title: Comparison of contractile responses relative to protein between isolated diabetic and non-diabetic rat aortae to KCl and alpha-adrenoceptor agonists in different extracellular calcium concentrations.
abstract: The influence of extracellular Ca2+ concentration on contractile responses of aortae isolated from diabetic rats to KCl and alpha-adrenoceptor agonists was compared with that of non-diabetic rat aortae. Diabetic rats 6 weeks after administration of streptozotocin showed significantly lower body weight and higher plasma glucose concentration, but the protein content per each aortic ring preparation was not significantly different from that of non-diabetic preparation. Both diabetic and non-diabetic aortae showed concentration-dependent contractile responses to norepinephrine, which were concentration-dependently inhibited by prazosin. On the other hand, clonidine induced small contractions in both aortae, which tended to be more inhibited by prazosin than yohimbine. In non-diabetic aortae, the contractile responses to KCl, norepinephrine, methoxamine and clonidine were significantly greater with 2.5 mmol/l of extracellular Ca2+ than 1.25 mmol/l. In diabetic aortae, however, the contractile responses were not significantly influenced by changes in extracellular Ca2+ concentration. Additionally, the contractile responses to each agonist were markedly greater in non-diabetic aortae than diabetic ones. The present results indicate that the contractions of diabetic vasculature do not respond to changes in extracellular Ca2+ concentration, suggesting that there may be some impairment of Ca2+ related mechanisms.
authors.affiliation: Department of Pharmacology, School of Medicine, University of the Ryukyus, Okinawa, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Nakasone
authors.forename: M
authors.initials: M
authors.lastname: Higuchi
authors.forename: K
authors.initials: K
authors.lastname: Miyagi
authors.forename: T
authors.initials: T
authors.lastname: Matsuzaki
authors.forename: K
authors.initials: K
authors.lastname: Noguchi
authors.forename: M
authors.initials: M
authors.lastname: Sakanashi
authors.forename: S
authors.initials: S
authors.lastname: Yamashiro
authors.forename: T
authors.initials: T
authors.lastname: Itomine
authors.forename: M
authors.initials: M
authors.lastname: Sakanashi
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects*; D002118:Calcium / Q000494:pharmacology*; D003000:Clonidine / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D008729:Methoxamine / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects; D009124:Muscle Proteins / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000316:Adrenergic alpha-Agonists; D009124:Muscle Proteins; D011189:Potassium Chloride; D008729:Methoxamine; D003000:Clonidine; D002118:Calcium; D009638:Norepinephrine