Effect of beta blockade on the erythrocyte transport of Na+: evaluation during stimulation by cold pressure test in patients with essential hypertension]

Abstract Several studies have shown in essential hypertension alterations of the transmembrane red blood cells sodium fluxes, as an involvement, especially in the early phases, also of the adrenergic system. In this study we evaluated the behaviour of red blood cells fluxes of sodium before, during and after the cold pressor test, a method used also to evoke an adrenergic stimulation, in twenty hypertensive subjects, 14 males and 6 females, with an average age of 43.2 +/- 5.7 years, with normal weight and without cardiovascular complications and metabolic diseases. The behaviour of the Na+ total efflux (Na+ TE), of the Na+/K+ pump, of the Na+K+ cotransport (Na+/K+ CT), of the Na+/Li+ counter transport (Na+/Li+ Cnt), of the Na+ passive permeability (Na+ PP), of the intracellular Na+ (I Na+) and of the plasmatic noradrenaline (NE) was evaluated basally, at the third minute during cold pressor test (CPT) and 20 minutes after the end of the test. The test, which the same method, was repeated after a 30 day treatment with propranolol at the dose of 240 mg/day in three daily administrations. The beta-blockade caused, besides the reduction of both the systolic and diastolic pressure values, a significant increase in the Na+/K+ CT (from 248 +/- 41 to 314 +/- 71 mmol/l/cells/h, p < 0.001) and a decrease in the Na+ PP (from 0.039 +/- 0.004 to 0.023 +/- 0.007 hr-1, p < 0.00001), probably directed towards the reduction of the accumulation of intracellular Na+, that could compete, among the other mechanisms, with the anti-hypertensive action of the beta-blockers. The CPT caused, before the beta-blockade, a significant depression of the Na+/K+ pump (from 2057 +/- 149 to 1610 +/- 101 mmol/l/cells/h, p < 0.00001) and of the Na+ TE (from 2640 +/- 397 to 2032 +/- 179 mmol/l/cells/h, p < 0.00001) inversely correlated to the levels of NE (r = -0.60, p < 0.003), with a consequent increase in I Na+ (from 6.2 +/- 0.6 to 7.5 +/- 1.5 mmol/l/cells, p < 0.001), showing how the adrenergic activation in hypertensive subjects is able to interfere with the systems of transmembrane transport with an inhibitory attitude, that is expressed by an increase in the levels of I Na+. The beta-blockade was able to outweigh the depression of the Na+/K+ pump (from 1843 +/- 584 to 1728 +/- 640 mmol/l/cells/h, p: ns) and the reduction of the Na+ TE, preventing the accumulation of I Na+ (from 6.3 +/- 1.6 to 6.6 +/- 1.3 mmol/l/cells, p: ns). Such data show an increased susceptibility of the Na+ transport systems to the adrenergic stimuli in hypertensive subjects with a tendency to favor the accumulation of I Na+ and that the beta-blockade is able to antagonize the effects, with a maintenance of the intracellular levels of Na+.