Vpress

Vpress Uses, Dosage, Side Effects, Food Interaction and all others data.

Vpress (arginine-vasopressin or antidiuretic hormone) is a nonapeptide primarily produced in the hypothalamus that exhibits diverse physiological functions related to diuresis, hemodynamic modulation, and behaviour. Vpress is very similar to oxytocin, differing in the third and eighth amino acids. Despite a wide variety of functions, exogenous vasopressin is primarily used to control blood pressure during systemic shock by increasing vasoconstriction and renal fluid reuptake by acting through V1 and V2 cellular receptors.

The vasopressive effect of posterior pituitary gland extracts was noted in 1895, while vasopressin itself was not purified until 1951. It has been used for more than five decades for varying conditions, including variceal bleeding, diabetes insipidus, and, more recently, vasodilatory shock. It is currently marketed under the trademark VASOSTRICT® by PAR Pharmaceuticals.

Vpress is a nonapeptide antidiuretic hormone involved in modulating various physiological processes, including autonomic signalling, stress response, behaviour, and memory; the most well-known modulation is of blood pressure. Vpress acts both within the brain and in the periphery to modulate blood pressure through sympathetic outflow, baroreflex modulation, vasoconstriction, and renal fluid retention. These mechanisms vary by location and physiological state, leading to occasionally contradictory responses to vasopressin. Although generally safe, vasopressin may worsen cardiac output in patients with impaired cardiac function. The cessation of vasopressin therapy may result in transient reversible diabetes insipidus, which may require additional desmopressin or vasopressin to manage.

Vpress
Uses
Dosage
Side Effect
Precautions
Interactions
Uses during Pregnancy
Uses during Breastfeeding
Accute Overdose
Food Interaction
Half Life
Volume of Distribution
Clearance
Interaction With other Medicine
Contradiction
Storage

Trade Name	Vpress
Availability	Prescription only
Generic	Vasopressin
Vasopressin Other Names	Vasopressin, unspecified, Vasopressina
Related Drugs	hydrochlorothiazide, propranolol, atenolol, amiodarone, lidocaine, epinephrine, ranitidine, simethicone, flecainide, Tenormin
Type	Injection
Formula	C₉₂H₁₃₀N₂₈O₂₄S₄
Weight	Average: 2140.46 Monoisotopic: 2138.869561874
Groups	Approved
Therapeutic Class
Manufacturer	Neon Laboratories
Available Country	India
Last Updated:	September 19, 2023 at 7:00 am

Uses

Vpress is a peptide hormone used to increase blood pressure in patients with vasodilatory shock who are resistant to fluid and catecholamine therapy.

Vpress is indicated to increase blood pressure in adults in vasodilatory shock refractory to the application of fluids and catecholamines.

Vpress is also used to associated treatment for these conditions: Acute Circulatory Failure, Dental Local Anesthesia

How Vpress works

Vpress, Cyclo (1-6) L-Cysteinyl-L-Tyrosyl-L-PhenylalanylL-Glutaminyl-L-Asparaginyl-L-Cysteinyl-L-Prolyl-L-Arginyl-L-Glycinamide, is a cyclic nonapeptide hormone primarily produced by the supraoptic and periventricular nuclei of the hypothalamus. Vpress release is mediated by sensory pathways, in which either a 2% increase in plasma osmolarity or a 10% decrease in blood pressure causes the release of endogenous vasopressin. Upon release, vasopressin mediates a variety of physiological effects, both centrally and systemically, primarily by binding to G-protein-coupled receptors termed V₁ (V_1A), V₂, and V₃ (V_1B).

