Atrial natriuretic factor and salt wasting after aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: The causes of volume depletion and hyponatremia after subarachnoid hemorrhage are not fully understood but may be in part due to natriuresis or "cerebral salt wasting." Because previous studies using infrequent hormone sampling have given inconsistent results, we determined if elevations in atrial natriuretic factor concentrations preceded negative sodium and fluid balances. METHODS: We measured diurnal atrial natriuretic factor and vasopressin concentrations and sodium balance for 5 days in 14 consecutive patients after aneurysmal subarachnoid hemorrhage. RESULTS: Plasma concentrations of atrial natriuretic factor on admission were elevated in subarachnoid hemorrhage patients (mean +/- SD 106 +/- 59 pg/ml) compared with acutely ill controls (39 +/- 30 pg/ml). In eight patients, high peak concentrations of atrial natriuretic factor, greater than 300 pg/ml or a twofold increase above baseline, were followed by natriuresis and a negative sodium balance. Three patients, two of whom became hyponatremic, developed cerebral infarcts after natriuresis. Vasopressin concentrations were slightly elevated just after hemorrhage but subsequently declined to normal values. CONCLUSIONS: A markedly increased atrial natriuretic factor concentration precedes natriuresis in some patients and, with other abnormalities of water handling possibly including a relatively diminished vasopressin concentration, may cause volume depletion. Patients with natriuresis appear to be at increased risk for delayed cerebral infarction after subarachnoid hemorrhage.     

Suprasellar and intraventricular blood predict elevated plasma atrial natriuretic factor in subarachnoid hemorrhage.

Following subarachnoid hemorrhage, the plasma concentration of atrial natriuretic factor is elevated and appears to be independent of atrial stretch. While the hypothalamus and circumventricular organs contribute to sodium and intravascular volume regulation, their influence on atrial natriuretic factor is not known. We tested the hypothesis that, following subarachnoid hemorrhage, suprasellar cisternal blood, intraventricular blood, or ventricular enlargement would be associated with elevated plasma levels of atrial natriuretic factor. Computed tomograms of 26 patients performed less than or equal to 3 days after hemorrhage were analyzed to determine the presence of suprasellar or intraventricular blood and enlargement of the third or lateral ventricle. These results were correlated with the plasma atrial natriuretic factor and serum sodium concentrations. The initial atrial natriuretic factor concentration was elevated and was higher in patients with suprasellar or intraventricular blood than in those without (suprasellar: 131 +/- 20 and 54 +/- 10 pg/ml, respectively; intraventricular: 137 +/- 25 and 84 +/- 31 pg/ml, respectively). The atrial natriuretic factor concentration remained higher over the week following hemorrhage in patients with suprasellar blood than in those without (127 +/- 16 and 68 +/- 12 pg/ml, respectively). The atrial natriuretic factor concentration was not correlated with hyponatremia (125-134 meq/l) or age-corrected ventricular size. Hyponatremia did not correlate with the presence of intraventricular or suprasellar blood. Our data suggest that suprasellar and intraventricular blood disturb hypothalamic function, resulting in an elevated plasma atrial natriuretic factor concentration. The presence of a direct relation between atrial natriuretic factor and hyponatremia remains unclear.     

