Description

Product Description

Nva-VYIHPF is a synthetic Angiotensin II analog engineered to mimic the biological activity of the endogenous octapeptide hormone Angiotensin II (HY-13948), a key effector of the renin-angiotensin system (RAS). By substituting the N-terminal asparagine with norvaline (Nva), this analog displays enhanced stability and modulated receptor interaction while retaining vasoactive potency.

Angiotensin II plays a central role in regulating blood pressure, fluid homeostasis, and vascular smooth-muscle contraction. Nva-VYIHPF is used to investigate how small structural modifications influence angiotensin receptor binding and signaling bias between AT₁ and AT₂ receptors. It is particularly useful in mechanistic research on hypertension, heart failure, renal function, and vascular remodeling.

Key Features

• Angiotensin II analog with N-terminal norvaline substitution

• High affinity for AT₁ and AT₂ receptors

• Modulates vascular tone and smooth muscle contraction

• Facilitates structure–activity relationship (SAR) studies of the RAS

• Useful for in-vitro and in-vivo cardiovascular research

The modification confers improved metabolic stability and altered signal bias, enabling researchers to distinguish between canonical G-protein-dependent and β-arrestin-dependent pathways in angiotensin signaling.

Product Specifications

Mechanism of Action

1. Renin–Angiotensin System Overview

The renin–angiotensin system is a hormonal cascade that controls blood pressure and fluid balance. Angiotensin II, the principal effector peptide, acts on specific receptors to induce vasoconstriction, aldosterone secretion, and sympathetic activation. Nva-VYIHPF retains the core sequence motifs responsible for binding to angiotensin receptors but exhibits altered metabolic behavior and slightly modified receptor bias.

2. AT₁ Receptor Activation

At physiological concentrations, Nva-VYIHPF binds to the AT₁ receptor, a GPCR predominantly expressed in vascular smooth muscle cells and the adrenal cortex. This interaction activates phospholipase C (PLC), leading to inositol-trisphosphate (IP₃) and diacylglycerol (DAG) generation, subsequent Ca²⁺ mobilization, and smooth muscle contraction. The result is transient vasoconstriction and an increase in arterial pressure, mirroring natural Ang II effects.

3. AT₂ Receptor Modulation

In contrast to the AT₁ pathway, the AT₂ receptor mediates vasodilation, anti-proliferation, and tissue repair. Nva-VYIHPF shows partial agonism at AT₂, providing a unique tool for studying the antagonistic balance between AT₁ and AT₂ signaling. It stimulates nitric oxide (NO) release and cyclic GMP accumulation in endothelial cells, which contributes to vascular relaxation and cytoprotection.

4. Signal Bias and Receptor Selectivity

The replacement of Asp¹ with Norvaline reduces peptide susceptibility to aminopeptidase cleavage, enhancing stability. Moreover, this substitution alters the electrostatic interactions within the receptor binding pocket, shifting downstream signaling from canonical Gq-mediated Ca²⁺ release toward non-canonical pathways such as ERK1/2 and β-arrestin signaling.

Such bias is valuable for probing the molecular basis of GPCR conformational selectivity and for designing next-generation angiotensin modulators with fewer side effects.

5. Physiological Consequences

• Induces reversible vasoconstriction in isolated arterial rings

• Promotes aldosterone and vasopressin release in endocrine models

• Enhances oxidative stress markers through NADPH oxidase activation (via AT₁)

• Counter-regulated by AT₂-mediated NO signaling that balances vascular tone

Overall, Nva-VYIHPF provides a precise means to decipher the complex interplay of Ang II receptor pathways and their pharmacological modulation.

Side Effects

Although Nva-VYIHPF is intended only for laboratory use, its bioactivity resembles Ang II and may cause the following effects in biological systems:

• Vasoconstriction and transient blood pressure elevation

• Increased aldosterone secretion leading to fluid retention in animal models

• Oxidative stress via AT₁ activation and ROS production

• Endothelial dysfunction at high concentrations

• Compensatory NO release through AT₂ stimulation

Care should be taken to titrate doses according to experimental objectives and cell types. The peptide should not be administered in clinical settings.

Disclaimer

For research use only. Not for human or veterinary use, diagnosis, or treatment.

Keywords

Nva-VYIHPF, Angiotensin II analog, Norvaline peptide, AT₁ receptor agonist, AT₂ modulator, renin-angiotensin system, hypertension research, vascular biology, GPCR bias, peptide analog.

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