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      Effect of Angiotensin II on ANP-Dependent Guanylyl Cyclase Activity in Cultured Mouse and Rat Podocytes

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          The presence of a well-developed contractile apparatus is the feature determining major roles of podocytes in the renal glomeruli. Receptors for a variety of vasoactive hormones are expressed in these cells; however, most of the signaling pathways are still unknown and remain to be elucidated. Angiotensin II (Ang II) and atrial natriuretic peptide (ANP), due to their opposite action, are the major modulators of glomerular filtration. In podocytes, Ang II induces rise in intracellular calcium concentration, whereas ANP stimulates generation of cGMP. The present study was designed to check whether ANP-stimulated cGMP synthesis in podocytes might be affected by Ang II. Cultured rat (RP) and mouse (MP) podocytes were stimulated with ANP, in the absence or presence of Ang II and cyclic GMP was determined by RIA method. Co-incubation of podocytes with ANP and Ang II caused significant (p < 0.01) suppression of ANP-dependent cGMP generation. The effect was prevented by saralasin, an inhibitor of angiotensin receptors. Phorbol-12-myristate-13-acetate (PMA) mimicked, whereas chelerythrine reversed inhibitory effect of Ang II. In conclusion, angiotensin II counteracts ANP-stimulated cGMP synthesis in cultured podocytes. It seems likely that the protein kinase C pathway is involved in this effect.

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          The multispecific organic anion transporter (OAT) family.

          Organic anion transporters play important roles in the elimination of a variety of endogenous substances, xenobiotics and their metabolites from the body. During the last decade, molecular cloning has identified several families of multispecific organic anion transporters mediating the renal and hepatic elimination of organic anions and, most recently, the OAT (organic anion transporter) family, the founding member of which (OAT1) is the basolateral p-aminohippurate (PAH) transporter in the renal proximal tubule. So far, four isoforms have been identified. OATs are membrane proteins with 12 putative membrane-spanning domains and function as sodium-independent exchangers or facilitators. OATs show weak structural similarity to organic cation transporters (OCTs) and OCTN/carnitine transporters. OATs are multispecific organic anion transporters, the substrates of which include both endogenous (e.g. cyclic nucleotides, prostaglandins, urate, dicarboxylates) and exogenous anions (various anionic drugs and environmental substances). All members of the OAT family are expressed in the kidney, while some are also expressed in the liver, brain and placenta. The OAT family represents the renal secretory pathway for organic anions and is also involved in the distribution of organic anions in the body.
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            Both subtype 1 and 2 receptors of angiotensin II participate in regulation of intracellular calcium in glomerular epithelial cells.

            We have documented that both receptors of angiotensin II (ANG II) (AT1 and AT2) are involved in regulation of intracellular signals in glomerular epithelial cells (GECs). We studied the role of these receptors in regulation of intracellular ionized calcium [Ca2(+)]i in GECs. Cells were loaded with Indo-1 (Ca2(+)) and SNARF-1 (pH) fluorescent dyes and then incubated with or without ANG II for 1 hour at 37 degrees C. In some experiments AT(1) and AT(2) receptor blockers (Losartan and PD 12339, respectively) were added. In additional experiments cells were incubated with thapsigargin (Tg) and bradykinin (BK) as well as ANG II. A four-channel fluorescence videomicroscope system was used to measure real-time [Ca2(+) ]i in individual cells. Levels of inositol triphosphate (IP(3)) were measured with radioimmunoassay. An amount of 100 nmol/L of ANG II caused a maximal increase in [Ca2(+)]i in calcium-containing buffer. ANG II had no effect on intracellular pH of GECs. Increase in [Ca2(+)]i by ANG II was prevented by the concurrent use of Losartan and PD 123319. BK caused a transient increase in [Ca2(+)]i, which was significantly decreased by ANG II; concurrent addition of Losartan and PD 123319 prevented ANG II effect. ANG II prevented the accumulation of Ca2(+) in intracellular stores. ANG II caused a significant but transient increase in levels of IP(3). In summary, ANG II increases extracellular/intracellular calcium dependent bidirectional Ca2(+) transport in GECs, inhibits BK induced release of Ca2(+) from IP(3) sensitive stores, and, in addition, reduces refilling of endoplasmic reticulum [Ca2(+)] depleted by repeated BK stimulation. Both receptor subtypes appear to be important in ANG II mediated physiologic responses of GECs and may participate in modulation of glomerular function in vivo.
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              Angiotensin II-Induced Phosphoinositide Production and Atrial Natriuretic Peptide Release in Rat Atrial Tissue


                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                28 November 2002
                : 25
                : 5
                : 296-302
                Departments of aImmunopathology and bPathophysiology, Medical University of Gdańsk, and cLaboratory of Cellular and Molecular Nephrology, Medical Research Centre of the Polish Academy of Sciences, Warsaw, Poland
                66790 Kidney Blood Press Res 2002;25:296–302
                © 2002 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 2, References: 37, Pages: 7
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/66790
                Original Paper

                Cardiovascular Medicine, Nephrology

                Angiotensin II, Natriuretic peptides, Guanylyl cyclases, Podocytes


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