Cerebrospinal fluid atrial natriuretic factor in intracranial disease

We tested the hypothesis that the concentration of atrial natriuretic factor in the cerebrospinal fluid is an indicator of brain injury in patients with intracranial disease. Atrial natriuretic factor concentration was measured in 72 samples of cerebrospinal fluid from 28 patients with intraventricular drains and in nine samples from outpatient controls undergoing diagnostic lumbar puncture. Levels were correlated with diagnosis; systemic fluid administration; concentration of atrial natriuretic factor in the plasma; intracranial pressure; sodium, glucose, and protein concentrations, osmolality, and cell count in the cerebrospinal fluid; sodium concentration in the serum; and hemodynamics. Atrial natriuretic factor concentration was highest in cerebrospinal fluid from patients with intracerebral hematoma, followed by those with obstructive hydrocephalus and subarachnoid hemorrhage (19 +/- 2, 13 +/- 3, and 8 +/- 2 pg/ml, respectively); atrial natriuretic factor concentration was less than 4 pg/ml in the controls. Patients treated with fluid restriction had significantly higher atrial natriuretic factor levels than those receiving maintenance or high-volume fluids (16 +/- 3, 8 +/- 2, 10 +/- 1 pg/ml, respectively). The concentration of atrial natriuretic factor in the plasma was significantly elevated in patients with intracerebral hematoma and subarachnoid hemorrhage (155 +/- 38 and 92 +/- 20 pg/ml, respectively) and did not correlate with fluid administration or the concentration of atrial natriuretic factor in the cerebrospinal fluid. Neither cerebrospinal fluid nor plasma concentrations of atrial natriuretic factor correlated with intracranial pressure; cerebrospinal fluid sodium, glucose, or protein concentrations, osmolality, or cell count; serum sodium concentration; or hemodynamics. We conclude that the concentration of atrial natriuretic factor in the cerebrospinal fluid is a nonspecific indicator of brain injury.(ABSTRACT TRUNCATED AT 250 WORDS)     

Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm

We studied the sodium balance and changes in plasma volume by an isotope dilution technique in the first week after an aneurysmal subarachnoid hemorrhage in 21 patients. In 11 of the patients, the plasma volume decreased by more than 10%. This was accompanied by a negative sodium balance and hyponatremia in 6 patients, a negative sodium balance without hyponatremia in 4 patients, and a positive sodium balance in 1 patient. Together with a decrease in plasma volume, blood urea nitrogen content increased and body weight decreased. Three patients developed hyponatremia without a decrease in plasma volume. Serum vasopressin was measured in 14 of the 21 patients. The values were elevated on admission and declined in the first week, regardless of the presence of hyponatremia. These findings indicate that natriuresis and hyponatremia in aneurysmal subarachnoid hemorrhage reflect salt wasting and not inappropriate secretion of antidiuretic hormone and that these changes should be corrected by fluid replacement rather than by fluid restriction.     

Atrial natriuretic peptide and arginine vasopressin secretion in schizophrenic patients

Plasma levels of arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) were measured in 15 patients with schizophrenic or schizoaffective disorders and 15 healthy volunteers during oral water loading at 20 ml/kg. In the patient group, plasma AVP was secreted even when plasma osmolality was below 270 mosmol kg, although the sensitivity of AVP secretion response to osmolality was lower than in the controls. The ANP level was higher in the group of patients than in the controls. There was a negative correlation between plasma ANP and osmolality in the patients. We speculate that the volume expansion caused by inappropriate AVP secretion stimulated plasma ANP release and that the natriuresis resulting from the elevated plasma ANP level might contribute to hyponatremia.     

Pathogenesis of hyponatremia observed in the treatment of acute subarachnoid hemorrhage]

The cause of hyponatremia following subarachnoid hemorrhage (SAH) has been understood as an inappropriate secretion of antidiuretic hormone (SIADH). Whereas, water restriction for the management of this condition sometimes induces a severe dehydration, resulting in vasospasm. To clarify the pathogenesis of hyponatremia following SAH, we measured the daily sodium and water balance with the plasma concentration of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in seventeen cases after subarachnoid hemorrhage. Although the patients received an adequate amount of fluid (more than 4080ml/day; daily average in seventeen cases) and sodium (more than 277 mEq/day; daily average in seventeen cases), eight out of the seventeen cases showed transient hyponatremia of a slight degree beginning on 8.8 days after SAH. ANP values were elevated markedly in fifteen out of the seventeen cases, remaining high during the first two weeks following SAH. ADH values were elevated remarkably in eight out of the seventeen cases. However, these values declined immediately to a normal range within two days following SAH. PRA were increased or came within the normal range, suggesting the lack of water retention. Overall sodium balance and water balance did not differ significantly between hyponatremia cases and normonatremia ones, whereas, sodium balance in acute phase was significantly negative, associated with marked natriuresis in patients with hyponatremia. These correlations suggested that hyponatremia after SAH is the result of natriuresis by an increased ANP rather than ADH. In conclusion, a greater replenishment of water and sodium is required to avoid hyponatremia with dehydration. This technique may be helpful for the prevention of vasospasms following SAH.     

