Effect of pioglitazone on vascular reactivity in vivo and in vitro. Am J Physiol 1996 Mar;270(3 Pt 2):R660-6
Date
03/01/1996Pubmed ID
8780234DOI
10.1152/ajpregu.1996.270.3.R660Scopus ID
2-s2.0-13344282090 (requires institutional sign-in at Scopus site) 71 CitationsAbstract
Pioglitazone (a thiazolidinedione derivative) increases insulin sensitivity and prevents hypertension in the Dahl-salt-sensitive (S) rat. The present study was undertaken to determine if pioglitazone modulates pressor responsiveness to vasoactive agents, both in vivo and in vitro. In vivo, pretreatment with pioglitazone inhibited (P < 0.02) pressor responses to both norepinephrine and angiotensin II in conscious Dahl-S, but not in Sprague-Dawley rats. In vitro, pioglitazone augmented the capacity of insulin to inhibit pressor responses of strips of thoracic aortas to norepinephrine, but not to angiotensin. Additionally, in vitro, incubation with insulin plus pioglitazone augmented acetylcholine-induced, but not nitroprusside-induced vasodilation. Pioglitazone pretreatment increased (P < 0.001) in vitro insulin-stimulated glucose uptake in adipose tissue, but not in thoracic aortas of Dahl-S. We hypothesize that pioglitazone attenuates hypertension by modulating the effects of insulin on vascular function, resulting in both blunted vasoconstriction and augmented acetylcholine-induced vasodilation. These alterations are not accounted for by an effect of pioglitazone on glucose uptake by vascular smooth muscle.
Author List
Kotchen TA, Zhang HY, Reddy S, Hoffmann RGMESH terms used to index this publication - Major topics in bold
AnimalsAorta
Cells, Cultured
Glucose
Hypoglycemic Agents
Insulin
Male
Rats
Rats, Sprague-Dawley
Thiazoles
Thiazolidinediones
Vasoconstriction
Vasodilation