**7. Vasopressin system**

Vasopressin (ADH) is released by the hypothalamus as a result of baroreceptor, osmotic, and neurohormonal stimuli. It normally maintains body fluid balance, vascular tone, and regulates contractility. Heart failure causes a paradoxical increase in AVP. The increased blood volume and atrial pressure in heart failure suggest inhibition of vasopressin secretion, but it does not occur. This phenomenon is related to SNS and RAAS activation overriding the volume and low-pressure cardiovascular receptors and osmotic vasopressin regulation causing increase in AVP secretion. It contributes to the increased systemic vascular resistance (V1 receptors) and to renal retention of fluid (V2 receptors). Stimulation of V1 receptors can also case vasoconstriction of the peripheral vessels, platelet aggregation, and adrenocorticotrophic hormone stimulation. Low-dose arginine infusion initiated in the operating room after complex neonatal cardiac surgery was associated with decreased fluid resuscitation and catecholamine. The vasopressin levels are usually high in the early phase of septic shock, but it's deficiency was noted in vasodilatory shock.

The important mechanism of vasopressin action in stress states is its potentiating effect on ACTH secretion leading to cortisol release. Although vasopressin is a powerful vasoconstrictor it dilates the pulmonary, cerebral, and myocardial circulations helping to preserve vital organ blood flow.

In our group of patients with single ventricle, there was a significant correlation between vasopressin concentration and disturbances of water – electrolyte balance in single ventricle patients. Higher vasopressin plasma levels were connected with greater propensity for fluid retention and prolonged pleural effusions (6).
