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

Acts at the GPCR Vasopressin receptors
V1 on vascular smooth muscle – vasoconstrictive – markedly less than ADH (1500x less than ADH)
V1 on platelets - increase platelet aggregation – more potent than ADH
V2 on the nephron - expressed in the renal collecting duct (CD) - antidiuretic actions (10x ADH)

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

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

Vasoconstriction – increased MAP
Pulmonary vasodilation

Increased vWF, factor VIII

Antidiuretic: reduced urine output, resolution of polydypsia

Vasoconstriction (less)
Increased platelet aggregation
Antidiuretic (more)

IV only

BA
SL: 0.25%
PO: 0.08-0.16%
Intranasal: 10%

limited data

No PB

20%

0.14 L/kg

0.2-0.32 L/kg

Metabolised by peptidases (Vasopressinases) to amino acids

Minimal hepatic metabolism

65% unchanged in urine

65% unchanged in urine

10-35 mins

2-3hrs

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

OD – Hyponatremia (Seizure, altered mental state, arrythmias, edema)

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

Deamino Arginine Vasopressin

Endogenous vasopressin hormone, clinically used as a non-adrenergic vasopressor.

NON-ADRENERGIC

Vasopressin Hormone

Vasopressin Analogue

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

Central DI – ADH replacement (Intranasal/parenteral)
Nocturnal polyuria (intranasal).
Haemostasis in Haemophilia with fVIII def or Type 1 Von Willebrand disease during surgical procedures and postoperatively to maintain hemostasis (parenteral).

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

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

Is a naturally occurring nonapeptide-9AA

Synthetic analogue of 8-arginine vasopressin (ADH)

Antidiuretic peptide drug

displays enhanced antidiuretic potency, fewer pressor effects due to V2-selective actions, and a prolonged half-life and duration of action compared to endogenous ADH

Level 1

Level 2

Acts at the GPCR Vasopressin receptors

Acts at the GPCR Vasopressin receptors

Rapid onset

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

sublingual tablet, intra nasal spray, IV/IM

IV infusion
0.01–0.04 units/min

sublingual tablet, intra nasal spray, IV/IM
0.1 to 1.2 mg divided into 2 or 3 doses