Hyponatraemia vasopressin

Several nonpeptidic, orally active vasopressin receptor antagonists have been developed. The dual V1A/V2R antagonist conivaptan is used in the treatment of hyponatraemia and could also become useful for diseases such as congestive heart failure, in which increased peripheral resistance and dilutional hyponatremia both are present [4]. Side effects of conivaptan include headache, injection site reactions, vomiting, diarrhoea, constipation and thirst. 

Ox ocin is a nonapeptide which is structurally related to vasopressin. It stimulates rhythmic uterine contractions and is widely used by intravenous infusion of a diluted solution to induce labour and to treat postpartum bleeding. In large doses, it may cause relaxation of vascular smooth muscle causing hypotension in patients with cardiac disease or who are dehydrated. It has water-retaining properties and when given for prolonged periods to patients whose intake is electrolyte-free it causes overhydration and hyponatraemia. This may result in convulsions in the newborn with the risk of cerebral damage. 

A variety of tumours, e.g. oat-cell limg cancer, can make vasopressin, and of course they are not subject to normal homeostatic mechanisms. SIADH also occurs in some CNS and respiratory disorders (infection). Dilutional hyponatraemia follows, i.e. low plasma sodium with an inappropriately low plasma osmolality and high urine osmolality. When the plasma sodium approaches 120 mmol/I treatment should be with fluid restriction (< 500 ml/day). Treatment is primarily of the imderlying disorder accompanied by fluid restriction. Chemotherapy to the causative tumour or infection is likely to be the most effective treatment. Demeclocycline, which inhibits the renal action of vasopressin, is useful Infusion of isotonic or hypertonic saline must be reserved for extreme emergencies, associated with stupor, and undertaken with great caution. Rapid correction of hyponatraemia must be avoided because of the risk of central pontine myelinolysis the rate of correction must not exceed 12 mmol/1 per 24 h. 

On presentation, this woman was sodium depleted with pre-renal uraemia. As her ECF was expanded with 0.9% sodium chloride, this improved her glomerular filtration rate which is sufficient, even in the absence of aldosterone, to correct the hyperkalaemia by increasing her urinary potassium excretion. The reduction in this patient s blood volume will stimulate vasopressin secretion, giving rise to the hyponatraemia. The sodium chloride infusion by restoring her blood volume will inhibit AVP secretion, enabling her to correct the hyponatraemia. 

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