title: Evidence for a common defect associated with pressure in the aorta of two hypertensive rat strains.
abstract: 1. Thoracic aortas of normotensive (Wistar-Kyoto (WKY) and Lyon normotensive (LN)) and hypertensive (spontaneously hypertensive rats (SHR) and Lyon hypertensive (LH)) rats from two groups (Japanese (WKY rats and SHR) and Lyon (LN and LH rats)) were compared using organ chambers. Changes in endothelium and smooth muscle reactivity to noradrenaline (NA), carbamylcholine and N omega-nitro-L-arginine (L-NNA) were analysed to distinguish between changes in reactivity that are associated with the presence of hypertension and those that are dependent on group (Japanese vs Lyon). 2. Aortas of hypertensive rats had lower pD2 values for NA than aortas from normotensive rats. These differences were associated with hypertension (P < 0.005 and P < 0.01) and group (P < 0.005 and P < 0.005) in presence or absence of endothelium, respectively, whereas no difference was seen in the maximal developed tension in response to NA. 3. Aortas also differed by a reduced ability to relax in response to carbamylcholine in hypertensive rats; this effect is hypertension (P < 0.05) and group (P < 0.005) dependent, without any change in carbamylcholine pD2 values. 4. Changes in maximum developed tension in the presence of L-NNA were found to be endothelium dependent and pressure and group independent. Furthermore, the change in tension induced by L-NNA appears significantly more pronounced in SHR than in LH rats (P < 0.05). 5. These results indicate that the common defect associated with hypertension appears to be linked to the endothelium through alpha-adrenoceptors and muscarinic receptors in both the Japanese and Lyon groups. However, SHR differs markedly from LH rats by having a higher developed tension in response to NA, this increased tension being counterbalanced by the release of nitric oxide, as observed in the presence of L-NNA.
authors.affiliation: INSERM U337 15, Broussais Hospital, Paris, France.
authors.forename: P
authors.initials: P
authors.lastname: Chamiot-Clerc
authors.forename: M H
authors.initials: MH
authors.lastname: Colle
authors.forename: M
authors.initials: M
authors.lastname: Legrand
authors.forename: J
authors.initials: J
authors.lastname: Sassard
authors.forename: M E
authors.initials: ME
authors.lastname: Safar
authors.forename: J F
authors.initials: JF
authors.lastname: Renaud
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000503:physiopathology*; D002217:Carbachol / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology*; D019335:Nitroarginine / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013045:Species Specificity
chemical_list: D019335:Nitroarginine; D002217:Carbachol; D009638:Norepinephrine