title: Noradrenergic transmission in the tail artery of hypertensive rats transgenic for the mouse renin gene Ren-2.
abstract: 1. The aim of the present study was to analyse the noradrenergic transmission in the tail artery of hypertensive rats transgenic for the mouse renin gene Ren-2 (TGR) in comparison with its control, the Sprague-Dawley (SD) rat. 2. Electrical field stimulation (EFS) of vascular segments produced frequency-dependent vasoconstrictions that were significantly greater in TGR arteries. 3. These contractions were abolished by tetrodotoxin (0.1 microM). Phentolamine (50 nM) and prazosin (1 - 10 nM) produced an inhibition of these responses that was significantly greater in SD arteries, whereas that produced by yohimbine (0.5-1 microM) was higher in TGR arteries. In both strains, propranolol (1 microM) potentiated the responses to EFS, and this increase was observed at lower frequencies in TGR arteries. 4. The EFS-evoked [3H]-noradrenaline (NA) release was significantly greater in TGR than in SD rats. However, NA (10 nM-10 microM) reduced and yohimbine and phentolamine (10 nM-10 microM) increased the tritium outflow to a similar degree in both strains. 5. Exogenous NA also induced greater vasoconstriction in TGR arteries. 6. These results suggest the existence in TGR tail artery of an increase in: (a) NA-release and alpha 2-adrenoceptor-mediated contractions, which could contribute to the elevated blood pressure in these rats; and (b) beta-adrenoceptor-mediated vasodilatations, which may be a mechanism to counteract high blood pressure.
authors.affiliation: Departamento de Farmacología y Terapeutica, Facultad de Medicina, Universidad Autónoma, Madrid, Spain.
authors.forename: S M
authors.initials: SM
authors.lastname: Arribas
authors.forename: M J
authors.initials: MJ
authors.lastname: Alonso
authors.forename: J
authors.initials: J
authors.lastname: Marín
authors.forename: F
authors.initials: F
authors.lastname: Fernandes
authors.forename: J L
authors.initials: JL
authors.lastname: Llergo
authors.forename: C F
authors.initials: CF
authors.lastname: Sánchez-Ferrer
authors.forename: M
authors.initials: M
authors.lastname: Salaices
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D001158:Arteries / Q000294:innervation; D004558:Electric Stimulation; D006973:Hypertension / Q000235:genetics* / Q000503:physiopathology*; D008297:Male; D051379:Mice; D009638:Norepinephrine / Q000494:pharmacology / Q000502:physiology*; D010646:Phentolamine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018341:Receptors, Adrenergic, alpha-2 / Q000187:drug effects / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology; D012083:Renin / Q000235:genetics*; D009435:Synaptic Transmission / Q000187:drug effects / Q000235:genetics* / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D018341:Receptors, Adrenergic, alpha-2; D011943:Receptors, Adrenergic, beta; D015016:Yohimbine; D013779:Tetrodotoxin; D012083:Renin; D009638:Norepinephrine; D011224:Prazosin; D010646:Phentolamine