Sodium depletion increases platelet and plasma catecholamines in hypertensive men.

Abstract

SUMMARY The catecholamine content in blood platelets is considerably higher than that in plasma, and platelet catecholamines must be taken up from plasma, since blood platelets lack enzymes for catecholamine synthesis. However, it is unknown whether platelets take up and store catecholamines during physiological in vivo increments in plasma catecholamines. Previously untreated 50-year-old men (n = 17) with mild to moderate essential hypertension were given a low sodium diet for 2 weeks. Urinary excretion of sodium decreased from 201 ±11 (SE) to 24 ± 5 and 19 ± 4 mmol/24 hr after 1 and 2 weeks, respectively. During the first week, the blood platelet concentration of norepinephrine increased from 27.2 ± 2.9 to 39.6 ± 4.7 pg/mg (p<0.005) and venous plasma norepinephrine increased from 254 ± 22 to 347 ± 28 pg/ml (p<0.001). The platelet concentration of dopamine increased from 3.7 ± 0.4 to 5.6 ± 0.5 pg/ml (p<0.005), and venous plasma dopamine increased from 26 ± 4 to 41 ± 5 pg/ml (p<0.05). During the second week, both plasma and platelet norepinephrine and dopamine remained elevated. Platelet epinephrine showed a small increase from baseline to the second week (p<0.05), but no concomitant increase in plasma epinephrine occurred. Thus, sodium depletion increases both platelet and plasma catecholamines and blood platelets may take up catecholamines in vivo. Platelet catecholamine content may be an integrated measure of plasma catecholamine concentrations during variations caused by sodium depletion. (Hypertension 11: 477-482, 1988) KEY WORDS • blood pressure * electrolytes • epinephrine * norepinephrine * sympathetic tone • thrombocytes S OME of the knowledge about platelet 5-hydroxytryptamine (5-HT) and catecholamine content has been summarized by Da Prada and Picotti.1 The platelet levels of these monoamines are much higher than corresponding plasma concentrations. However, the molar contents of norepinephrine, dopamine, and epinephrine are several thousand times lower than the molar content of 5-HT. Platelet catecholamines are essentially free (unconjugated), and the subcellular localization in the platelets seems to be the 5-HT organelles (dense granules). Since platelets lack enzymes for catecholamine synthesis, it may be that the catecholamines can be actively transported and taken up through the platelet 5-HT carrier mechanism, although at a relatively low receptor/carrier affinity.

Decreased Platelet-Free Dopamine and Unchanged Noradrenaline and Adrenaline in Essential Hypertension

“…Zweifler and Julius (11) found increased platelet content of noradrenaline and adrenaline in patients with pheochromocytoma. It may be that platelet catecholamine content under certain circumstances is an integrated measure of plasma catecholamine concentrations over time (5,6). However, the platelet content of noradrenaline and adrenaline was unchanged in patients with essential hypertension despite their high plasma catecholamines (11).…”

“…There is some evidence that platelet content may be an integrated measure of plasma catecholamine concentrations over time (5,6). In essential hypertension, reduced 5-HT content in platelets has consistently been reported (7)(8)(9)(10) .…”

Role of catecholamines in platelet function: pathophysiological and clinical significance

“…Increased platelet levels of adrenaline and noradrenaline have been found in patients following prolonged sodium depletion, which increases adrenergic tone [319].…”

Neurogenic and behavioral influences on plasma lipids.

“…As expected, because the sympathetic nervous system regulates body salt and water balance (Esler, 1990), both diuretics and dietary sodium restriction stimulate noradrenergic activity, with associated significant elevation of plasma total and LDL cholesterol levels (E. A. Anderson et al, 1989;Egan, Weder, Petrin, & Hofman, 1991;Kjeldsen et al, 1988;LuR et al, 1979;Ruppert et al, 1991;Weidmann et al, 1983). The evidence strongly suggests a major role of the sympathetic nervous system in the elevated plasma lipids (Egan et al, 1991;Ruppert et al, 1991).…”