Diurnal variation in water homeostasis among schizophrenic patients subject to water intoxication

Among seven schizophrenic patients subject to water intoxication (six men and one woman, mean age 39.1 +/- 6.9 years), we measured serum sodium, plasma arginine vasopressin, and urine osmolality at 7 a.m. and 4 p.m. on eight consecutive Thursdays. On the days of greatest diurnal change in serum sodium, the 7 a.m. serum sodium was 141.1 +/- 1.8 mEq/l and the 4 p.m. value was 129.9 +/- 3.2 mEq/l. Plasma vasopressin also tended to be lower at 4 p.m. but, in many cases, was inadequately suppressed for the level of hyponatremia. The urine was dilute at both 7 a.m. and 4 p.m. and mean urine osmolality did not differ at the two times. In three patients, urine osmolality was consistently subnormal relative to plasma vasopressin at both 7 a.m. and 4 p.m. This abnormality was consistent with nephrogenic diabetes insipidus secondary to lithium and, possibly, phenytoin which the patients received to protect them against hyponatremia. We conclude that the combination of polydipsia and abnormal osmoregulation of vasopressin secretion contributes importantly to the afternoon hyponatremia found in schizophrenic patients subject to water intoxication.     

The Regulation of Serum Sodium After REeplacing Carbamazepine with Oxcarbazepine

PURPOSE: To evaluate changes in serum electrolyte balance and underlying regulatory mechanisms in 10 male patients with epilepsy 2 and 6 months after replacing long-term carbamazepine (CBZ) monotherapy with oxcarbazepine (OCBZ) monotherapy. Arginine vasopressin (AVP) is thought to be most important underlying mechanism of CBZ-related hyponatremia via direct or kidney tubular mechanisms. Furthermore, AVP is as well hormonally regulated by the renin-angiotensin-aldosterone system and atrial natriuretic peptide (ANP). METHODS: The medication of the patients was changed from CBZ to OCBZ. Serum electrolytes, creatinine, albumin, aldosterone, and the N-terminal fragment of ANP (NT-proANP) concentrations were measured before and 2 and 6 months after the change in the medication. RESULTS: The mean serum sodium level diminished after the medication was changed. Serum sodium levels decreased below the reference range in two (20%) patients during OCBZ medication. Serum sodium levels decreased altogether in four patients, and remained unaltered in six patients. Serum aldosterone levels increased in the six patients whose serum sodium concentrations did not decrease, but no increase was found in the patients with decreased sodium levels during OCBZ medication. Serum NT-proANP levels decreased in all patients. CONCLUSIONS: Serum sodium levels decrease after replacing CBZ with OCBZ. The low serum NT-proANP concentrations appear to reflect the decreased serum sodium levels, but a compensatory aldosterone response may prevent the development of hyponatremia in some patients during OCBZ medication.     

Management of sodium abnormalities in patients with CNS disease.

The CNS plays an integral role in the neuroendocrine regulation of sodium and water homeostasis. Therefore, disturbances of this function are common in patients with CNS disease. The body's sodium and water content are tightly regulated in order to maintain normal osmolality and intravascular volume. Complex neural, humoral, and renal mechanisms integrate information regarding osmolality, intravascular volume, blood pressure, and intake of sodium and water. They act to modify intake and excretion of sodium and water and vascular tone. Most sodium abnormalities in patients with CNS disease result from altered water excretion secondary to disturbed release of antidiuretic hormone (ADH). Insufficient release is seen with lesions in or near the optic chiasm and pituitary gland and results in diabetes insipidus (DI). DI is common following surgery or trauma in this region and care must be exercised in treating these patients because of the potentially variable and transient nature of the disturbance. The syndrome of inappropriate release of ADH is seen in a wide variety of CNS disorders and produces a dilutional hyponatremia. Symptomatic hyponatremia should be managed aggressively with diuretics and hypertonic saline followed by fluid restriction. However, very rapid correction or overcorrection should be avoided. In some patients, especially those with acute subarachnoid hemorrhage, disturbed sodium regulation appears to contribute to hyponatremia. Patients with subarachnoid hemorrhage and hyponatremia should not be fluid restricted, because of the risk of exacerbating vasospasm, but treated with large volumes of isotonic saline.     

