atrial

Atrial Natriuretic Peptide (1-28), human, porcine, Biotin-labeled, is one of three mammalian natriuretic peptides (NPs) that exerts endocrine effects on fluid homeostasis and blood pressure. Atrial Natriuretic Peptide holds promise for cardiovascular diseases research.

Prepro-Atrial Natriuretic Factor (26-55) (human) is a polypeptide that elevates cyclic GMP levels in the renal cortex and medulla and enhances renal guanylate cyclase activity [1].

Atrial natriuretic peptide (3-28) (human) (ANP (3-28) (human)), a peptide hormone produced by the atrial myocardium, plays a critical role in the regulation of blood pressure, fluid balance, and electrolyte homeostasis [1] [2].

Atrial Natriuretic Peptide (ANP) (1-28),rat (TFA) is the main circulating forms of Atrial Natriuretic Peptide (ANP) in rats, which strongly inhibit the secretion of Ang II - stimulated endothelin-1.

Atrial Natriuretic Peptide (1-28), rat is the major circulating form of ANP in rats.

Atrial natriuretic factor (1-28) from both human and porcine sources is a powerful suppressor of pro-opiomelanocortin (POMC) mRNA, while it only has a modest inhibition effect on βEP-LI release.

ANP (1-11), rat acetate (Atrial natriuretic factor (1-11) acetate) is one of the atrial natriuretic factors, inhibitors of CRF-stimulated ACTH secretion.

Auriculin B (ANP (126-150) (Rat)), a rat-derived atrial natriuretic peptide, exhibits potent vasodilatory and diuretic properties [1].

Carperitide acetate (Atrial Natriuretic Peptide (ANP) (1-28), human, porcine Acetate), a 28-amino acid hormone, is naturally produced and released by the human heart upon cardiac injury or mechanical stretch. This compound effectively inhibits the secretion of endothelin-1 in a dose-dependent manner.

Carperitide, a 28-amino acid hormone known as Atrial Natriuretic Peptide (ANP) (1-28), is naturally synthesized and released by the human heart in reaction to cardiac injury and mechanical stretch. This compound effectively suppresses endothelin-1 secretion in a dose-dependent manner.

ATX-II, an Na+ channel modulator toxin derived from the sea anemone (Anemonia sulcata), causes delayed inactivation of the Na+ channels and has been linked to pulmonary vein arrhythmogenesis and atrial fibrillation [1] [2]. It exhibits interaction with halothane, caffeine, and ryanodine.

AP 811 acetate is a selective antagonist of the atrial natriuretic peptide clearance receptor (ANP-CR, NPR3), demonstrating high affinity with a K_i value of 0.48 nM and exhibiting over 20,000-fold selectivity for NPR3 compared to NPR1. It effectively inhibits ANP-induced pump stimulation [1] [2].

Atriopeptin III (rat) (ANP 127-150), a 24-amino acid atrial peptide, functions as a powerful vasodilator and natriuretic/diuretic agent, enhancing renal functions and reducing blood pressure in a rat model with ureter-obstructed kidneys. It is utilized in research concerning chronic renal failure [1].

AP 811, a selective antagonist of the atrial natriuretic peptide clearance receptor (APN-CR, NPR3) with a K i value of 0.48 nM, exhibits remarkable selectivity for NPR3 over NPR1 by more than 20,000-fold. Moreover, AP 811 effectively eliminates ANP-induced pump stimulation.

Atrial Natriuretic Peptide (ANP) has the sequence of H-Ser-Leu-Arg-Arg-Ser-Ser-Cys-Phe-Gly-Gly-Arg-OH, is a 28 amino acid peptide. ANP is a powerful vasodilator, and a protein (polypeptide) hormone secreted by heart muscle cells. It is involved in the hom

BNP (1-21), Pro (Human) is a 21-amino acid peptide and a form of B-Type Natriuretic Peptide (BNP), a cardiac natriuretic hormone. It coexists with the homologous atrial natriuretic peptide in the heart's dual natriuretic peptide system. BNP plays a critical role in heart organogenesis and the transition to extrauterine life [1] [2] [3].

Auriculin A, a synthetic atrial natriuretic factor (ANF), exhibits hemodynamic properties by antagonizing renal vasoconstriction in dogs and affects arterial baroreflex regulation of heart rate, systemic blood pressure, and constant flow-perfused hind limb perfusion pressure in rabbits [1] [2].

ATX-II TFA, a specific Na+ channel modulator toxin, is derived from the venom of the sea anemone (Anemonia sulcata). This compound impedes the inactivation of Na+ channels and has been associated with arrhythmogenesis in the pulmonary vein and atrial fibrillation [1] [2]. It interacts with halothane, caffeine, and ryanodine in this modulation.

M65 is a PAC1 receptor-specific antagonist that inhibits the secretion of atrial natriuretic peptide (ANP) [1].

Vasonatrin peptide (VNP) is a chimera of atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) with potent venodilating and natriuretic activity.

A-71915 (TFA) is a selective inhibitor of ANP receptor (atrial natriuretic peptide-receptor), induces apoptosis and decreases insulin secretion in RINm5F pancreatic β-cells.

Prepro-ANF (56-92), human, a precursor to the human atrial natriuretic factor, serves as an activator of guanylate cyclase, specifically enhancing particulate guanylate cyclase activity within the renal membrane and unit [1].

Vasonatrin Peptide (VNP) TFA, a chimeric compound derived from atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP), exhibits venodilating properties reminiscent of CNP, natriuretic effects akin to ANP, as well as unique arterial vasodilating capabilities not characteristic of either parent peptide. Additionally, VNP TFA confers cardioprotection in diabetic ischemia-reperfusion injury by attenuating endoplasmic reticulum (ER) stress through the cGMP-PKG signaling cascade [1] [2] [3].

ANP (1-30), frog, a peptide fragment sourced from atrial natriuretic peptide of frog origin, exhibits natriuretic, diuretic, and vasorelaxant properties.

A-71915 (TFA) is a selective atrial natriuretic peptide-receptor (ANP receptor) inhibitor that promotes apoptosis and reduces insulin secretion in RINm5F pancreatic β-cells [1].

A 71915, an atrial natricuretic factor receptor antagonist, blocks physiological effects of angiotensin.