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Angiotensin I (human, mouse, rat)

Catalog No.
A1006
Precursor of angiotensin II
Grouped product items
SizePriceStock Qty
5mg
$60.00
In stock
10mg
$100.00
In stock
25mg
$140.00
In stock
For scientific research use only and should not be used for diagnostic or medical purposes.

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Email: [email protected]

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Background

Angiotensin I (human, mouse, rat; CAS 484-42-4) is a decapeptide (sequence: H-Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu-OH) resulting from the renin-catalyzed cleavage of angiotensinogen. Angiotensin I itself lacks direct biological activity and functions primarily as the immediate precursor of angiotensin II (Ang II). Conversion occurs via angiotensin-converting enzyme (ACE), which removes two amino acids, yielding Ang II. Ang II mediates biological effects by activating Gq protein-coupled receptors in vascular smooth muscle cells, triggering IP3-dependent intracellular pathways that result in vasoconstriction and elevated blood pressure. Angiotensin I serves as an essential research tool to investigate renin-angiotensin system regulation, cardiovascular disease mechanisms, and antihypertensive drug screening.

Product Citation

Chemical Properties

Physical AppearanceA solid
StorageDesiccate at -20°C
M.Wt1296.5
Cas No.484-42-4
FormulaC62H89N17O14
SynonymsAsp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu
Solubility≥129.6 mg/mL in DMSO; ≥124.2 mg/mL in H2O; ≥9.16 mg/mL in EtOH
Chemical NameAngiotensin I (human, mouse, rat)
SDFDownload SDF
Canonical SMILESCCC(C)C(C(=O)NC(CC1=CN=CN1)C(=O)N2CCCC2C(=O)NC(CC3=CC=CC=C3)C(=O)NC(CC4=CN=CN4)C(=O)NC(CC(C)C)C(=O)O)NC(=O)C(CC5=CC=C(C=C5)O)NC(=O)C(C(C)C)NC(=O)C(CCCN=C(N)N)NC(=O)C(CC(=O)O)N
Shipping ConditionSmall Molecules with Blue Ice, Modified Nucleotides with Dry Ice.
General tips We do not recommend long-term storage for the solution, please use it up soon.

Protocol

Animal experiment:[1]

Animal models

Time-dated pregnant ewes (gestational day 125 ± 5, term ~ 145 days)

Dosage form

5 μg/kg

Intracerebroventricular injection

Applications

Intracerebroventricular injection of Ang I significantly increased fetal blood pressure and c-fos expression in the supraoptic nuclei (SON) and the paraventricular nuclei (PVN) in the hypothalamus, accompanied by an increase of fetal plasma arginine vasopressin (AVP). Double labeling experiments showed colocalization of AT1 receptor and c-fos expression in both SON and PVN following Ang I treatment. The results indicate that central angiotensin I increases fetal AVP neuron activity and pressor responses.

Note

The technical data provided above is for reference only.

References:

1. Shi L, Mao C, Zeng F, et al. Central angiotensin I increases fetal AVP neuron activity and pressor responses. American Journal of Physiology - Endocrinology and Metabolism, 2010, 298(6): E1274-1282.

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