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Article: Endothelium-dependent relaxation and hyperpolarization evoked by bradykinin in canine coronary arteries: Enhancement by exercise-training

TitleEndothelium-dependent relaxation and hyperpolarization evoked by bradykinin in canine coronary arteries: Enhancement by exercise-training
Authors
Issue Date1996
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 1996, v. 117 n. 3, p. 413-418 How to Cite?
Abstract1. Kinins, which are produced locally in arterial walls, stimulate the release of endothelium-derived vasodilator substances. Therefore, they may participate in the metabolic adaptation to chronic exercise that occurs in the coronary circulation. Experiments were designed to compare the reactivity to bradykinin in coronary arteries isolated from sedentary and exercised-trained dogs (for 8-10 weeks). 2. The organ chambers used in this study were designed for measurement of isometric tension and cell membrane potential with glass microelectrodes. Rings of canine isolated coronary arteries with endothelium were suspended in the organ chambers filled with modified Krebs-Ringer bicarbonate solution (37°C, gassed with 5% CO2 in 95 O2), and were all treated with indomethacin to prevent interference from prostaglandins. 3. Bradykinin evoked concentration-dependent relaxations of the coronary arteries. However, the kinin was significantly less potent in relaxing coronary arteries from the sedentary dogs than those from the trained ones. 4. In the presence of N(G)-nitro-L-arginine (an inhibitor of nitric oxide synthases), concentration-relaxation curves to bradykinin were shifted to the right in both types of preparations. Nonetheless, the peptide was still significantly more potent in arteries from exercise-trained animals. 5. In the electrophysiological experiments, concentration-hyperpolarization curves to bradykinin obtained in arteries from sedentary dogs were also significantly to the right of those in vessels from exercise-trained animals. Thus, in arteries from exercised animals, bradykinin more potently evoked the release of both nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). 6. The angiotensin converting enzyme (ACE)-inhibitor, perindoprilat, shifted to the left the concentration-relaxation curves to bradykinin obtained under control conditions and in the presence of N(G)-nitro-L-arginine. The concentration-hyperpolarization curves to bradykinin were also shifted to the left by perindoprilat. The shift induced by the ACE-inhibitor in either type of preparation was not significantly different. 7. These findings demonstrate that exercise-training augments the sensitivity of the coronary artery of the dog to the endothelium-dependent effects of bradykinin. This sensitization to bradykinin may reflect an increased role of both NO and EDHF, and is not the consequence of differences in ACE activity in the receptor compartment.
Persistent Identifierhttp://hdl.handle.net/10722/171187
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMombouli, JVen_US
dc.contributor.authorNakashima, Men_US
dc.contributor.authorHamra, Men_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:35Z-
dc.date.available2012-10-30T06:12:35Z-
dc.date.issued1996en_US
dc.identifier.citationBritish Journal Of Pharmacology, 1996, v. 117 n. 3, p. 413-418en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171187-
dc.description.abstract1. Kinins, which are produced locally in arterial walls, stimulate the release of endothelium-derived vasodilator substances. Therefore, they may participate in the metabolic adaptation to chronic exercise that occurs in the coronary circulation. Experiments were designed to compare the reactivity to bradykinin in coronary arteries isolated from sedentary and exercised-trained dogs (for 8-10 weeks). 2. The organ chambers used in this study were designed for measurement of isometric tension and cell membrane potential with glass microelectrodes. Rings of canine isolated coronary arteries with endothelium were suspended in the organ chambers filled with modified Krebs-Ringer bicarbonate solution (37°C, gassed with 5% CO2 in 95 O2), and were all treated with indomethacin to prevent interference from prostaglandins. 3. Bradykinin evoked concentration-dependent relaxations of the coronary arteries. However, the kinin was significantly less potent in relaxing coronary arteries from the sedentary dogs than those from the trained ones. 4. In the presence of N(G)-nitro-L-arginine (an inhibitor of nitric oxide synthases), concentration-relaxation curves to bradykinin were shifted to the right in both types of preparations. Nonetheless, the peptide was still significantly more potent in arteries from exercise-trained animals. 5. In the electrophysiological experiments, concentration-hyperpolarization curves to bradykinin obtained in arteries from sedentary dogs were also significantly to the right of those in vessels from exercise-trained animals. Thus, in arteries from exercised animals, bradykinin more potently evoked the release of both nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). 6. The angiotensin converting enzyme (ACE)-inhibitor, perindoprilat, shifted to the left the concentration-relaxation curves to bradykinin obtained under control conditions and in the presence of N(G)-nitro-L-arginine. The concentration-hyperpolarization curves to bradykinin were also shifted to the left by perindoprilat. The shift induced by the ACE-inhibitor in either type of preparation was not significantly different. 7. These findings demonstrate that exercise-training augments the sensitivity of the coronary artery of the dog to the endothelium-dependent effects of bradykinin. This sensitization to bradykinin may reflect an increased role of both NO and EDHF, and is not the consequence of differences in ACE activity in the receptor compartment.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_US
dc.relation.ispartofBritish Journal of Pharmacologyen_US
dc.subject.meshAngiotensin-Converting Enzyme Inhibitors - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiologyen_US
dc.subject.meshCricetinaeen_US
dc.subject.meshDinoprost - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshEndothelium, Vascular - Drug Effectsen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshHeart Rate - Drug Effectsen_US
dc.subject.meshIsometric Contraction - Drug Effectsen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Drug Effects - Physiologyen_US
dc.subject.meshMuscle Relaxation - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshNitric Oxide Synthase - Antagonists & Inhibitorsen_US
dc.subject.meshNitroarginine - Pharmacologyen_US
dc.subject.meshPhysical Conditioning, Animalen_US
dc.titleEndothelium-dependent relaxation and hyperpolarization evoked by bradykinin in canine coronary arteries: Enhancement by exercise-trainingen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1476-5381.1996.tb15206.x-
dc.identifier.pmid8821528-
dc.identifier.scopuseid_2-s2.0-0030022212en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030022212&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume117en_US
dc.identifier.issue3en_US
dc.identifier.spage413en_US
dc.identifier.epage418en_US
dc.identifier.isiWOS:A1996TY67600003-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridMombouli, JV=7004285772en_US
dc.identifier.scopusauthoridNakashima, M=35599797500en_US
dc.identifier.scopusauthoridHamra, M=6602722404en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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