Comparison of contractile responses relative to protein between isolated diabetic and nondiabetic rat aortae to KCl and alpha-adrenoceptor agonists in different extracellular calcium concentrations

Citation
J. Nakasone et al., Comparison of contractile responses relative to protein between isolated diabetic and nondiabetic rat aortae to KCl and alpha-adrenoceptor agonists in different extracellular calcium concentrations, ARZNEI-FOR, 50(12), 2000, pp. 1078-1083
Citations number
22
Categorie Soggetti
Pharmacology & Toxicology
Journal title
ARZNEIMITTEL-FORSCHUNG-DRUG RESEARCH
ISSN journal
00044172 → ACNP
Volume
50
Issue
12
Year of publication
2000
Pages
1078 - 1083
Database
ISI
SICI code
0004-4172(200012)50:12<1078:COCRRT>2.0.ZU;2-V
Abstract
The influence of extracellular Ca2+ concentration on contractile responses of aortae isolated from diabetic rats to KCl and alpha -adrenoceptor agonis ts was compared with that of non-diabetic rat aortae. Diabetic rats 6 weeks after administration of streptozotocin showed significantly lower body wei ght and higher plasma glucose concentration, but the protein content per ea ch aortic ring preparation was not significantly different from that of non -diabetic preparation. Both diabetic and non-diabetic aortae showed concent ration-dependent contractile responses to norepinephrine, which were concen tration-dependently inhibited by prazosin. On the other hand, clonidine ind uced small contractions in both aortae, which tended to be more inhibited b y prazosin than yohimbine. In non-diabetic aortae, the contractile response s to KCI, norepineyhrine, methoxamine and clonidine were significantly grea ter with 2.5 mmol/l of extracellular Ca2+ than 1.25 mmol/l. In diabetic aor tae, however, the contractile responses were not significantly influenced b y changes in extracellular Ca2+ concentration. Additionally, the contractil e responses to each agonist were markedly greater in non-diabetic aortae th an diabetic ones. The present results indicate that the contractions of dia betic vasculature do not respond to changes in extracellular Ca2+ concentra tion, suggesting that there may be some impairment of Ca2+ related mechanis ms.