There is a growing body of evidence linking insulin resistance and hyperinsulinaemia with hypertension. Vascular delivery of insulin and glucose to the striated muscle may be rate-limiting for them to exercise their effects. We therefore studied the effects of experimentally induced hypertension (renovascular and DOCA-salt) on muscle uptake of [(3)H]-deoxyglucose ([(3)H]-DOG)(non-metabolized glucose analog). In both models of induced hypertension uptake of [(3)H]-DOG was compared with the corresponding normotensive controls. Spontaneously hypertensive rats (SHR), however, had a reduced [(3)H]-DOG muscle uptake relative to normotensive WKY rats. To clarify a pro-hypertensive role on insulin it was administered by means of a sustained release subcutaneous implant to normotensive rats for 2 months and we could not detect hypertension in the resting state, though a transient hypertensive response to acute saline loading was present. On the other hand, young SHR made hyperinsulinaemic by the same method had an accelerated development of hypertension relative to control SHR. Thus it is not hypertension as such but the genetic susceptibility that is associated with insulin effects on blood pressure. In human hypertension we evaluated exercise (a maneuver known to improve insulin-sensitivity and reduce blood pressure) in non-obese essential hypertensive subjects. Three months of exercise training was associated with improved glucose tolerance and insulin clearance rate, but had no effect on 24-h ambulatory blood pressure. Thus, in essential hypertension insulin does not contribute significantly to the maintenance of hypertension. Taken together, our data indicate that hypertension does not cause insulin resistance and that exogenous hyperinsulinaemia does not produce hypertension in normotensive rats. However, in genetically determined hypertension insulin may play a role in its development.
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