Exogenous Vasopressin-Induced Hyponatremia in Patients With Vasodilatory Shock

Abstract

Vasopressin has gained wide support as an adjunct vasopressor in patients with septic shock. This agent exerts its vasoconstriction effects through smooth muscle V1 receptors and also has antidiuretic activity via renal V2 receptors. This interaction with the renal V2 receptors results in the integration of aquaporin 2 channels in the apical membrane of the renal collecting duct leading to free water reabsorption. Thus, water intoxication with subsequent hyponatremia, although rare, is a potentially serious side effect of exogenous vasopressin administration. We present 2 patients who developed hyponatremia within hours of initiation of vasopressin infusion. Extensive diuresis followed its discontinuation with subsequent normalization of serum sodium. One of the patients required the use of hypertonic saline for more rapid normalization of serum sodium due to concerns for potential seizure activity. A review of the literature relevant to the incidence of vasopressin-induced hyponatremia is provided as well as discussion on additional factors relevant to septic shock that should be considered when determining the relative risk of hyponatremia in patients receiving vasopressin.

Translational and therapeutic potential of oxytocin as an anti-obesity strategy: Insights from rodents, nonhuman primates and humans

“…However, pre-labor uterine sensitivity to OT stems from a more than 150-fold up-regulation in myometrial OTRs [232], and this increase in OTR expression appears to be primed by high estrogen levels just prior to term [233] suggesting that it is unlikely to elicit uterine cramping in non-pregnant women. One potential concern is whether chronic OT, at doses that elicit weight loss, may also interact with vasopressin 2 receptors (V 2R s) in sufficient concentrations to cause hyponatremia (serum sodium b 135 mmol/L) [234]. This complication is not likely, however, given that OT has nearly a 90-fold higher affinity for the OTRs than the V 2R s [235].…”

The use of crystalloids in traumatic brain injury

“…It is the antidiuretic hormone, which is secreted by the posterior pituitary gland following hypovolaemia and a rapid increase in plasma osmolality. Although a decline in plasma sodium concentration was observed 16-24 hours after beginning vasopressin administration, in 16% of the TBI patients hyponatremia developed earlier (2-4 days after injury) and was associated with lesions in the limbic system, presumably resulting in inappropriate vasopressin secretion [67,74]. Hyponatremia also occurs in more than 10% of patients on the first day of mannitol administration and more than 20% of patients receiving mannitol for 7-days [63,75].…”

Terlipressin Versus Norepinephrine for Septic Shock: A Systematic Review and Meta-Analysis

“…Previous study investigated that activation of the V1 receptor results in vasoconstriction and arterial blood pressure ascent . However, arginine-vasopressin (AVP) has no selectivity for the V1 receptor and may produce side effects due to activation of the other receptors (Torgersen et al, 2010;Salazar et al, 2015). TP has a much stronger selectivity to the V1 receptor than to other receptors.…”