Troglitazone and vascular reactivity: role of glucose and calcium.
Metabolism
; 48(1): 125-30, 1999 Jan.
Article
en En
| MEDLINE
| ID: mdl-9920156
ABSTRACT
We sought to determine whether insulin/insulin-like growth factor-1 (IGF-1) and an insulin-sensitizing agent, troglitazone, have additive vasodilatory effects and the possible involvement of intracellular Ca2+ ([Ca2+]i) and/or glucose utilization in these effects. Contractile responses to norepinephrine (NE) and potassium chloride (KCl), as well as relaxation to endothelium-dependent (acetylcholine [Ach]) and -independent (sodium nitroprusside [NaNP]) agents, were examined in rat tail artery rings in the presence of insulin/IGF-1 and/or troglitazone. Endothelium-intact tail artery rings stretched to 1 g tension were preincubated with troglitazone (3 micromol/L) and/or insulin/IGF-1 (100 nmol/L) prior to addition of graded doses of NE and KCI. A 90-minute exposure to troglitazone attenuated the maximal contraction to graded doses of NE and KCI (P<.0001). Incubation in glucose-free medium decreased the responses only to NE; troglitazone further attenuated the NE-induced contraction (P = .001). In submaximally precontracted endothelium-intact rings, troglitazone increased the relaxation both to NaNP (P<.0001) and to Ach (P = .001). Contraction experiments in depolarizing KCI (25 mmol/L) or Ca2+ -free buffer showed that troglitazone and insulin have a similar Ca2+ dependency. In conclusion, troglitazone, like insulin/IGF-1, attenuates responses to vasoactive agonists through a Ca2+ -dependent mechanism that may require the presence of glucose but is independent of insulin action and nitric oxide (NO) production.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Tiazoles
/
Vasodilatadores
/
Calcio
/
Cromanos
/
Tiazolidinedionas
/
Glucosa
/
Hipoglucemiantes
Límite:
Animals
Idioma:
En
Revista:
Metabolism
Año:
1999
Tipo del documento:
Article
País de afiliación:
Estados Unidos