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Conference Paper: Attenuated [Ca2+]i and [pH]i responses to kappa-opioid receptor stimulation in the heart of rats subjected to chronic hypoxia

TitleAttenuated [Ca2+]i and [pH]i responses to kappa-opioid receptor stimulation in the heart of rats subjected to chronic hypoxia
Authors
Issue Date1999
PublisherMedcom Limited. The Journal's web site is located at http://www.hkcchk.com/journals.php
Citation
The 3rd Annual Scientific Meeting of The Institute of Cardiovascular Science and Medicine (ICSM), Hong Kong, 30 October 1999. In Journal of Hong Kong College of Cardiology, 1999, v. 7 n. 2, p. 141, abstract no. 61 How to Cite?
AbstractIn the present study WC determined the [Ca2+]i and [PH]i responses to k-opioid receptor stimulation in the hypertrophied right heart induced by chronic hypoxia. U50,488H, a selective k-opioid receptor agonist, at IO - 30 µM, dose-dependently decreased the electrically-induced [CA2+]i transient. 20 µM U50,488H also increased the [pH]i. The effects of the k-opioid receptor agonist at 20 µM were completely abolished by 5 µM nor-binaltorphimine (nor-BNI), a selective K-opioid receptor antagonist and I µM calphostin C, a specific inhibitor of protein kinase C (PKC). We further investigated the [Ca2+]i and [pH]i responses to activation of PKC, known to mediate the actions of k-opioid receptor stimulation. PMA, an activator of PKC, at 0.01 - 1 µM also dose-dependently decreased the electrically-induced [Ca2+]i transient and at 0. 1 µM it increased the [pH]i. The effects of 0.1 µM PMA were abolished by 1 µM calphostin C. The effect of 0.1 µM PMA on [pH]i was also blocked by EIPA, a potent Na+-H+ exchange (NHE) blocker. In the right hypertrophied heart of rat subjected to hypoxia for 4 weeks, the effects of U50,488H and PMA on [Ca2+]i transient and [pH]i were significantly attenuated and completely abolished, respectively. The responses to The results demonstrated for the first time that the [Ca2+]i transient and [pH]i responses to k-opioid receptor stimulation were impaired in the heart of rats subjected to chronic hypoxia, which may be due to impaired PKC functions. (Supported by a grant from the Institute of Cardiovascular Science and Medicine)
DescriptionConference Theme: Bridging Cardiovascular Science and Medicine
Persistent Identifierhttp://hdl.handle.net/10722/104891
ISSN
2015 SCImago Journal Rankings: 0.102

 

DC FieldValueLanguage
dc.contributor.authorPei, JM-
dc.contributor.authorBian, JS-
dc.contributor.authorYu, XM-
dc.contributor.authorFung, ML-
dc.contributor.authorWong, TM-
dc.date.accessioned2010-09-25T22:11:42Z-
dc.date.available2010-09-25T22:11:42Z-
dc.date.issued1999-
dc.identifier.citationThe 3rd Annual Scientific Meeting of The Institute of Cardiovascular Science and Medicine (ICSM), Hong Kong, 30 October 1999. In Journal of Hong Kong College of Cardiology, 1999, v. 7 n. 2, p. 141, abstract no. 61-
dc.identifier.issn1027-7811-
dc.identifier.urihttp://hdl.handle.net/10722/104891-
dc.descriptionConference Theme: Bridging Cardiovascular Science and Medicine-
dc.description.abstractIn the present study WC determined the [Ca2+]i and [PH]i responses to k-opioid receptor stimulation in the hypertrophied right heart induced by chronic hypoxia. U50,488H, a selective k-opioid receptor agonist, at IO - 30 µM, dose-dependently decreased the electrically-induced [CA2+]i transient. 20 µM U50,488H also increased the [pH]i. The effects of the k-opioid receptor agonist at 20 µM were completely abolished by 5 µM nor-binaltorphimine (nor-BNI), a selective K-opioid receptor antagonist and I µM calphostin C, a specific inhibitor of protein kinase C (PKC). We further investigated the [Ca2+]i and [pH]i responses to activation of PKC, known to mediate the actions of k-opioid receptor stimulation. PMA, an activator of PKC, at 0.01 - 1 µM also dose-dependently decreased the electrically-induced [Ca2+]i transient and at 0. 1 µM it increased the [pH]i. The effects of 0.1 µM PMA were abolished by 1 µM calphostin C. The effect of 0.1 µM PMA on [pH]i was also blocked by EIPA, a potent Na+-H+ exchange (NHE) blocker. In the right hypertrophied heart of rat subjected to hypoxia for 4 weeks, the effects of U50,488H and PMA on [Ca2+]i transient and [pH]i were significantly attenuated and completely abolished, respectively. The responses to The results demonstrated for the first time that the [Ca2+]i transient and [pH]i responses to k-opioid receptor stimulation were impaired in the heart of rats subjected to chronic hypoxia, which may be due to impaired PKC functions. (Supported by a grant from the Institute of Cardiovascular Science and Medicine)-
dc.languageeng-
dc.publisherMedcom Limited. The Journal's web site is located at http://www.hkcchk.com/journals.php-
dc.relation.ispartofJournal of Hong Kong College of Cardiology-
dc.titleAttenuated [Ca2+]i and [pH]i responses to kappa-opioid receptor stimulation in the heart of rats subjected to chronic hypoxia-
dc.typeConference_Paper-
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1027-7811&volume=7 &issue=2&spage=141&epage=&date=1999&atitle=Attenuated+[Ca2+]i+and+[pH]i+responses+to+kappa-opioid+receptor+stimulation+in+the+heart+of+rats+subjected+to+chronic+hypoxia.en_HK
dc.identifier.emailFung, ML: fungml@hku.hk-
dc.identifier.emailWong, TM: wongtakm@hkucc.hku.hk-
dc.identifier.authorityFung, ML=rp00433-
dc.identifier.hkuros53378-
dc.identifier.volume7-
dc.identifier.issue2-
dc.identifier.spage141, abstract no. 61-
dc.identifier.epage141, abstract no. 61-
dc.publisher.placeHong Kong-

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