The PTH-(1-84)/C-PTH fragment ratio predicts bone turnover with acceptable precision for biological measurements. Moreover, a change in serum calcium levels is one of the regulators of the relative amount of circulating PTH-(1-84) and its large C-PTH fragments.

To examine the mechanisms underlying the sensitivity to sodium intake in a subset of patients with essential hypertension, we studied the effects of different sodium intake (10, 100, 200 mEq/day) on blood pressure, the function of the renin-angiotensin-aldosterone system, and on blood levels of catecholamines in 20 patients with essential hypertension and 10 normal subjects. Mean blood pressure (MBP) was not different in hypertensive and normal subjects during low sodium diet. But, with high sodium intake, MBP increased by at least 10% in 12 patients (salt-sensitive), whereas in the remaining 8 patients (salt-resistant) and in normal subjects, MBP did not change significantly. This phenomenon cannot be attributed to differences in sodium retention because the percent change in body weight ad the urinary sodium excretion in the salt-sensitive patients was not different than it was in salt-resistant patients or in normal subjects. The observed difference in blood pressure response to high sodium intake in salt-sensitive patients is also not dependent on an impaired suppressibility of the renin-angiotensin-aldosterone system because there were no significant differences in the basal levels of PRA and aldosterone between the groups, and because the orthostatic increments in PRA were significantly lower in salt sensitive than they were in the salt-resistant patients and in normal subjects. Plasma norepinephrine (NE) levels were not significantly different between normal subjects or hypertensive patients while on low sodium intake. But during high sodium intake, they decreased significantly (P less than 0.05) in normal subjects (from 22 +/- 3.4 to 12 +/- 2.3 ng/dl) and in salt-resistant patients (from 17 +/- 4.5 to 13 +/- 2.4 ng/dl) but not in salt-sensitive patients (from 20 +/- 1.9 to 22 +/- 3.2 ng/dl). Furthermore, the majority of salt-sensitive patients displayed inappropriately high plasma NE in relation to their urine excretion of sodium during high sodium intake. Finally, the increments in plasma NE after 5 min of standing were significantly greater in salt-sensitive patients than they were in salt-resistant patients and normal subjects during both low or high sodium intake. These data indicate that a subset of patients with essential hypertension may have impaired suppressibility of plasma NE during high sodium intake, which suggests hyperactivity of the sympathetic nervous system in these patients. These aberrations may be responsible for the increase in MBP in the salt-sensitive patients during high sodium intake.

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Changes in the tubular reabsorption of sodium independent of aldosterone activity may play an important role in determining sodium excretion. Several studies in the dog employing clearance techniques have demonstrated that infusions of isotonic saline (1-5) or plasma-like solutions (1, 2) result in a depression of the over-all net tubular reabsorption of sodium as the excretion of sodium increases. Dirks, Cirksena, and Berliner have demonstrated by micropuncture studies in the dog that this depression of tubular reabsorption during the infusion of saline occurs specifically in the proximal tubule (6). These same authors reported that acute constriction of the thoracic inferior vena cava, a maneuver known to inhibit sodium excretion and to lead to chronic sodium retention and the formation of ascites (7), prevents this depression of proximal reabsorption during saline infusion (8). Such studies indicate that nonaldosterone factors determining the rate of sodium reabsorption by the proximal tubule could play a major role in the normal physiologic regulation of sodium balance and also may be involved in the pathogenesis of sodium retention in disorders characterized by the accumulation of ascites and edema.Although the factors that determine the rate of proximal tubular reabsorption are unknown, recent studies from our laboratory have demonstrated that renal vascular resistance and perfusion pressure may affect the over-all tubular reabsorp-

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