The syndrome of psychosis, intermittent hyponatremia, and polydipsia: evidence for diurnal volume expansion

Seven patients (6 men and 1 woman, mean age 39.1 +/- SD 6.9 years) with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) underwent serial determinations of serum sodium (SOD), plasma atrial natriuretic peptide (ANP), and urinary osmolality (UOSM) at 7 AM and 4 PM. There was a diurnal increase in ANP (7 AM 17.9 +/- 5.1 pg/ml and 4 PM 27.7 +/- 9.0 pg/ml, p = 0.02), a diurnal decrease in serum sodium (7 AM 141.1 +/- 1.7 mEq/l, 4 PM 129.9 +/- 3.2 mEq/l, p less than 0.0001) and no diurnal change in UOSM. The diurnal increase in ANP in the the PIP syndrome contrasts to the diurnal decrease in ANP reported in normal subjects. Our data, while preliminary, suggest that patients with the PIP syndrome have increased intravascular volume leading to ANP secretion, natriuresis, and hyponatremia.     

Significance of plasma atrial natriuretic peptide measurement during the management of hyponatremia in neurosurgical patients]

We have examined the total number of admitted cases to clarify the pathogenesis of hyponatremia during the management of neurosurgical patients. We experienced 32 cases of hyponatremia during the past year by measuring the sodium balance and atrial natriuretic peptide (ANP) level. According to these two factors, we divided the cases into three groups. The first group shows normal ANP levels in spite of hyponatremia. Low administration of the sodium was thought to be the cause in these cases. The second group shows the elevated ANP levels with a positive sodium balance. Elevated circulatory volume due to the inadequate level of antidiuretic hormone and mild heart and/or kidney failures cause these conditions. Water restriction and/or diuresis were effective methods in the management of the cases. The last group shows the elevated ANP levels with a negative sodium balance. There is a statistically significant negative correlation between sodium balance and the ANP level. Marked natriuresis due to the elevated ANP causes the decrement of the circulatory volume in these cases. Pathogenesis of the last group is very important in the management of neurosurgical patients in an acute state, especially in subarachnoid hemorrhage cases. The decrement of the systemic circulatory volume would jeopardize the patient's neurological condition. In this group, water restriction that has been commonly recommended is contraindicated. Satisfactory water and sodium replenishment seems to be the best recommended treatment for this group.     

Hyponatremia and cerebral infarction in patients with ruptured intracranial aneurysms: Is fluid restriction harmful?

We studied retrospectively the relationship between hyponatremia and cerebral infarction in 134 consecutive patients with aneurysmal subarachnoid hemorrhage. In 44 patients sodium levels fell below 135 mmol/L on at least two consecutive days between the second and the tenth day after the hemorrhage. Twenty-five of these patients fulfilled the criteria for the syndrome of inappropriate secretion of antidiuretic hormone. Cerebral infarction developed in 27 of the 44 patients with hyponatremia and in 19 of the 90 patients with normal serum sodium levels (p less than 0.001). Cerebral infarctions were more often fatal in patients with hyponatremia (p less than 0.01). Twenty-six of the 44 patients had been treated with fluid restriction to correct the serum sodium levels, and infarctions developed in 21. Fluid restriction to correct hyponatremia appears to be potentially dangerous in patients with aneurysmal subarachnoid hemorrhage.     

The effect of fludrocortisone acetate on plasma volume and natriuresis in patients with aneurysmal subarachnoid hemorrhage

In order to prevent hypovolemia fludrocortisone acetate treatment was started on admission in 39 consecutive patients with CT evidence of subarachnoid hemorrhage. In 28 patients an aneurysm was proven or probable, and in 21 of these the effects of fludrocortisone acetate on sodium balance and on plasma volume could be studied. In the first five days plasma volume decreased more than 10% in four patients, decreased less than 10% in five and increased in 12. The cumulative sodium balance measured over five days was negative in seven of the 21 patients. Plasma renin values were measured in 15 of the 21 patients and also in stored samples of 18 patients who were not treated with fludrocortisone acetate. Plasma renin values were less high in patients treated with fludrocortisone acetate, regardless of the presence of a negative sodium balance. In three of the 39 patients signs of pulmonary edema developed, and low serum potassium values were observed in four of the 21 patients. In comparison with previous studies, these findings suggest that fludrocortisone acetate is an effective method of decreasing the incidence of volume depletion and negative sodium balance.     

