AT(1) receptor antagonists. Treatment with angiotensin II abolished the effect of a subsequent treatment with angiotensin IV whereas two successive angiotensin IV-dependent [Ca2+](i) peaks were obtained. Angiotensin II increased [Ca2+](i) in a Ca2+-free medium whereas angiotensin IV was inactive. Leucine-valine-valine-hemorphin 7, a hemorphin specific for the angiotensin AT(4) receptor, was devoid of any agonistic or antagonistic effect. In contrast, angiotensin-(1-7), if without influence on basal [Ca2+](i), inhibited angiotensin II- and angiotensin IV-dependent [Ca2+](i) increases. Total inhibition of the angiotensin IV effect was obtained whereas association of angiotensin-(1-7) to 8-(NN-diethylamino)-octyl-3,4,5-trimethoxybenzoate, an inhibitor of inositol phosphate-mediated Ca2+ release, was necessary to suppress the effect of angiotensin II. These results provide evidence that angiotensin II metabolites may participate in the control of [Ca2+](i) in mesangial cells at the initial stage of binding to the angiotensin AT(1) receptors.
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            Improved Survival in Rats Administered NG-Nitro L-Arginine Methyl Ester Due to Converting Enzyme Inhibition

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              Blockade of nitric oxide formation inhibits the stimulation of the renin system by a low salt intake


                Author and article information

                Nephron Exp Nephrol
                Cardiorenal Medicine
                S. Karger AG
                November 2003
                17 November 2004
                : 95
                : 3
                : e119-e128
                aInserm 489, Hôpital Tenon, bInserm 36, Collège de France, and cAP-HP, Department of Physiology, Hôpital St-Antoine, Paris, France
                74328 Nephron Exp Nephrol 2003;95:e119–e128
                © 2003 S. Karger AG, Basel

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                : 26 June 2003
                : 27 October 2003
                Page count
                Figures: 6, References: 34, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/74328
                Self URI (text/html): https://www.karger.com/Article/FullText/74328
                Self URI (journal page): https://www.karger.com/SubjectArea/Nephrology
                Original Paper

                Cardiovascular Medicine,Nephrology
                Angiotensin II,Nitric oxide,Glomerulus,Mesangial cell,Angiotensin-converting enzyme,Type I angiotensin II receptor


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