Role of the Central Nervous System in Metabolism of Electrolytes and Water

Welt, Louis G.

doi:10.1001/archinte.1952.00240090076007

Cited by 155 publications

(19 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Other factors producing natriuresis seems to be involved in the mechanisms of hyponatremia [3]. This kind of hyponatremia has been called "central salt-wasting syndrome" [4][5][6][7][8], the causes of which appear to be multifactorial.…”

mentioning

confidence: 99%

Involvement of Arginine Vasopressin and Renal Sodium Handling in Pathogenesis of Hyponatremia in Elderly Patients.

Ishikawa¹,

Fujita²,

Fujisawa³

et al. 1996

Endocr J

View full text Add to dashboard Cite

Abstract. The present study was undertaken to determine the pathophysiological role of arginine vasopressin (AVP) in elderly patients with hyponatremia, and the efficacy of fludrocortisone acetate in treating their hyponatremia. Eleven hospitalized patients aged 65 years or older whose serum sodium levels were less than 130 mEq/l were examined. The hyponatremic patients included two groups of patients: syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and central salt-wasting syndrome. And 24 healthy, young subjects aged 20 to 34 years, and 24 healthy, elderly subjects aged 65 to 80 years were recruited by community announcement. The elderly subjects had decreased urinary concentrating ability and exaggerated response of AVP secretion to osmotic and nonosmotic stimuli, as compared to the young subjects. All the patients had hyponatremia, with the exaggerated urinary loss of Na. Plasma AVP levels were elevated despite hypoosmolality in all the 2 groups of hyponatremic, elderly patients. Plasma renin activity and plasma aldosterone concentrations were low in the patients with SIADH and central salt-wasting syndrome. Fludrocortisone acetate therapy was effective in the patients with central salt-wasting syndrome and 3 patients with SIADH whose hyponatremia remained unchanged after water restriction. Water restriction therapy normalized serum Na levels in only 3 patients with SIADH. These results indicate that AVP is involved in the mechanism for hyponatremia in the elderly patients with SIADH and central salt-wasting syndrome. Severe hyponatremia associated with SIADH and central salt-wasting syndrome responds well to mineralocorticoid therapy. Both the secretion of AVP and renal sodium handling may be involved in the mechanisms of action of the disorders. The diagnostic criteria for SIADH in the elderly patients may have to be reevaluated and should be considered to indicate fludrocortisone acetate therapy.

show abstract

mentioning

confidence: 99%

Involvement of Arginine Vasopressin and Renal Sodium Handling in Pathogenesis of Hyponatremia in Elderly Patients.

Ishikawa¹,

Fujita²,

Fujisawa³

et al. 1996

Endocr J

View full text Add to dashboard Cite

show abstract

“…Intact pituitary and adrenal function but renal defect in preserving sodium and chloride was found in later studies. 16,17 Natriuresis and volume depletion with increased vasopressin secretion are typical presentations in CSW patients. There are several factors contributing to the development of CSW.…”

