Hypothalamic pressor responses and salt-induced hypertension in Dahl rats.

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Abstract
Interactions between abnormal salt intake and central sympathetic function were studied by recording pressor and sympathetic effects of hypothalamic stimulation in Dan salt-resistant (DR) and salt-sensitive (DS) rats. All DS rats, including those fed a low-salt diet since weaning, became hypertensive by 11 wk of age. Increased salt intake aggravated hypertension in DS rats without affecting blood pressure in DR rats. Basal sympathetic tone determined during urethane anesthesia, from the frequency of splanchnic nerve potentials as well as the magnitude of hypotension induced by .alpha.-adrenergic blockade with phentolamine, was consistently lower in low-salt DR rats than in any others. Pressor responses to electrical stimulation of the ventromedial hypothalamus, whether expressed as absolute or percent increases in mean pressure, were invariably enhanced in DS rats. On the other hand, attendant increases in sympathetic nerve firing were significantly higher in DS rats, but only when expressed as absolute changes and not when expressed as percent changes. Consequently, pressor and sympathetic responses became dissociated in magnitude such that low-salt DR rats which had the weakest pressor responses also had the highest percent increases in sympathetic nerve firing. Peripheral increases in cardiovascular reactivity were considered unlikely because pressor responses to drugs like norepinephrine, tyramine and vasopressin, were unaltered. Although 5-wk-old DS rats that were not exposed to high-salt intake remained normotensive, basal sympathetic activity and pressor responsiveness to hypothalamic stimulation were already enhanced. Since sympathetic and hypothalamic enhancement occurred before any other changes could be detected it was considered possible that sympathetic hyperactivity of hypothalamic origin may be involved in initiating genetic hypertension. Apparently, induction of hypertension in DS rats might depend on genetic transmission of hypersensitivity not only to salt but also to stressful stimuli.