Effect of Sodium Intake on Plasma Catecholamines in Normal Subjects*

Abstract

The effect of the state of sodium balance on the activity of the sympathetic nervous system has been evaluated previously by measuring urinary catecholamine excretion. Since urinary catecholamine may be affected by factors such as renal function or renal production of catecholamines, blood catecholamines may provide a better index of the activity of the sympathetic nervous system. The present study was undertaken to evaluate the effect of varying sodium intake on blood catecholamines.Thirteen normal subjects were studied for a period of 3 weeks in a metabolic ward. They received during the first, second, and third week 10, 100, and 200 meq sodium/day, respectively. On the seventh day of each week, when the patients had achieved sodium balance, urinary sodium excretion as well as blood levels of PRA, norepinephrine (NE), epinephrine (Ep), and dopamine (D) were measured in the supine position, at 5, 10, 15, and 20 min of upright posture, and at the end of 40 min of ambulation.The results show that: 1) blood levels of NE, Ep, and D as well as PRA were significantly higher during low sodium intake than during medium or high sodium intake, 2) as in the case of PRA, there was an inverse relationship between the blood levels of NE, Ep, and urinary sodium excretion; 3) upright posture produced a significant increment in the blood levels of NE which was not affected by sodium intake; and 4) the increment in PRA with posture was significantly greater during low sodium intake than with medium high sodium intake.The data demonstrate that: 1) the plasma levels of NE, Ep, and D are affected by the state of sodium balance, particularly during marked sodium depletion; and 2) meaningful interpretation of the significance of the blood levels of catecholamines should be made with reference to indices of sodium balance, such as urinary sodium excretion. (JClin Endocrinol Metab 48: 26, 1978) S EVERAL lines of evidence point toward the possible role of increased activity of the sympathetic nervous system in the genesis of essential hypertension (1-3). Esler et al. found hemodynamic evidence of sympathetic hyperactivity in a group of patients with high renin hypertension (4). However, Mitchell et al. (5) did not find differences in plasma catecholamine levels among hypertensive patients with different levels of PRA. The data on the relationship between urinary or blood catecholamines and essential hypertension are controversial. Some investigators have reported elevated levels of urinary catecholamines in 5-33% of patients (6-9), whereas others have found decreased excretion (10). Measurements of blood levels of catecholamines did not reveal a

The Influence of NaCl Supplementation on the Postnatal Development of Urinary Excretion of Noradrenaline, Dopamine, and Serotonin in Premature Infants

“…Our present findings support the view that sodium depletion enhances the activity of the renal sympathetic nervous system (2,22,25) even in low birth weight premature infants. In this regard, it is to be considered that, in addition to neural release, urinary CAs may be derived from glomerular filtration and tubular secretion (4).…”

The effect of angiotensin II and noradrenaline alone and in combination on renal sodium excretion in man.

“…Similarly the baseline plasma NA levels in our subjects were at the upper part of the normal range for resting supine subjects. The increase in plasma NA (mean 316 ± 51 pg m-1') and final levels achieved (Table 2) are slightly higher than those that might be expected in upright salt depleted subjects and are similar to those seen during submaximal exercise (Robertson et al, 1979;Romoff et al, 1979;Seidelin et al, 1987). These levels are also comparable with those found in patients with heart failure (Levine et al, 1982;Fitzpatrick et al, 1985).…”

Salt Sensitivity of Blood Pressure

“…55 In SS hypertensive subjects, plasma catecholamines do not decrease in response to a salt load as they do in normotensive or SR hypertensive subjects, likely contributing to the hypertensive response to salt. [56][57][58][59][60] In contrast, plasma catecholamine responses to salt depletion are exaggerated in SS compared with SR hypertensive subjects, perhaps reflecting sympathetic stimulation by the decrease in BP. 47,61 Renal natriuretic dopamine fails to be normally stimulated whereas renal norepinephrine fails to be normally inhibited during a salt load in SS hypertensive subjects, leading to an altered urine ratio between these catechols that may be related to impaired sodium excretion.…”