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      A Forskolin Derivative, Colforsin Daropate Hydrochloride, Inhibits the Decrease in Cortical Renal Blood Flow Induced by Noradrenaline or Angiotensin II in Anesthetized Rats

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          Abstract

          A forskolin derivative, colforsin daropate hydrochloride (CDH), acts directly on adenylate cyclase to increase the intracellular cyclic adenosine monophosphate levels which produce a positive inotropic effect and a lower blood pressure. However, little is known about the effects of CDH on the renal function. We used laser Doppler flowmetry to measure the cortical renal blood flow (RBF) in male Wistar rats given a continuous intravenous infusion of CDH and evaluated the effects of CDH on the noradrenaline (NA) and angiotensin II (AngII) induced increases in blood pressure and reductions in RBF. Continuous intravenous administration of CDH at 0.25 µg/kg/min did not affect the mean arterial pressure (MAP), but increased heart rate and RBF. Continuous intravenous administration of CDH at high doses (0.5–0.75 µg/kg/min) decreased the MAP, with little effect on the RBF. The administration of exogenous NA (1.7 µg/kg) increased the MAP and decreased the RBF. However, a bolus injection of NA did not decrease the RBF during continuous intravenous administration of CDH, and CDH did not affect the NA-induced increase in MAP. The administration of exogenous AngII (100 ng/kg) increased MAP and decreased RBF and heart rate, but a bolus injection of AngII did not decrease RBF during continuous intravenous administration of CDH. These results suggest that CDH plays a protective role against the pressor effects and the decrease in RBF induced by NA or AngII.

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          Most cited references 7

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          Protective effect of cystathionine on acute gastric mucosal injury induced by ischemia-reperfusion in rats.

          We studied the protective effect of cystathionine on acute gastric mucosal injury induced by ischemia-reperfusion in rats. Under pentobarbital anesthesia, the celiac artery was clamped for 30 min and reperfused. Sixty minutes after the reperfusion, the total area of erosions and thiobarbituric acid-reactive substances in the stomach, as an index of lipid peroxidation, were measured and compared between control and cystathionine-treated groups. Intraperitoneal administration of cystathionine (1-20 mg/kg) 10 min before the ischemia significantly reduced both the total area of erosions and the level of thiobarbituric acid-reactive substances. When cystathionine (10 mg/kg) was administered orally, the significant reductions in the total area of erosions and level of thiobarbituric acid-reactive substances were also observed. There was a good correlation between the total area of erosions and the level of thiobarbituric acid-reactive substances. Cystathionine did not affect blood flow during ischemia-reperfusion. These results indicate that the protective effect of cystathionine on acute gastric mucosal injury induced by ischemia-reperfusion may be due to the scavenging action against superoxide radicals in vivo.
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            Modulation of cAMP-mediated vasorelaxation by endothelial nitric oxide and basal cGMP in vascular smooth muscle.

            Recent in vitro evidence shows a role of endothelial nitric oxide (NO) in the modulation of isoproterenol-induced vasorelaxation. To elucidate roles of endothelial cells and NO in cyclic adenosine monophosphate (cAMP)-mediated vasodilators we examined the effects of removal of endothelium and a NO synthase (NOS) inhibitor on relaxant responses in vitro of rat aortic strips to beta-adrenoceptor stimulants and colforsin dapropate, a water-soluble forskolin, and changes in cAMP and cyclic guanosine monophosphate (cGMP) contents. Relaxant responses of rat aorta to isoproterenol, denopamine, salbutamol, colforsin, and dibutyryl cAMP (dbcAMP) were blunted by removal of endothelial cells or treatment with NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). Relaxant response of endothelium-intact segments to isoproterenol was associated with increases in tissue cAMP and cGMP contents. Removal of endothelium or treatment with L-NAME markedly reduced basal cGMP and abolished the isoproterenol-induced increase in cGMP but not cAMP content. In endothelium-removed segments, pretreatment with sodium nitroprusside (SNP) restored the diminished relaxant response to isoproterenol and increased basal cGMP (from 0.08 +/- 0.01 to 0.16 +/- 0.02 pmol/mg protein), whereas it did not affect the isoproterenol-induced increase in cAMP. The diminished relaxant response of endothelium-removed segments to dbcAMP was not restored by SNP pretreatment. The results suggest that relaxant response of rat aorta to cAMP-mediated vasodilators is mediated, in part, by NO production in endothelium and subsequent increase in cGMP in vascular smooth-muscle cells.
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              Effects Of NKH477 On Endothelin-1-Induced Renal Responses In Anaesthetized Dogs

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                Author and article information

                Journal
                NEP
                Nephron Physiol
                10.1159/issn.1660-2137
                Nephron Physiology
                S. Karger AG
                1660-2137
                2004
                February 2004
                27 February 2004
                : 96
                : 2
                : p59-p64
                Affiliations
                aDepartment of Anesthesiology, University of Occupational and Environmental Health, School of Medicine, Kitakyushu, bKitakyushu Nephro Clinic, Kitakyushu, cDepartment of Pharmacology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, and dKitakyushu Institute of Biophysics, Kitakyushu, Japan
                Article
                76409 Nephron Physiol 2004;96:p59–p64
                10.1159/000076409
                14988663
                © 2004 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 3, References: 22, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/76409
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