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      Size Dependence of Functional Alterations in Mesenteric Arteries from the Aldosterone-Salt Hypertensive Rat

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          Abstract

          We tested the hypothesis that an elevated potassium-42 (<sup>42</sup>K<sup>+</sup>) efflux (highly dependent on Ca<sup>2+</sup>) and an increase in the sensitivity of contraction and <sup>42</sup>K<sup>+</sup> efflux to norepinephrine (NE) in conduit arteries of aldosterone-salt hypertensive rats (AHR) exended to smaller, distributing arteries. Functional endpoints were compared in two sizes of arteries from the mesenteric bed: second-order branches of the superior mesenteric artery (SMA branches) and the SMA. Contraction and free cytosolic Ca<sup>2+</sup> concentration ([Ca<sup>2+</sup>]<sub>c</sub>; fura-2 microfluorometry) were measured simultaneously and <sup>42</sup>K<sup>+</sup> efflux was measured separately in SMA branches. Contraction and <sup>42</sup>K<sup>+</sup> efflux were measured separately in SMA. Basal tone, [Ca<sup>2+</sup>]<sub>c</sub>, and <sup>42</sup>K<sup>+</sup> efflux were similar in SMA branches from AHR and control-salt rats (CSR). However, basal <sup>42</sup>K<sup>+</sup> efflux was elevated in SMA from AHR compared to CSR. The sensitivity of the contractile, [Ca<sup>2+</sup>]<sub>c</sub>, and <sup>42</sup>K<sup>+</sup> efflux responses to NE was similar in SMA branches. In contrast, the sensitivity of the contractile and <sup>42</sup>K<sup>+</sup> efflux responses to NE was enhanced in SMA from AHR compared to CSR. Inhibiton of endothelium-derived vasoactive substances by pretreatment with N<sub>ω</sub>-nitro- L-arginine methyl ester and indomethacin significantly shifted the NE concentration-response relationships to the left for contraction, [Ca<sup>2+</sup>]<sub>c</sub>, and <sup>42</sup>K<sup>+</sup> efflux in both SMA branches and SMA from CSR. A similar shift to the left was observed in AHR for contraction but not consistently for [Ca<sup>2+</sup>]<sub>c</sub> and <sup>42</sup>K<sup>+</sup> efflux. We conclude that SMA branches from AHR demonstrate neither the elevated basal <sup>42</sup>K<sup>+</sup> efflux, nor the NE supersensitivity exhibited by SMA. Endothelial function was not impaired both in SMA and SMA branches.

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          α1- and α2-adrenoceptor agonist-induced contraction in rat mesenteric artery upon removal of endothelium

          Contractile response to norepinephrine, methoxamine and clonidine were determined in rat mesenteric arteries with and without an intact endothelium. Removal of the endothelial cell layer markedly enhanced the maximum contractile effect of norepinephrine (2.8 fold), methoxamine (4.0 fold) and clonidine (13.0 fold). Furthermore, there was a significant decrease in the EC50 values for these agonists. These findings indicate that both alpha 1- and alpha 2-adrenoceptor agonists can induce contraction of mesenteric arteries which is modulated by the endothelial cell layer.
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            Involvement of α-adrenoceptors in the endothelium-dependent depression of noradrenaline-induced contraction in rat aorta

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              Author and article information

              Journal
              JVR
              J Vasc Res
              10.1159/issn.1018-1172
              Journal of Vascular Research
              S. Karger AG
              1018-1172
              1423-0135
              1999
              October 1999
              28 October 1999
              : 36
              : 5
              : 404-414
              Affiliations
              Department of Physiology, School of Medicine, Dalton Cardiovascular Research Center, University of Missouri, Columbia, Mo., USA
              Article
              25680 J Vasc Res 1999;36:404–414
              10.1159/000025680
              10559681
              91c3eab1-595b-4e09-a518-8c1e8417e97b
              © 1999 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.

              History
              Page count
              Figures: 5, Tables: 4, References: 31, Pages: 11
              Categories
              Research Paper

              General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
              Mineralocorticoid hypertension,Vascular smooth muscle,Mesenteric arteries,Norepinephrine,Fura-2,Endothelium,Calcium,Potassium isotopes

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