title: Adventitia removal does not modify the alphaID-adrenoceptors response in aorta during hypertension and ageing.
abstract: 1 The aim of the current study was to characterize the alpha(1)-adrenergic receptors (alpha(1)-ARs) present in the isolated tunica media of aorta, in normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats during the course of ageing and hypertension (rats of 1, 3, 6 and 12 months of age). In all vessels, endothelium was removed. 2 In isolated aortic rings, phenylephrine increased contraction in a concentration- and age-dependent manner and was impaired in old SHR compared with WKY rats. 3 The alpha(1)-AR selective antagonist prazosin showed high affinity (pA(2)) in vessels from both rat strains. 4 The potency of the alpha(1A)-AR selective antagonists, RS 100329 (5-methyl-3-[3-[4-[2-(2,2,2,-trifluoroethoxy) phenyl]-1-piperazinyl] propyl]-2,4-(1H)-pyrimidinedione) and 5-methylurapidil in antagonizing aortic phenylephrine-responses was low. 5 The alpha(1D)-AR selective antagonist, BMY 7378 (8-[2-[4-(2-methoxyphenyl)-1 piperazynil] ethyl]-8-azaspiro [4.5] decane-7,9-dione) potently blocked phenylephrine-induced responses in aorta from both strains and at all ages. 6 Adventitia removal decreased E(max) in older rats and modified the relative affinity (pD(2)), but did not affect the affinity of the selective antagonists. 7 The results suggest that aorta tunica alpha(1D)-AR is the main subtype involved in phenylephrine-induced contraction of rat aorta, while alpha(1A)-AR plays only a minor role. 8 Ageing and hypertension did not modify alpha(1)-ARs in the blood vessel and the tunica adventitia does not seem to participate in contraction, even though alpha(1)-ARs are expressed.
authors: Departamento de Farmacobiología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Sede Sur, México, D.F.
authors: J H
authors: JH
authors: Gómez-Zamudio
authors: R
authors: R
authors: Villalobos-Molina
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000375:Aging / Q000502:physiology*; D000818:Animals; D004730:Endothelium, Vascular / Q000502:physiology*; D005347:Fibroblasts / Q000502:physiology; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D009119:Muscle Contraction / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D032389:Myocytes, Smooth Muscle / Q000502:physiology; D010879:Piperazines / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D018340:Receptors, Adrenergic, alpha-1 / Q000187:drug effects / Q000502:physiology*; D013941:Thymine / Q000494:pharmacology; D017540:Tunica Media / Q000502:physiology; D015430:Weight Gain / Q000502:physiology
chemical_list: C547721:Adra1d protein, rat; D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists; D010879:Piperazines; D012333:RNA, Messenger; C120711:RS 100329; D018340:Receptors, Adrenergic, alpha-1; C057446:5-methylurapidil; D013941:Thymine