Section: Discussionmentioning

confidence: 99%

Recurrent Hyponatremia After Traumatic Brain Injury

Chang

Liao

Chuang

et al. 2008

The American Journal of the Medical Sciences

View full text Add to dashboard Cite

Dysregulation of the neuroendocrine system is a frequent complication after traumatic brain injury (TBI). Symptoms of these hormonal abnormalities might be subtle and thus easily ignored. Hyponatremia usually indicates underlying disorders that disrupt fluid homeostasis. In most patients with TBI, hyponatremia is a feature of the syndrome of inappropriate antidiuretic hormone (SIADH) secretion due to pituitary dysfunction after head injury. Usually TBI-associated hyponatremia is transient and reversible. We report the case of a 48-year-old man with TBI-associated hyponatremia with delayed recovery and recurrent hyponatremia precipitated by subsequent surgery. In this report, we emphasize the importance of identifying patients with slow recovery of the injured brain, which could complicate with SIADH and acute hyponatremia. Differentiating TBI-associated SIADH from other important causes of hyponatremia such as cerebral salt wasting, and hypocortisonism are also reviewed. Prevention of its recurrence by avoiding further risk is mandatory in managing patients with TBI. KEY H yponatremia is a common disorder encountered in various settings. 1 In most cases, hyponatremia manifests as an underlying disease and degree of hyponatremia usually indicates severity of etiology, and can even correlate with patient outcome. 2 Clinical features of hyponatremia are confined to most neurological manifestations, but vary with severity and rate of progression. Hyponatremia is one of the clues for diagnosing disease that might not be detected directly. Moreover, in certain circumstances, hyponatremia can even provide significant prognostic implications. 1 Traumatic brain injury (TBI) may severely impair brain function. In addition to structural damage, neuroendocrine dysfunction is an important complication. 3 The pituitary insult can manifest with any hormone dysregulation involving either the anterior or posterior pituitary gland. 4,5 Most TBI-associated hyponatremia is mild and asymptomatic, and lasts only a short time. The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) commonly underlies acute hyponatremia in these patients. 6 Because the neurological manifestations of hyponatremia and acute brain injury are quite similar, differentiation may be difficult. Furthermore, unresolved recurrent hyponatremia with obvious clinical manifestations has rarely been described. We report here a patient with recurrent symptomatic hyponatremia after head injury. Case ReportA 48-year-old man was sent to our emergency department because of an accidental fall, and head injury 4 days before admission. He had originally been admitted to a local hospital where brain computed tomography revealed no intracranial hemorrhage or skull fracture. However, he developed progressive headaches, deteriorated consciousness, and vomiting that were refractory to medical treatment. Repeated brain computed tomography at our institution disclosed minimal bilateral frontal subdural hematoma. Biochemical examination found a rapid drop ...

show abstract

“…Also, their lesions were complete ventral hypothalamectomies rather than the discrete small lesions induced by us. Prior to this time there was already evidence for a central nervous system (CNS) role in natriuresis since a number of patients with brain lesions and hypernatremia had been reported (7). McCann et al (8) observed hypernatremia in a number of cats with large lesions of the median eminence (ME) and ventral hypothalamus associated with diabetes insipidus.…”

Section: Sm Mccann Et Almentioning

confidence: 99%

Neuroendocrine control of body fluid homeostasis

McCann

Gutkowska²,

Antunes‐Rodrigues

2003

Braz J Med Biol Res

View full text Add to dashboard Cite

Angiotensin II and atrial natriuretic peptide (ANP) play important and opposite roles in the control of water and salt intake, with angiotensin II promoting the intake of both and ANP inhibiting the intake of both. Following blood volume expansion, baroreceptor input to the brainstem induces the release of ANP within the hypothalamus that releases oxytocin (OT) that acts on its receptors in the heart to cause the release of ANP. ANP activates guanylyl cyclase that converts guanosine triphosphate into cyclic guanosine monophosphate (cGMP). cGMP activates protein kinase G that reduces heart rate and force of contraction, decreasing cardiac output. ANP acts similarly to induce vasodilation. The intrinsic OT system in the heart and vascular system augments the effects of circulating OT to cause a rapid reduction in effective circulating blood volume. Furthermore, natriuresis is rapidly induced by the action of ANP on its tubular guanylyl cyclase receptors, resulting in the production of cGMP that closes Na + channels. The OT released by volume expansion also acts on its tubular receptors to activate nitric oxide synthase. The nitric oxide released activates guanylyl cyclase leading to the production of cGMP that also closes Na + channels, thereby augmenting the natriuretic effect of ANP. The natriuresis induced by cGMP finally causes blood volume to return to normal. At the same time, the ANP released acts centrally to decrease water and salt intake.

show abstract

Role of the Central Nervous System in Metabolism of Electrolytes and Water

Cited by 155 publications

References 49 publications

Involvement of Arginine Vasopressin and Renal Sodium Handling in Pathogenesis of Hyponatremia in Elderly Patients.

Involvement of Arginine Vasopressin and Renal Sodium Handling in Pathogenesis of Hyponatremia in Elderly Patients.

Recurrent Hyponatremia After Traumatic Brain Injury

Neuroendocrine control of body fluid homeostasis

Contact Info

Product

Resources

About