Atriopeptin 6x1mg

USD425.00

ANP (Atriopeptin) is a powerful vasodilator and a protein secreted by heart muscle cells. It is released by muscle cells in the upper chambers of the heart, in response to high blood volume. ANP acts to reduce water and adipose loads on the circulatory system thereby reducing blood pressure.

• Decreases systemic vascular resistance and systemic arterial pressure
• Reduce arterial pressure
• Reduces cardiac output by decreasing ventricular preload
• Reduce blood volume
• Reduce pulmonary capillary wedge pressure
• Promotes the excretion of sodium ions in the urine

BROCHURE FACT SHEET

Category:

Description

Purity: > 95%
Synonyms: ANH; ANF; PND; NPPA; Atrial Natriuretic Factor; Atrial Natriuretic Hormone; Atriopeptin; Natriuretic Peptide Precursor A
Molecular Formula: C128H205N45O39S2
Molecular Weight: 41.1 kDa
Sequence (three-letter code): {SER}{LEU}{ARG}{ARG}{SER}{SER}{CYS}{PHE}{GLY}{GLY}{ARG}{MET}{ASP}{ARG} {ILE}{GLY}{ALA}{GLN}{SER}{GLY}{LEU}{GLY}{CYS}{ASN}{SER}{PHE}{ARG}{TYR}

Description
Atrial natriuretic peptide (ANP) is a 28-amino acid peptide that is synthesized, stored, and released by atrial myocytes in response to atrial distension, angiotensin II stimulation, endothelin, and sympathetic stimulation (beta-adrenoceptor mediated). Therefore, elevated levels of ANP are found during hypervolemic states (elevated blood volume), such as occurs in heart failure. ANP is first synthesized and stored in cardiac myocytes as prepro-ANP, which is then cleaved to pro-ANP and finally to ANP.

Dosing Protocol
Use one vial mixed with 2.5ml sterile water, sub-contaneus (under the skin). For best results use 1 x 1mg vial every 3-4 days for 6 treatments.

Ingredients
1mg ATRIAL NATRIURETIC PEPTIDE (3-28) (98%).

Storage
Keep Refrigerated when possible and out of direct sunlight.

Clinical Research
Beneficial effects seen in animal models of AKI led researchers to conduct clinical trials with different ANP preparations. Early clinical trials were underpowered and showed mixed results. Subsequently, Allgren et al. conducted a large trial of ANP in critically ill patients with acute tubular necrosis . The administration of ANP in this study did not improve the overall rate of dialysis-free survival; however, some benefits were observed in a subgroup of patients with oliguria. Since the publication of this study, there have been multiple clinical trials evaluating ANP for prevention and treatment of AKI. We conducted a comprehensive review of the existing literature on this topic. Our results show that there are a too few large, high-quality studies on this topic to make any definite statement regarding the efficacy of ANP in the management of AKI. However, analysis of the existing studies shows that ANP, when used in low doses for prevention of AKI, is well tolerated and may be associated with some improvement in clinical outcomes (requirement of RRT, lengths of ICU stay, and hospitalization). Its effects are most robust when analyzed in a postsurgery setting (such as cardiovascular surgery). High-dose ANP in the treatment of established AKI was not associated with any significant clinical improvements. By causing hypotension, high-dose ANP preparations may jeopardize renal perfusion, particularly in AKI that is characterized by loss of auto regulatory capacity, and further negate the possible benefits of ANP

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