To study the relationship between serum Na concentration and impairment of homeostatic mechanisms in advanced congestive heart failure (CHF), we evaluated the status of the sympathetic nervous system, renin-angiotensin system, and regional visceral blood flow in 26 patients with this syndrome. Compared with normal subjects, hyponatremic patients had marked stimulation of PRA (P = 0.012), norepinephrine (P less than 0.001), and epinephrine (P less than 0.001) with severe impairment of renal (P less than 0.001) and hepatic (P less than 0.003) plasma flows. In contrast, normonatremic patients, with an apparently similar degree of CHF, demonstrated less pronounced abnormalities in all of these parameters. Moreover, the responses of neurohormones and regional blood flow to orthostatic stress were greatly attenuated in the hyponatremic patients, whereas, the normonatremic subjects had more normal responses. We conclude that serum Na concentration serves as a useful index of activation of the sympathetic nervous system, renin-angiotensin system, and impairment of regional perfusion in patients with advanced CHF.
SUMMARY To assess the contribution of the renln-angiotensin-aldosterone system and renal hemodynamics to acute renal sodium handling in essential hypertension we studied 21 subjects who had essential hypertension (16 with normal renin, 5 with low renin) and 9 normal subjects. All were in balance on a 10 mEq sodium intake before receiving a small sodium load, 60 mEq intravenously over 1 hour. Hypertensive subjects with low renin showed the anticipated exaggerated natriuresis, which was transient and occurred without a rise in blood pressure. Natriuresis in hypertensive subjects with normal renin was either normal or blunted; delayed sodium excretion occurred in a subset, along with delayed suppression of the renin-angiotensin-aldosterone system by the saline load. Neither renal plasma flow nor glomerular filtration rate changed during the saline load. After 72 hours of converting enzyme inhibition with enalapril, renal plasma flow increased substantially more in the subjects with a blunted renin response and their natriuretic response to the sodium load returned to normal. These results indicate that when prior sodium intake is controlled, large sodium loads are avoided, and low renin hypertension is removed as a confounding variable, blunted rather than exaggerated natriuresis is the common feature of essential hypertension. Equally well documented has been the sensitivity of hypertension to sodium intake. 43 It has been difficult to reconcile the two phenomena -accelerated sodium excretion and sensitivity of the hypertension to sodium intake -in a single pathogenetic sequence, in which sodium is responsible for the hypertension. Without exception, however, the acute sodium load employed in earlier studies has been very large, and with few exceptions, the state of sodium balance before administration of the sodium load was uncontrolled. One goal of this study was to assess the rate of sodium Received April 4, 1985; accepted August 27, 1985. excretion after a much more physiological sodium load, 60 mEq, or about the quantity of sodium in a typical meal, in subjects whose sodium balance was controlled before administration of the sodium load. In response to a large sodium load, suppression of the renin-angiotensin-aldosterone system is delayed in some subjects with normal renin and essential hypertension.6 These subjects also have disordered angiotensin-mediated control of renal perfusion and aldosterone release with shifts in sodium balance.7 A second goal of this study was to examine the response of the renin system to a much smaller sodium load and to relate the magnitude of renin suppression to the rate of sodium excretion following the sodium load. Our working premise was that sodium excretion must reflect, at least in part, the state and responsiveness of the renin-angiotensin-aldosterone system and the renal blood supply.Because earlier studies have shown especially pronounced exaggerated natriuresis in subjects with low renin essential hypertension, "10 we included a subgroup in this category as a posi...
We tested the hypothesis that 1-desamino-8-D-arginine vasopressin (DDAVP), a V2-receptor agonist, could inhibit the diuresis induced by water immersion in humans. Water and electrolyte excretion, plasma atrial natriuretic factor concentration, and plasma aldosterone concentration were measured initially and after 3 h of water immersion in 13 healthy sodium-replete men given either placebo or 20 micrograms of intranasal DDAVP. Guanosine 3',5'-cyclic monophosphate and urea excretion and urine osmolality were also determined. DDAVP inhibited the diuresis induced by water immersion in men: 758 +/- 168 (SE) ml/3 h in the placebo group vs. 159 +/- 28 ml/3 h in the DDAVP group (P less than 0.05). After 3 h of water immersion, plasma atrial natriuretic factor concentrations were increased from 11 +/- 2 to 20 +/- 4 pg/ml in the placebo group and from 14 +/- 2 to 33 +/- 4 pg/ml in the DDAVP group (P less than 0.05). Plasma aldosterone concentrations were decreased from 98 +/- 18 to 45 +/- 6 pg/ml in the placebo group (P less than 0.05) and from 54 +/- 17 to 25 +/- 5 pg/ml in the DDAVP group (P less than 0.05). Despite these changes in aldosterone and atrial natriuretic factor concentrations, which should increase sodium excretion, DDAVP decreased the natriuresis induced by water immersion in humans: 56 +/- 8 meq Na+/3 h in the placebo group vs. 36 +/- 6 meq Na+/3 h in the DDAVP group (P less than 0.05). DDAVP may be used to prevent the diuresis associated with central redistribution of blood volumes that occur during water immersion.(ABSTRACT TRUNCATED AT 250 WORDS)
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