- Acts primarily directly at alpha-1-adrenoreceptors (phospholipase C → IP3 → increased calcium)
- To a lesser extent acts on beta 1>beta 2 effects

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

Low doses: β - ↑ino+chronotropy
increased MVO2
Higher doses: 1 -
peripheral vasocontriction.
↑systolic/diastolic pressures
may cause reflex bradycardia

Detail:
CVS
- Increased SVR leading to increased SBP/DBP/MAP
- Increased afterload - leading to increased myocardial oxygen consumption, slight decrease in cardiac output and may lead to reflex bradycardia (through beta-1 effects limit this)
- Coronary artery vasodilation increased coronary O2 delivery
- Pulmonary vascular resistance is increased
- Excessive doses may lead to limb or organ ischaemia
- Extravasation may lead to tissue necrosis

CNS
- Generally improves cerebral blood flow by way of improved CPP more than it decreases CBF by cerebral vasoconstriction

Renal/GU
- Decreases renal blood flow
- Causes uterine constriction (may lead to fetal asphyxia)

GIT:
- Decreased splanchnic blood flow

Metabolic
- Less hyperglycaemia/acidosis, although it may decrease insulin secretion

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

IV only
Clear Solution 1:1000
8-12 mcg/min uptitrated to effect
onset / duration immediate / 1-2 minutes

IV only

doesn’t cross the BBB

limited data

No PB

0.14 L/kg

Rapidly metabolised into adrenaline by MAO (Uptake 1, Nv terminal)
COMT (Uptake 2 circulation)

25% removed in the lungs

Metabolised by peptidases (Vasopressinases) to amino acids

urine as inactive metabolites (84-96%)

65% unchanged in urine

2 minutes

10-35 mins

Excessive doses cause severe hypertension
Reduced flow to organs
splanchnic
renal
Issues with increased MVO2 and IHD

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

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

ADRENERGIC

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

Used to treat hypotension due to decreased SVR

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

Is a naturally occurring catecholamine released in post ganglionic SNS, medulla (20:80 Adr)

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

Level 1

Level 1

Alpha and beta adrenergic receptor activity

Acts at the GPCR Vasopressin receptors

Rapid onset

injectable solution only, 1mg/mL in 2 mL vials diluted in 5D or NS.
CVC only due to risk of extravasation associated necrosis

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

IV infusion- 0.05-0.5mcg/kg. Through a central line diluted with glucose or saline.

IV infusion
0.01–0.04 units/min