V₁ receptors are abundantly expressed in the brain whereby vasopressin binding can increase blood pressure through autonomic pathways. Peripherally, V₁ is localized in the blood vessels (vascular smooth muscle), platelets, adrenal glands, kidneys, and liver. Vpress binding to V₁ causes hydrolysis of phosphatidylinositol-4,5-bisphosphate into inositol triphosphate (IP₃) and diacylglycerol (DAG) by phospholipase C, which in turn release intracellular calcium and activate protein kinase C (PKC) to open voltage-gated calcium channels (VGCCs) while closing potassium channels. Overall, intracellular calcium levels rise, which bind calmodulin and cause muscular contraction, resulting in vasoconstriction. This is balanced by the apparent ability of vasopressin to induce vasodilation through binding oxytocin receptors and activating endothelial nitric oxide (NO) synthase; NO acts antagonistically to reduce muscle contraction. It is also thought that vasopressin, acting through both V₁ and oxytocin receptors, causes the cardiac release of atrial natriuretic peptide (ANP), which has a negative inotropic effect; indeed, vasopressin tends to decrease heart rate and cardiac output, although the opposite effect has been noted with low doses.

V₂ receptors are abundantly expressed in the distal convoluted tubules and the collecting ducts of the kidneys. Vpress binding to V₂ causes activation of a G_s protein that subsequently activates protein kinase A (PKA) through adenylyl cyclase-mediated increase in cyclic adenosine monophosphate (cAMP), which leads to phosphorylation of the water channel aquaporin-2 (AQP2) and its trafficking to the cell surface. Increased AQP2 levels lead to increased water reabsorption and explains vasopressin's antidiuretic effects.

V₃ (formerly V_1B) receptors are primarily located in the anterior pituitary and brain. Vpress released during acute stress causes adrenocorticotropic hormone (ACTH) release from the pituitary through V₃ and by potentiating the effects of corticotrophin-releasing factor. Within the brain itself, V₃ activation modulates various effects, including recognition, memory, aggression, anxiety, and depression.

Thus, vasopressin can affect a wide variety of physiological processes, often in apparently contradictory ways depending on the patient's dose and physiological state. Vasodilatory shock causes an immediate release of vasopressin from 20 to 200 times its normal serum concentration, which falls again to normal levels in prolonged shock; in this context, normal serum levels are insufficient to control the pathologic vasodilation. In these cases, vasopressin acts to depolarize hyperpolarized vascular smooth muscle cells, restore sensitivity to catecholamines, and inhibit excessive nitric oxide production, primarily through acting through V₁ receptors. Therefore, vasopressin helps decrease the dose requirement for norepinephrine and is routinely administered together with norepinephrine to restore normal blood pressure in shock states.

Toxicity

Vpress overdose is expected to present with consequences related to excessive vasoconstriction of peripheral, mesenteric, coronary vascular beds, hyponatremia, and possibly with ventricular tachyarrhythmias, rhabdomyolysis, and gastrointestinal symptoms. As vasopressin is rapidly metabolized and cleared, symptoms will resolve with cessation of vasopressin administration.

Food Interaction

[Moderate] MONITOR: Alcohol may decrease the antidiuretic effect of vasopressin.

Clinical studies found that plasma vasopressin levels often decrease during alcohol consumption and increase upon cessation of consumption.

In addition, alcoholics were found to have a more pronounced decrease in plasma vasopressin levels when drinking and suppressed vasopressin levels even during alcohol withdrawal as compared to non-alcoholic individuals.

The mechanism of this interaction is not fully understood.

MANAGEMENT: Patients should be advised to abstain from alcohol during vasopressin treatment.

Hemodynamic monitoring is suggested for patients known to drink alcohol while receiving vasopressin.

Vpress Drug Interaction

Moderate: ciprofloxacin, norepinephrine, promethazine, ketorolac, ondansetronMinor: furosemideUnknown: amoxicillin, lorazepam, amoxicillin / clavulanate, diphenhydramine, diltiazem, glucose, hydromorphone, naloxone, acetaminophen, dexmedetomidine, methylprednisolone, levothyroxine, diazepam, midazolam

Vpress Disease Interaction

Major: nephritis, renal impairment, vascular disease, fluid overload/hyponatremia

Half Life

Vpress administered at 0.01-0.1 U/min has an apparent t_1/2 of ≤10 minutes, although half-lives of up to 44 minutes have been reported in the literature.