by Julien Demiselle, Nicolas Fage, Peter Radermacher and
Pierre Asfar
Abstract
Activation of arginine–vasopressin is one of the hormonal
responses to face vasodilation-related hypotension. Released from the
post-pituitary gland, vasopressin induces vasoconstriction through the
activation of V1a receptors located on vascular smooth muscle cells. Due to its
non-selective receptor affinity arginine–vasopressin also activates V2 (located
on renal tubular cells of collecting ducts) and V1b (located in the anterior
pituitary and in the pancreas) receptors, thereby potentially promoting undesired
side effects such as anti-diuresis, procoagulant properties due to release of
the von Willebrand’s factor and platelet activation. Finally, it also
cross-activates oxytocin receptors. During septic shock, vasopressin plasma
levels were reported to be lower than expected, and a hypersensitivity to its
vasopressor effect is reported in such situation. Terlipressin and selepressin
are synthetic vasopressin analogues with a higher affinity for the V1 receptor,
and, hence, potentially less side effects. In this narrative review, we present
the current knowledge of the rationale, benefits and risks of vasopressin use
in the setting of septic shock and vasoplegic shock following cardiac surgery.
Clearly, vasopressin administration allows reducing norepinephrine
requirements, but so far, no improvement of survival was reported and side
effects are frequent, particularly ischaemic events. Finally, we will discuss
the current indications for vasopressin and its agonists in the setting of
septic shock, and the remaining unresolved questions.
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