Level 1

Catecholamine sparing drug in shock
Diabetes insipidus
Bleeding in vWF def / mild haemophilia

Prod hypothal.
released by the posterior pituitary
similar to oxytocin complex molecule wt

measured in international units
20 IU/ml vial
requiring dilution for eff¬ective delivery.
It cannot be given orally as it is
inactivated by trypsin

Acts at the GPCR Vasopressin receptors

Acts at the GPCR Vasopressin receptors

V1 on vascular smooth muscle
Inc intracellular Ca conc, vasoconstrictive
V1 on platelets
increase platelet aggregation

V2 on the nephron
Aquaporin-2 trafficking from intracellular vesicle membrane – allowing water reabsorption
V2 on endothelial cells – allow vWF release that prevents breakdown of factor VIII

V3 (prev V1b) on pituitary
Contribute to ACTH release

Rapid onset

Hyponatraemia with H2O retention
May cause severe vasoconstriction -CVC only
Arrhythmias at higher doses
GIT smooth muscle constriction
cramping, nausea, diarrhoea

IV only

limited data

No PB

0.14 L/kg

Metabolised by peptidases (Vasopressinases) to amino acids

65% unchanged in urine

10-35 mins

IV infusion
0.01–0.04 units/min

NON-ADRENERGIC

Is a naturally occurring nonapeptide-9AA.
Produced hypothal.
released by the posterior pituitary.
similar to oxytocin complex molecule wt

CVS:
- in the presence of shock, vasopressin causes an increase in MAP and SVR via its vasoconstrictor effect.
- In low doses it causes vasodilation in certain vascular beds in animal models.
- It causes pulmonary vasodilation in hypoxic and physiological conditions.

GU:
a reduction in urine output and polydipsia is seen following administration in DI

GIT:
Gastric smooth muscle contraction

Other: Increase in vWF and Factor 8 can be detected

Vasopressin Hormone

Is a naturally occurring nonapeptide-9AA

Vasoconstriction – increased MAP
Pulmonary vasodilation

Increased vWF, factor VIII

Antidiuretic: reduced urine output, resolution of polydypsia