Clinical significance of natriuretic peptides in patients with aneurysmal subarachnoid hemorrhage]

Hyponatremia and hypovolemia following aneurysmal subarachnoid hemorrhage (SAH) might be speculated by exaggerated secretion of natriuretic peptides and resulted ischemic sequela caused by cerebral vasospasm. We measured serum concentration of natriuretic peptides and investigated their influence on post-SAH hyponatremia. Among 49 patients of SAH, their plasma concentration of the natriuretic peptides (atrial natriuretic peptide: ANP and brain natriuretic peptide: BNP) were measured at the day of ictus and 7th day of SAH. The correlation between concentration of natriuretic peptides and location of aneurysm, severity of SAH, incidence of hyponatremia and symptomatic vasospasm were elucidated. The plasma concentration of ANP did not alter on admission and 7th day post SAH, whereas that of BNP increased in the patients with moribund SAH and those with ruptured A-com aneurysm. The initial increase of BNP following SAH could be attributed to direct damage of SAH on the hypothalamus. Hyponatremia and symptomatic vasospasm tended to occur in the patients who had persistent increase of plasma BNP concentration during one week post SAH. Therapeutic intervention to maintain normonatremia by fluid-management decreased occurrence of symptomatic vasospasm, even though patients with increased plasma BNP concentration. It might be concluded that increased secretion of BNP following SAH is caused by direct effect to the hypothalamus and prolonged hyper secretion of BNP resulted hyponatremia, hypovolemia and exaggerated symptomatic vasospasm.     

垂体腺瘤患者围手术期血钠与血浆醛固酮、心钠素关系

目的研究垂体腺瘤患者血钠与血浆醛固酮（ALD）、心钠素（ANP）的变化,探讨手术后发生低血钠的原因,为低钠血症的预防及处理提供一种可行性方法.方法随机选择垂体腺瘤患者20例,分别测定术前及术后第一个24 h尿钠丢失量及血清钠、血浆ALD、ANP含量.结果20例患者手术后血钠下降9例,其中2例发生低钠血症;该9例患者术后尿钠丢失量明显增加（P＜0.05）,血浆ALD分泌减少.11例患者术后血钠不下降,尿钠丢失量无明显变化,血浆ALD分泌增加.血浆ANP含量在手术前、后均高于正常对照组（P＜0.05）.结论垂体腺瘤患者排钠因素占优势,尿钠丢失增加与血浆ALD代偿不足有关,是引起血钠下降主要原因之一.     

Cerebral salt-wasting syndrome in a patient with neuroleptic malignant syndrome

BACKGROUND: Hyponatremia associated with neuroleptic malignant syndrome has thus far been described as a syndrome of inappropriate secretion of antidiuretic hormone. OBJECTIVES: To ascertain and describe the role of cerebral salt-wasting syndrome as the cause of hyponatremia in a patient with neuroleptic malignant syndrome. PATIENT: A psychotic patient being treated with olanzapine presenting with sopor, muscle rigidity, polyuria, tachycardia, pyrexia, and severe hyponatremia. METHODS: Serial serological examinations of plasma tonicity (sodium level and osmolality), brain natriuretic peptide, and antidiuretic hormone were performed, and sodium excretion and urine osmolality were determined from 24-hour urine collection. In addition, markers for rhabdomyolysis were monitored. RESULTS: The patient shows clear symptoms of cerebral salt-wasting syndrome in association with neuroleptic malignant syndrome, characterized by severe hyponatremia, volume depletion, and elevated brain natriuretic peptide but normal antidiuretic hormone levels. Cerebral salt-wasting syndrome improved under dantrolene sodium treatment and concomitant fluid and sodium replacement. CONCLUSION: Hyponatremia in patients with neuroleptic malignant syndrome might more likely reflect cerebral salt-wasting syndrome than a syndrome of inappropriate secretion of antidiuretic hormone as an additional aspect of autonomic dysregulation caused by antidopaminergic drugs.     

