BACKGROUND: It has been studied whether an adrenergic stimulation induced by the cold pressor test (CPT) could influence the behaviour of the transmembrane transport systems of sodium in hypertensive subjects compared to a normotensive control population. MATERIALS AND METHODS: Twenty-two hypertensive subjects (average age 43.2 +/- 5.7 years), with normal weight, without signs of cardiovascular and metabolic diseases, underwent the cold pressor test. The dynamic behaviour of sodium erythrocytic transport systems and plasmatic norepinephrine was evaluated basally, at the third minute during the cold pressor test and 20 minutes after the end of the test. The same test was carried out in a control population made up of 20 normotensive subjects (average age 41.9 +/- 4.8 years), selected on the basis of the absence of any cardiovascular or metabolic pathology and without family history of arterial hypertension. RESULTS: The cold pressor test did not cause significant changes in the sodium transmembrane transport systems in normotensive subjects, while in the hypertensive subjects a significant reduction was observed, during the test, in the total efflux of sodium and in the sodium/potassium pump, respectively from 2636 +/- 296 mumol/l/red blood cells/hr to 2032 +/- 178 mumol/l/red blood cells/hr (p < 0.0001) and from 2156 +/- 149 mumol/l/red blood cells/hr to 1610 +/- 101 mumol/l/red blood cells/hr (p < 0.0001); the intraerythrocytic sodium increased from 6.5 +/- 1.0 mmol/l/cells to 7.2 +/- 1.1 mmol/l/cells (p < 0.04) and the passive permeability decreased from 0.039 +/- 0.004 hr-1 to 0.018 +/- 0.006 hr-1 (p < 0.0001). During cold pressor test the increase in the plasma norepinephrine levels was correlated to the reduction in the total efflux of sodium (r = -0.60; p < 0.003) and in the sodium/potassium pump (r = -0.59; p < 0.003) only in hypertensive subjects. CONCLUSIONS: Our data show that an adrenergic stimulation, induced by the cold pressor test, is able to significantly influence the behaviour of transmembrane fluxes of sodium in hypertensive subjects, and it causes an inhibitory effect on the sodium/potassium pump and an increase in the intraerythrocytic sodium. Such data show the existence in hypertensive subjects of an interrelationship between adrenergic activity and sodium transport systems that could cooperate in causing and/or in maintaining the hypertensive syndrome.