title: Influence of endothelium on beta-adrenoceptor-mediated mechanical and electrical functions in rat pulmonary artery.
abstract: The effect of isoprenaline on mechanical and electrical functions was studied in intact and denuded rat isolated pulmonary arteries. In intact blood vessels, isoprenaline-induced relaxation was significantly attenuated by acidification of buffer, presence of Ba(2+) and/or ouabain. Isoprenaline produced hyperpolarisation of vascular muscle cells increasing E(m) from -61.0+/-0.44 (n=190 cells) to -70.0+/-0.74 mV (n=31 cells; mean+/-SE). The latter effect was inhibited by acidification of buffer, tetraethylammonium (TEA), Ba(2+) and/or ouabain. Isoprenaline-mediated relaxation was also significantly inhibited by the removal of endothelial cells. Acidification of buffer, or the presence of Ba(2+), or ouabain alone did not result in further inhibition of relaxation to isoprenaline in denuded tissues. However, Ba(2+) and ouabain combined caused further inhibition of the relaxant responses to isoprenaline in denuded tissues analogous to intact tissue. Combined Ba(2+), TEA and ouabain also caused substantial inhibition of relaxant response to isoprenaline. Inclusion of Ba(2+), TEA or ouabain in acidic buffer did not further inhibit relaxation to isoprenaline when compared to Ba(2+), TEA and ouabain combined in regular buffer. Denudation of blood vessels resulted in a significant hyperpolarisation of vascular muscle (-67.4+/-0.35 mV; n=195 cells) due to the activation of K channels and Na(+)/K(+)-ATPase. In denuded tissue, isoprenaline was unable to further increase E(m) (-68.8+/-0.44 mV n=36). Isoprenaline-induced hyperpolarisation involves activation of K channels and Na(+)/K(+)-ATPase of smooth muscle cells possibly in parallel but mutually dependent on the presence of endothelial cells.
authors.affiliation: Division of BioMedical Sciences, Faculty of Medicine, Memorial University, St. John's, NL, Canada.
authors.forename: Puneet
authors.initials: P
authors.lastname: Mahajan
authors.forename: Reza
authors.initials: R
authors.lastname: Tabrizchi
mesh_terms: D000818:Animals; D017609:Barium Compounds / Q000494:pharmacology; D002712:Chlorides / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D009419:Nerve Tissue Proteins; D010042:Ouabain / Q000494:pharmacology; D024683:Potassium Channels, Tandem Pore Domain / Q000378:metabolism; D011651:Pulmonary Artery / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D019789:Tetraethylammonium / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects
chemical_list: D017609:Barium Compounds; D002712:Chlorides; D009419:Nerve Tissue Proteins; D024683:Potassium Channels, Tandem Pore Domain; D011943:Receptors, Adrenergic, beta; C024986:barium chloride; C420132:potassium channel subfamily K member 3; D010042:Ouabain; D019789:Tetraethylammonium; D000254:Sodium-Potassium-Exchanging ATPase; D007545:Isoproterenol