Vasopressin is a nonapeptide synthesised in the hypothalamus and released upon stimulations such as hyperosmolality, hypotension and hypovolaemia. In acute shock states serum vasopressin levels increase rapidly and decrease in prolonged septic shock. The administration of vasopressin in healthy subjects has little effect, whereas in vasodilatory shock it increases the mean arterial pressure through V1 receptors and decreases the cardiac output.
Vasopressin stimulates the V2 receptors in the kidney
leading to reabsorption of water through aquaporin 2.
However, in vasodilatory shock the antidiuretic effects are overcome by the effect vasopressin has on the kidneys: improvement of renal blood flow leading to water excretion.
Twenty-four studies on the use of vasopressin in patients
with vasodilatory shock are reviewed. They show that
vasopressin potentiates norepinephrine effects, increases
blood pressure significantly in patients with vasodilatory
shock and may improve renal function. Side effects
ranging from ischaemic skin lesions to possible intestinal
ischaemia should not be underestimated. Above a dose
of 0.04 U/min it may lead to cardiac arrest. Effects on
mortality cannot be interpreted from these studies. Broad clinical use should await controlled trials to clarify its effects on clinical outcomes such as organ failure and mortality.