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Several lines of evidence suggest that insulin resistance and the resultant hyperinsulinaemia are causally related to hypertension. Insulin actions are initiated by binding to a high-affinity transmembrane protein receptor which is present in all mammalian cells. These effects are predominant in skeletal muscle, liver, and fat and involve a number of tissue-specific and biochemically diverse events. Less well known are effects of insulin occurring in tissues not usually considered as insulin targets, which are hypothetical contributors to the pro-hypertensive action of the hormone. These effects include activation of renal sodium reabsorption, stimulation of the sympathetic nervous system, growth-promoting activity on vascular smooth muscle cells, and modulation of transmembrane cation transport. Epidemiological investigations have implicated sodium intake in the pathogenesis of hypertension. Because of the sodium-retaining effects of insulin, it has been postulated that insulin resistance with associated hyperinsulinaemia may be critical for the pathogenesis of salt-sensitivity in essential hypertensive subjects. Insulin resistance is present also in strains of rats with genetic hypertension that can be utilized as models to study the molecular mechanisms of this abnormality. In the present article, we summarize the current knowledge of the mechanisms of insulin resistance in rat models of arterial hypertension in which decreased sensitivity to insulin occurs and propose a rationale hypothesis that links insulin resistance with salt-sensitivity and hypertension.