Endothelium-dependent modulation of the pressor activity of arginine vasopressin in the isolated superior mesenteric arterial bed of the rat (original) (raw)
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α1D - Journal of Pharmacology and Experimental
2001
The vasodilator activity of ␣ 1-adrenoceptor agonists was tested in the rat mesenteric vascular bed (MVB), and the mechanism involved was investigated in cultured endothelial cells isolated from the bovine coronary vascular bed. In preparations preconstricted by U46619, noradrenaline and phenylephrine induced a slight relaxant effect at nanomolar concentrations. This effect was abolished in endothelium-denuded preparations and in preparations pretreated with 100 M N-nitro-L-arginine methyl ester plus 3 M indomethacin. Both the phospholipase C inhibitor U73122 and the endoplasmic reticulum Ca 2ϩ-ATPase inhibitor thapsigargin inhibited the vasorelaxant effect of phenylephrine. The cellular level of inositol monophosphate (IP 1) in bovine endothelial cells doubled after a 15-min exposure to 0.03 to 0.1 nM phenylephrine. The activity of cNOS was significantly increased following exposure to the same concentrations of phenylephrine. Both chloroethylclonidine and the selective ␣ 1D-adrenoceptor antagonist BMY 7378 reduced, in a This study was supported by a grant from the
Journal of Vascular Research, 2005
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 fl ow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change 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. 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 or, in the case of photocopying, direct payment of a specifi ed fee to the Copyright Clearance Center (see 'General Information').
Journal of Pharmacological Sciences, 2006
The aims of this study were to investigate the role of endothelin-1 in FK506-induced hypertension and vascular dysfunction of rats treated with the drug for 8 (short-term) or 30 (long-term) days and to measure malondialdehyde levels in the kidneys. Kidney and mesentery of rats were perfused. In the short-term treated groups, there was no significant change in systolic blood pressure. The response to noradrenaline only in renal vascular beds was significantly increased by FK506 and this increase was prevented by Bosentan. FK506 had no significant effect on sodium nitroprusside-induced vasodilation in comparison with solvent in both vascular beds. Bosentan failed to prevent these responses. In the long-term treated groups, at the end of the treatment with FK506, there was a significant increase in blood pressure, but no change in the response to noradrenaline in either kidneys or mesentery. The increase in blood pressure was prevented by bosentan treatment. FK506 increased malondialdehyde levels in the kidneys of the rats from only the long-term treated groups. Bosentan did not change this increase. Our results indicated that endothelin-1 plays a key role in the FK506-induced change in vascular reactivity to noradrenaline in renal vascular beds and drug-induced hypertension in the rats. There was no relationship between oxidative stress and FK506-induced hypertension.
British Journal of Pharmacology, 2000
In the presence of L-NNA (100 mM), indomethacin (10 mM) and ODQ (10 mM), acetylcholine induced a concentration-dependent vasorelaxation of guinea-pig mesenteric and middle cerebral arteries precontracted with cirazoline or histamine, but not with high K + , indicating the contribution of an endothelium-derived hyperpolarizing factor (EDHF). 2 In cerebral arteries, charybdotoxin (ChTX; 0.1 mM) completely inhibited the indomethacin, L-NNA and ODQ-insensitive relaxation; iberiotoxin (IbTX, 0.1 mM), 4-aminopyridine (4-AP, 1 mM), or barium (30 mM) signi®cantly reduced the response; in the mesenteric artery, ChTX and IbTX also reduced this relaxation. Glibenclamide (10 mM) had no aect in either the mesenteric or cerebral artery. 3 Neither clotrimazole (1 mM) nor 7-ethoxyresoru®n (3 mM) aected EDHF-mediated relaxation in the mesenteric artery, but abolished or attenuated EDHF-mediated relaxations in the cerebral artery. AM404 (30 mM), a selective anandamide transport inhibitor, did not aect the vasorelaxation response to acetylcholine in the cerebral artery, but in the mesenteric artery potentiated the vasorelaxation response to acetylcholine in an IbTX, and apamin-sensitive, but SR 141816Ainsensitive manner. Ouabain (100 mM) almost abolished EDHF-mediated relaxation in the mesenteric artery, but enhanced the relaxation in the cerebral artery whereas the addition of K + (5 ± 20 mM) to precontracted guinea-pig cerebral or mesenteric artery induced further vasoconstriction. 4 These data suggest that in the guinea-pig mesenteric and cerebral arteries dierent EDHFs mediate acetylcholine-induced relaxation, however, EDHF is unlikely to be mediated by K + .
Vasodilator Effects of the Sodium Acetate in Pooled Protein Fraction
Annals of Surgery, 1979
Paradoxical hypotension during rapid infusion of plasma protein fraction (PPF) has been attributed to vasodilation by bradykinin in PPF. This study employed a canine, controlled right heart bypass preparation to assess changes in systemic vascular resistance and venous capacitance during infusion of PPF and other possibly vasoactive mediators. Plasma protein fraction caused consistent vasodilation, whereas purified human albumin did not. This vasodilation could be ascribed entirely to acetate, present in PPF as a buffer. Bradykinin in PPF had no effect during venous infusion. Acetate is used widely as a buffer in intravenous and dialysate solutions. Its vasoactive properties must be recognized when such solutions are administered to patients with limited capacity to compensate for sudden vasodilation. P ARADOXICAL HYPOTENSION during rapid administration of human plasma protein fraction (PPF) was reported preliminary by Harrison et al. in Australia in 1971.11 Torda et al.,18 as well as Bland and co-workers4 in this country, confirmed and expanded these observations in 1973. Some of the reported reactions occurred during cardiopulmonary bypass, when PPF was infused into the extracorporeal circuit. Other reactions, however, were docu'mented during venous infusion in patients with intact circulation. A fall in systemic vascular resistance was documented in both circumstances. Vasoactive amines, most specifically bradykinin, were known to be present in PPF, and on the basis of both direct and indirect evidence13 they were soon implicated as the possible vasodilator elements. Since bradykinin was known to be inactivated within the pulmonary capillary bed6 and because sensitivity to PPF had been thought by some to be greater during arterial infusion, it Was recommended by manufacturers that PPF be given only into the systemic venous system, presumably to obviate the adverse effects of bradykinin.1