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(Hypertension. 1997;30:825-829.)
© 1997 American Heart Association, Inc.

Articles

Endothelin Mediation of Insulin and Glucose-Induced Changes in Vascular Contractility

Pilar Nava María; Teresa Collados; Felipe Massó; ; Verónica Guarner

From the Cellular Physiology Department, National Institute of Cardiology "Ignacio Chávez" (T.C., F.M., V.G.), and Mexican Faculty of Medicine, La Salle University (P.N.), México, D.F.

Correspondence to Verónica Guarner, PhD, Departamento de Fisiología Celular, Instituto Nacional de Cardiología "Ignacio Chávez," Juan Badiano 1, Tlalpan, México, D.F. 14080.

Abstract Although the prevalence of hypertension in diabetic patients is high and many factors participate, hyperinsulinemia cannot be discarded as a contributing factor. Insulin could act directly on smooth muscle altering intracellular calcium levels that mediate contraction and glucose transport or could induce the secretion of endothelin by the endothelial cells lining the vessels. The aim of the present report was to study the effect of different glucose and insulin concentrations on rat vascular smooth-muscle contractile characteristics and to determine whether insulin effects are mediated by endothelin. Femoral arteries obtained from Wistar rats were placed in an in vitro chamber and superfused with different glucose and/or insulin solutions. The contractile response to KCl 80 mmol/L, measured by the force generated, showed a significant decrease with high extracellular glucose concentrations (11 mmol/L). Insulin caused a dose-dependent increase in arterial contraction induced by KCl. This increase was significant when arteries were stimulated with 80 mmol/L KCl in the presence of 5.5 mmol/L glucose, but when 40 mmol/L KCl was used, an increase was observed with both 5.5 and 11 mmol/L glucose. The insulin-induced contraction was significantly reduced in the presence of hyperimmune anti-endothelin serum and in the presence of endothelin receptor ET_A and ET_B antagonists PD 151,242 and BQ-788, respectively. These results suggest that hyperinsulinemia and hyperglycemia may contribute to hypertension in diabetes and that responses to insulin are mediated partially by endothelin, thus explaining why non–insulin-dependent diabetes mellitus patients show an increase in arterial pressure before the onset of nephropathy.

Key Words: muscle, smooth, vascular • insulin • glucose • endothelin

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