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Vasopressin infusions are also used as second line therapy for septic shock patients not responding to fluid resuscitation or infusions of catecholamines (e.g., dopamine or norepinephrine) to increase the blood pressure while sparing the use of catecholamines. These argipressins have much shorter elimination half-life (around 20 minutes ...
Also, systemic corticosteroids have been shown to suppress endogenous vasopressin production and release. [31] Neonates and children recovering from cardiac surgery who are receiving systemic corticosteroid therapy may also be optimal candidates for vasopressin therapy should hemodynamic instability be present.
The arginine vasopressin (AVP) gene is a gene whose product is proteolytically cleaved to produce vasopressin (also known as antidiuretic hormone or ADH), neurophysin II, and a glycoprotein called copeptin. AVP and other AVP-like peptides are found in mammals, as well as mollusks, arthropods, nematodes, and other invertebrate species. [5]
In refractory vasodilatory shock, the patient has both vasopressin secretion deficit and an advanced resistance to vasopressin-induced blood-pressure changes. [23] Some have hypothesized that patients with vasopressin deficiency, including a decrease in baroreceptor stimulation, appear to have impaired autonomic reflexes. [ 23 ]
Angiotensin II causes the release of anti-diuretic hormone (ADH), [6] also called vasopressin – ADH is made in the hypothalamus and released from the posterior pituitary gland. As its name suggests, it also exhibits vaso-constrictive properties, but its main course of action is to stimulate reabsorption of water in the kidneys.
This is in contrast to central or neurogenic diabetes insipidus, which is caused by insufficient levels of vasopressin (also called antidiuretic hormone, ADH). Nephrogenic diabetes insipidus is caused by an improper response of the kidney to vasopressin, leading to a decrease in the ability of the kidney to concentrate the urine by removing ...