Studies of vasopressin in the human cerebrospinal fluid

Abstract

The development of sensitive radioimmunoassays has permitted measurement of the low concentration of vasopressin in the human cerebrospinal fluid. There is accumulating evidence to suggest that vasopressin is involved in a variety of brain functions. As an effective blood-cerebrospinal fluid barrier to vasopressin has been demonstrated, the concentration of vasopressin in the cerebrospinal fluid probably reflects the release of vasopressin within the brain. In human subjects without intracranial disease, the concentration of vasopressin in the cerebrospinal fluid is in the range 0.5-2.0 pg/ml with only little diurnal variation. Intracranial disorders associated with increased intracranial pressure may cause increased cerebrospinal fluid vasopressin concentrations, whereas degenerative brain diseases are associated with low concentrations. Only little is known about the physiologic stimuli which alter the concentration of vasopressin in cerebrospinal fluid. The concentration in cerebrospinal fluid is not influenced by a number of stimuli that cause release of vasopressin into the blood, i.e. changes in plasma osmolality, postural changes, and nausea. Elevation of the intracranial pressure, changes in the composition of the cerebrospinal fluid, electrical stimulation of the hypothalamus, and severe hemorrhage provoke an increase in cerebrospinal fluid vasopressin level.

The ependyma: A protective barrier between brain and cerebrospinal fluid

“…The ependyma is postulated to regulate movement of water between the extracellular compartment and CSF (Pollay and Curl, 1967). Vasopressin concentration in CSF is increased when intracranial pressure is raised and it can increase ependymal permeability to water (Chen et al, 1993;Rosenberg et al, 1986;Sorensen, 1986). The probable sources of vasopressin are circumventricular organs or vasopressinergic axons which terminate in the ependymal layer (Dubois-Dauphin et al, 1990;Lepetit et al, 1993).…”

Cerebral Salt-Wasting Syndrome: Does It Exist?

“…Support for a renal salt wasting might come from studies reported by Rudman et al [71]in tube-fed elderly, including Alzheimer’s disease patients who developed hyponatremia only if salt intake was lowered to 1 g/day, while the water intake was kept constant at 1.725 liters/day. Hyponatremia rarely occurs in the elderly, in part because of a blunted thirst mechanism and in Alzheimer’s disease patients because of lower plasma ADH levels and decreased ADH response to metoclopramide stimulation [72, 73]. On a broader scale, renal salt wasting might be a common abnormality in elderly patients who have a delayed adjustment to an acute reduction in salt intake [74].…”

Alterations in vasopressin regulation in Alzheimer's disease.

“…4 The main mechanisms controlling hypothalamic AVP secretion"6 are changes in blood osmolality and decrease in blood pressure and/or blood volume. An increase in blood osmolality is sensed by the osmoreceptor sited in the anterior hypothalamus.…”