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- Publisher Website: 10.1172/JCI116907
- Scopus: eid_2-s2.0-0027132065
- PMID: 8254041
- WOS: WOS:A1993ML64300042
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Article: Endothelium-dependent hyperpolarization caused by bradykinin in human coronary arteries
Title | Endothelium-dependent hyperpolarization caused by bradykinin in human coronary arteries |
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Authors | |
Keywords | Angiotensin-converting enzyme inhibitor Endothelium-derived hyperpolarizing factor Endothelium-derived relaxing factor Potassium channels Relaxation |
Issue Date | 1993 |
Publisher | American Society for Clinical Investigation. The Journal's web site is located at http://www.jci.org |
Citation | Journal Of Clinical Investigation, 1993, v. 92 n. 6, p. 2867-2871 How to Cite? |
Abstract | The present study was designed to determine whether bradykinin induces endothelium-dependent hyperpolarization of vascular smooth muscle in human coronary arteries, and if so, to define the contribution of this hyperpolarization to endothelium-dependent relaxations. The membrane potential of arterial smooth muscle cells (measured by glass microelectrodes) and changes in isometric force were recorded in tissues from six patients undergoing heart transplantation. In the presence of indomethacin and N(G)- nitro-L-arginine (NLA), the membrane potential was -48.3±0.6 and -46.9±0.6 mV, in preparations with and without endothelium, respectively, and was not affected by treatment with perindoprilat, an angiotensin-converting enzyme inhibitor. In the presence of both indomethacin and NLA, bradykinin evoked transient and concentration-dependent hyperpolarizations only in tissues with endothelium, which were augmented by perindoprilat and mimicked by the calcium ionophore A23187. Glibenclamide did not inhibit membrane hyperpolarization to bradykinin. In rings contracted with prostaglandin F(2α), the cumulative addition of bradykinin caused a concentration- dependent relaxation during contractions evoked by prostaglandin F(2α), which was not abolished by NLA and indomethacin. The present findings demonstrate the occurrence of endothelium-dependent hyperpolarization, and its contribution to endothelium-dependent relaxations, in the human coronary artery. |
Persistent Identifier | http://hdl.handle.net/10722/171080 |
ISSN | 2023 Impact Factor: 13.3 2023 SCImago Journal Rankings: 4.833 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Nakashima, M | en_US |
dc.contributor.author | Mombouli, JV | en_US |
dc.contributor.author | Taylor, AA | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:12:07Z | - |
dc.date.available | 2012-10-30T06:12:07Z | - |
dc.date.issued | 1993 | en_US |
dc.identifier.citation | Journal Of Clinical Investigation, 1993, v. 92 n. 6, p. 2867-2871 | en_US |
dc.identifier.issn | 0021-9738 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171080 | - |
dc.description.abstract | The present study was designed to determine whether bradykinin induces endothelium-dependent hyperpolarization of vascular smooth muscle in human coronary arteries, and if so, to define the contribution of this hyperpolarization to endothelium-dependent relaxations. The membrane potential of arterial smooth muscle cells (measured by glass microelectrodes) and changes in isometric force were recorded in tissues from six patients undergoing heart transplantation. In the presence of indomethacin and N(G)- nitro-L-arginine (NLA), the membrane potential was -48.3±0.6 and -46.9±0.6 mV, in preparations with and without endothelium, respectively, and was not affected by treatment with perindoprilat, an angiotensin-converting enzyme inhibitor. In the presence of both indomethacin and NLA, bradykinin evoked transient and concentration-dependent hyperpolarizations only in tissues with endothelium, which were augmented by perindoprilat and mimicked by the calcium ionophore A23187. Glibenclamide did not inhibit membrane hyperpolarization to bradykinin. In rings contracted with prostaglandin F(2α), the cumulative addition of bradykinin caused a concentration- dependent relaxation during contractions evoked by prostaglandin F(2α), which was not abolished by NLA and indomethacin. The present findings demonstrate the occurrence of endothelium-dependent hyperpolarization, and its contribution to endothelium-dependent relaxations, in the human coronary artery. | en_US |
dc.language | eng | en_US |
dc.publisher | American Society for Clinical Investigation. The Journal's web site is located at http://www.jci.org | en_US |
dc.relation.ispartof | Journal of Clinical Investigation | en_US |
dc.subject | Angiotensin-converting enzyme inhibitor | - |
dc.subject | Endothelium-derived hyperpolarizing factor | - |
dc.subject | Endothelium-derived relaxing factor | - |
dc.subject | Potassium channels | - |
dc.subject | Relaxation | - |
dc.subject.mesh | Aged | en_US |
dc.subject.mesh | Angiotensin-Converting Enzyme Inhibitors - Pharmacology | en_US |
dc.subject.mesh | Arginine - Analogs & Derivatives - Pharmacology | en_US |
dc.subject.mesh | Benzopyrans - Pharmacology | en_US |
dc.subject.mesh | Bradykinin - Pharmacology | en_US |
dc.subject.mesh | Calcimycin - Pharmacology | en_US |
dc.subject.mesh | Child | en_US |
dc.subject.mesh | Coronary Vessels - Drug Effects - Physiology - Physiopathology | en_US |
dc.subject.mesh | Cromakalim | en_US |
dc.subject.mesh | Dinoprost - Pharmacology | en_US |
dc.subject.mesh | Endothelium, Vascular - Physiology - Physiopathology | en_US |
dc.subject.mesh | Glyburide - Pharmacology | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Indoles - Pharmacology | en_US |
dc.subject.mesh | Indomethacin - Pharmacology | en_US |
dc.subject.mesh | Infant | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Membrane Potentials - Drug Effects | en_US |
dc.subject.mesh | Middle Aged | en_US |
dc.subject.mesh | Muscle Relaxation - Drug Effects | en_US |
dc.subject.mesh | Muscle, Smooth, Vascular - Drug Effects - Physiology - Physiopathology | en_US |
dc.subject.mesh | Nitroarginine | en_US |
dc.subject.mesh | Pyrroles - Pharmacology | en_US |
dc.subject.mesh | Vasodilator Agents - Pharmacology | en_US |
dc.title | Endothelium-dependent hyperpolarization caused by bradykinin in human coronary arteries | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1172/JCI116907 | - |
dc.identifier.pmid | 8254041 | - |
dc.identifier.scopus | eid_2-s2.0-0027132065 | en_US |
dc.identifier.volume | 92 | en_US |
dc.identifier.issue | 6 | en_US |
dc.identifier.spage | 2867 | en_US |
dc.identifier.epage | 2871 | en_US |
dc.identifier.isi | WOS:A1993ML64300042 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Nakashima, M=35599797500 | en_US |
dc.identifier.scopusauthorid | Mombouli, JV=7004285772 | en_US |
dc.identifier.scopusauthorid | Taylor, AA=8157815100 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0021-9738 | - |