title: Vasopressin and its immune effects in septic shock.
abstract: Vasopressin is a stress hormone. However, vasopressin levels are inappropriately low in septic shock. Vasopressin stimulates AVPR1a, AVPR1b, AVPR2 and purinergic receptors. Vasopressin increases blood pressure by occupying AVPR1a receptors on vascular smooth muscle. An increase in ventricular afterload due to vasopressor administration limits ventricular systolic ejection, an effect that becomes increasingly important as systolic contractility is decreased. Stimulation of AVPR1a receptors may also decrease edemagenesis. Stimulation of AVPR1b by vasopressin releases ACTH and cortisol. AVPR2 stimulation increases retention of water by increasing cyclic AMP. Yet, vasopressin infusion may increase urine output, creatinine clearance and improve renal function in septic shock. Vasopressin has many effects on immune function such as altering cytokines, neuroimmunity, prostaglandins, humoral immunity and immune cells. For example, vasopressin decreases sepsis-induced pulmonary inflammation, could have renal anti-inflammatory effects and may decrease prostaglandin levels in a dose-dependent manner. Vasopressin may also modulate responses to stress by expression and release from immune cells. Interestingly, there are vasopressin receptors on immune cells. Many small clinical studies of vasopressin infusion in septic shock have shown that vasopressin infusion increases blood pressure, decreases requirements for norepinephrine and improves renal function. However, vasopressin could decrease coronary, cerebral and mesenteric perfusion. A multicenter trial of vasopressin versus norepinephrine in septic shock found no overall difference in mortality. Vasopressin may decrease mortality in patients with less severe septic shock. Vasopressin plus corticosteroid treatment may decrease mortality compared to corticosteroids plus norepinephrine. Potential mechanisms are that vasopressin plus corticosteroids beneficially alter immunity in septic shock.
authors.affiliation: Heart and Lung Institute, St. Paul's Hospital, University of British Columbia, Vancouver, B.C., Canada. Jim.Russell@hli.ubc.ca
authors.forename: James A
authors.initials: JA
authors.lastname: Russell
authors.forename: Keith R
authors.initials: KR
authors.lastname: Walley
mesh_terms: D000818:Animals; D006801:Humans; D051379:Mice; D008958:Models, Molecular; D009638:Norepinephrine / Q000627:therapeutic use; D016032:Randomized Controlled Trials as Topic; D051381:Rats; D017483:Receptors, Vasopressin / Q000737:chemistry / Q000378:metabolism; D012772:Shock, Septic / Q000188:drug therapy* / Q000276:immunology* / Q000401:mortality; D016896:Treatment Outcome; D014667:Vasopressins / Q000737:chemistry / Q000627:therapeutic use*
chemical_list: D017483:Receptors, Vasopressin; D014667:Vasopressins; D009638:Norepinephrine