title: Functional characteristics of alpha adrenergic and endothelinergic receptors in pressurized rat mesenteric veins.
abstract: Increasing transmural pressure can alter the functional role of post-junctional receptor subtypes. Under conditions of changing transmural pressure, we investigated the relative contributions of alpha adrenergic (α-ARs) and endothelinergic receptors to norepinephrine (NE) and endothelin (ET-1) contractile responses, respectively, in third-order rat mesenteric small veins (MSV) and arteries (MSA). NE, phenylephrine (PE), clonidine, and ET-1 concentration-response curves were constructed in the absence and presence of α-adrenergic and ET-1 receptor antagonists, respectively. MSV were more sensitive to NE, PE, and ET-1 compared with MSA. The sensitivity of MSV to NE was higher than that to PE. Phentolamine (α1-AR/α2-AR antagonist) and prazosin (α1-AR antagonist) completely abolished NE responses. Yohimbine (α2-AR antagonist) reduced NE and clonidine contractile responses in MSV. Clonidine contractile responses were reduced by prazosin in MSA. In MSA and MSV, BQ-610 (ET(A) receptor antagonist) but not BQ-788 (ET(B) receptor antagonist) reduced ET-1 contractile responses. Combined application of BQ-610 and BQ-788 caused further reduction in ET-1 concentration-response curves obtained in MSV. These results suggest that in addition to α1-ARs and ET(A) receptors, α2-ARs and ET(B) receptors also mediate NE and ET-1 contractile responses in MSV, respectively, with no change in the participation of these receptors as transmural pressure is increased.
authors.affiliation: Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, ON N1G 2W1, Canada.
authors.forename: Saad
authors.initials: S
authors.lastname: Enouri
authors.forename: Gabrielle
authors.initials: G
authors.lastname: Monteith
authors.forename: Ron
authors.initials: R
authors.lastname: Johnson
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists / Q000494:pharmacology; D058669:Adrenergic alpha-2 Receptor Antagonists / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D003000:Clonidine / Q000494:pharmacology; D065130:Endothelin A Receptor Antagonists; D065131:Endothelin B Receptor Antagonists; D019332:Endothelin-1 / Q000378:metabolism; D008297:Male; D008642:Mesenteric Veins / Q000187:drug effects / Q000378:metabolism*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D044022:Receptor, Endothelin A / Q000378:metabolism*; D044023:Receptor, Endothelin B / Q000378:metabolism*; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism*; D018341:Receptors, Adrenergic, alpha-2 / Q000378:metabolism*; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D058668:Adrenergic alpha-1 Receptor Antagonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D065130:Endothelin A Receptor Antagonists; D065131:Endothelin B Receptor Antagonists; D019332:Endothelin-1; D044022:Receptor, Endothelin A; D044023:Receptor, Endothelin B; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2; D010656:Phenylephrine; D003000:Clonidine; D009638:Norepinephrine