血浆脑利钠肽与蛛网膜下腔出血后脑血管痉挛及低钠血症的关系

目的　探讨血浆脑利钠肽(BNP)与蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)及低钠血症的关系。方法　动态测定30例SAH患者发病后1~3d、4~6d、7~9d及10~12d4个时段的血浆BNP和血钠水平,对血浆BNP和血钠水平进行相关性分析;比较有无CVS及有症状与无症状CVS患者的血浆BNP水平。同时检测18名健康人的血浆BNP水平作为对照。结果　SAH患者血浆BNP水平明显高于对照组(P<0. 01),虽然无CVS及无症状CVS患者血浆BNP水平在SAH后4个时段中逐渐下降,但有症状CVS患者第3时段血浆BNP水平明显高于第1时段(P<0. 01 );第2 ~4时段血钠与血BNP水平呈显著负相关(r2 =-0 .763,r3 =-0 .681,r4 =-0 .764,均P<0 .01)。结论　BNP可能导致和参与了SAH后CVS及低钠血症的发生,并在SAH后CVS的发病机制中起重要的作用。     

Paroxetine-induced hyponatremia in the elderly due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH)

This study investigated the development of hyponatremia and its underlying mechanism in elderly patients prescribed paroxetine. Patients were 15 men and women (mean age, 75.7 +/- 5.3 years) who were participants in a treatment study of late-life depression and who were without medical illness or other medications known to cause hyponatremia or alter antidiuretic hormone (ADH) secretion. Blood samples for measurement of plasma sodium, ADH, blood urea nitrogen (BUN), creatinine, glucose, and osmolality were determined prior to initiation of paroxetine (week 0) and at 2, 4, 6, and 12 weeks of treatment with paroxetine. Hyponatremia (serum sodium < 135 mEq/L) was identified in 6 of 15 patients after 2 weeks of treatment with paroxetine. Despite low plasma osmolality, ADH levels were not suppressed appropriately. Data suggest hyponatremia is a common adverse event in elderly patients prescribed paroxetine and implicates inappropriate secretion of ADH as the potential mechanism.     

Cerebral salt wasting syndrome in patients with aneurysmal subarachnoid hemorrhage

OBJECTIVE: Hydroelectrolytic disturbances are part of the complications of subarachnoid hemorrhage. Cerebral salt wasting syndrome (CSWS) must be considered when hyponatremia is associated with a decrease in circulating volume. We performed this study to determine the clinical characteristics and management paradigm of patients with serum sodium concentration abnormalities and aneurysmatic subarachnoid hemorrhage. METHODS: We analyzed retrospectively clinical and laboratory data from eight patients with subarachnoid hemorrhage due to rupture of an intracranial saccular aneurysm and cerebral salt wasting syndrome. Their course, as well as their clinical findings and treatment, are described. RESULTS: In eight patients, hyponatremia that lasted for more than 24 hours was detected (serum sodium under 135 mEq/l). The sodium disturbance occurred between day 3 and day 10 in all cases, in six of them in day 7 or day 8. The specific treatment for CSWS was to increase volume delivery according to the characteristics of the patient. Except for one case, none of the remaining patients required more than 72 hours of treatment to correct hyponatremia. No treatment-related complications were found CONCLUSION: Cerebral salt wasting syndrome, occurring in some patients with subarachnoid hemorrhage, is more commonly related to certain specific anatomic locations of the ruptured aneurysm, responds to sodium replacement therapy and fluids and can be diagnosed and treated based on the clinical, hydroelectrolytic and hemodynamic course of the patient. Further studies are needed to define the underlying mechanism of this condition.     

Severe hyponatremia in a case of severe spinal injury: sequential examination of factors affecting water-electrolyte balance]

Although hyponatremia has been known to occur in patients with severe spinal cord injury with highly incidence, its mechanism has not been understood well. We examined a 64-year-old patient with severe hyponatremia after spinal cord injury by sequential measuring of the factors affecting water-electrolyte balance, such as antidiuretic hormone, renin, angiotensin II, atrial natriuretic peptide, and brain natriuretic peptide. The patient showed severe hypotension due to dysfunction of the sympathetic nerve. The hyponatremia gradually resolved with the improvement of sympathetic nerve function. According to those results, the sympathetic nerve dysfunction was thought to correlate with the hyponatremia, and it was suggested that the unknown sympathetic regulation of water-electrolyte balance existed.