The arterial hypertension that frequently coexists with ventromedial hypothalamic (VMH) lesion-induced obesity has been obtained in rats chronically sustained on diets of standard-to-high salt content. Since VMH lesions also compromise the renal circulation and enhance ingestion of salt-loaded diets, the resulting haemodynamic adjustments, including hypertension, have been interpreted as possibly being sodium-dependent. This notion implies that chronically restricting dietary salt would ameliorate the hypertension, whereas the persistence of hypertension under such a regimen would suggest the potential contribution of non-sodium-related factors. This study assessed whether chronic maintenance of a low-salt diet would buffer the hypertensive and haemodynamic consequences of obesity, accompanying electrolytic VMH lesions in male Wistar-Kyoto (WKY) rats, compared with sham-treated controls. Despite the low-salt diet, the results showed that VMH obesity was accompanied by hypertension, elevated plasma norepinephrine, and redistribution of blood flow away from the brain, kidney and splanchnic organs. The compatibility of these results with earlier studies permitting salt ingestion, is difficult to reconcile with the notion that VMH-hypertension is sodiumdependent. Instead, it suggests that the VMH obesity-hypertension syndrome may provide a useful model for clarifying the autonomic consequences of either augmented carbohydrate ingestion of hyper-insulinaemia.