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To determine whether insulin regulates vascular smooth muscle Na+, K(+)-ATPase activity and if impaired insulin stimulation of vascular smooth muscle Na+, K(+)-ATPase activity could be a cause of increased vascular reactivity to norepinephrine and angiotensin II in diabetic states, the effects of insulin on Na+, K(+)-ATPase activity were examined in normal rabbit aortic intima-media incubated with normal plasma glucose and myo-inositol levels for 30 min. Insulin at 100 microU/ml (600 pmol/l) had no effect on Na+, K(+)-ATPase activity. At 250 microU/ml it caused a 4.2 +/- 0.8% increase, and at 500 microU/ml insulin caused a 17.7 +/- 1.4% increase in Na+, K(+)-ATPase activity that was completely inhibited by amiloride (1 mmol/l). Human insulin-like growth factor I (600 pmol/l) caused an 18.0 +/- 1.0% increase in Na+, K(+)-ATPase activity that was inhibited by amiloride. Insulin does not regulate (stimulate) aortic vascular smooth muscle Na+, K(+)-ATPase activity. Supraphysiological insulin concentrations, probably acting through an insulin-like growth factor I receptor, stimulate Na+/H+ exchange in aortic vascular smooth muscle and cause small secondary increases in Na+, K(+)-ATPase activity. In aortic intima-media incubated with normal plasma glucose and myo-inositol levels, endogenously released adenosine stimulates and maintains a component of resting Na+, K(+)-ATPase activity and stimulates acute increases in activity when norepinephrine (1 mumol/l) or angiotensin II (100 nmol/l) is added. These adenosine-stimulated components of Na+, K(+)-ATPase activity are selectively inhibited when the medium glucose is raised to 30 mmol/l during a 30-min equilibration and 30-min incubation.(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin does not regulate vascular smooth muscle Na+, K+-ATPase activity in rabbit aorta