(D-Pro⁷)-Angiotensin I/II (1-7)
Catalog No.: GA20155Purity:98.68%
(D-Pro⁷)-Angiotensin I/II (1-7) is a peptide antagonist of the Mas receptor, engineered by replacing the C-terminal Pro⁷ of Angiotensin-(1-7) with a D-proline.
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Cas No.: 586962-44-9
1mgIn Stock
$85.00
1
5mgIn Stock
$255.00
1
| Pack Size | Price | Availability | Quantity | Action |
|---|---|---|---|---|
| 1mg | $85.00 | In Stock | 1 | |
| 5mg | $255.00 | In Stock | 1 |
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Citations
1 publicationsPublications from researchers using this productDescription
(D-Pro⁷)-Angiotensin I/II (1-7) is a peptide antagonist of the Mas receptor, engineered by replacing the C-terminal Pro⁷ of Angiotensin-(1-7) with a D-proline[1]. The Mas receptor, a G-protein-coupled receptor for Ang-(1-7), elicits vasodilatory, anti-proliferative and anti-fibrotic protective signals upon activation[2]. (D-Pro⁷)-Angiotensin I/II (1-7) competitively blocks the binding of Angiotensin-(1-7) to Mas and is widely used to selectively interrupt ACE2/Ang-(1-7)/Mas-axis signaling in research[3].
In vitro, pretreatment of human pulmonary microvascular endothelial cells (PMVEC) with 100nM (D-Pro⁷)-Angiotensin I/II (1-7)(30min) completely abolished the protective effect of Ang-(1-7) against thrombin induced barrier disruption, reducing the trans-endothelial electrical resistance (TEER)[4]. In rat aortic vascular smooth muscle cells (VSMC) cultured in high glucose (25mM), 72h co-incubation with 1μM (D-Pro⁷)-Angiotensin I/II (1-7) reversed the inhibitory effect of Ang-(1-7) on high glucose-induced ErbB2 phosphorylation, restoring the p-ErbB2/t-ErbB2 ratio[5].
In vivo, (D-Pro⁷)-Angiotensin I/II (1-7) (10μM; 20min pre-incubation in isolated organ bath) reduced the maximal vasorelaxation evoked by Ang-(1-7) in rat renal arteries, completely blocking Ang-(1-7)-induced vasodilation and abolishing Ang-(1-7)-mediated activation of the NO-sGC-cGMP pathway[6]. (D-Pro⁷)-Angiotensin I/II (1-7) (0.1μM; 20min pre-incubation; vascular-bath perfusion) blocks an A-779-insensitive novel Ang-(1–7) receptor subtype and completely reverses the endothelium-dependent relaxation induced by Ang-(1–7) in isolated thoracic aortic rings from Sprague–Dawley rats[7].
References:
[1] Santos RA, Haibara AS, Campagnole-Santos MJ, et al. Characterization of a new selective antagonist for angiotensin-(1-7), D-pro7-angiotensin-(1-7). Hypertension. 2003;41(3 Pt 2):737-743.
[2] Santos RAS, Sampaio WO, Alzamora AC, et al. The ACE2/Angiotensin-(1-7)/MAS Axis of the Renin-Angiotensin System: Focus on Angiotensin-(1-7). Physiol Rev. 2018;98(1):505-553.
[3] Santos RA, Frézard F, Ferreira AJ. Angiotensin-(1-7): blood, heart, and blood vessels. Curr Med Chem Cardiovasc Hematol Agents. 2005;3(4):383-391.
[4] Klein N, Gembardt F, Supé S, et al. Angiotensin-(1-7) protects from experimental acute lung injury. Crit Care Med. 2013;41(11):e334-e343.
[5] Akhtar S, Chandrasekhar B, Attur S, Dhaunsi GS, Yousif MH, Benter IF. Transactivation of ErbB Family of Receptor Tyrosine Kinases Is Inhibited by Angiotensin-(1-7) via Its Mas Receptor. PLoS One. 2015;10(11):e0141657.
[6] Yousif MHM, Benter IF, Diz DI, Chappell MC. Angiotensin-(1-7)-dependent vasorelaxation of the renal artery exhibits unique angiotensin and bradykinin receptor selectivity. Peptides. 2017;90:10-16.
[7] Silva DM, Vianna HR, Cortes SF, Campagnole-Santos MJ, Santos RA, Lemos VS. Evidence for a new angiotensin-(1-7) receptor subtype in the aorta of Sprague-Dawley rats. Peptides. 2007;28(3):702-707.
Protocol
| Cell experiment [1]: | |
Cell lines | Human pulmonary microvascular endothelial cells |
Preparation Method | Human pulmonary microvascular endothelial cells (PMVECs, passages 4–8) were grown to confluence in polycarbonate wells containing gelatin-coated gold microelectrodes. Following a 30 minute recording of baseline resistance, the Ang-(1–7) receptor blocker (D-Pro⁷)-Angiotensin I/II (1-7)(100nM), the bradykinin receptor blocker icatibant (1µM), the NO synthase inhibitor Nω-nitro-L-arginine methyl ester (l-NAME; 1mM), or respective vehicle controls were added, followed after 15 minutes by Ang-(1–7) (100nM) or vehicle and after an additional 30 minutes by thrombin (0.2U/mL). Transendothelial electrical resistance (TEER) measurements were performed using an electrical cell substrate impedance sensing system. TEER values were recorded continuously up to 75 minutes after thrombin stimulation. |
Reaction Conditions | 100nM; 30min |
Applications | Pretreatment of human pulmonary microvascular endothelial cells (PMVEC) with (D-Pro⁷)-Angiotensin I/II (1-7) completely abolished the protective effect of Ang-(1-7) against thrombin induced barrier disruption, reducing the trans-endothelial electrical resistance (TEER). |
| Animal experiment [2]: | |
Animal models | Sprague–Dawley rats |
Preparation Method | 7–9-month-old male Hanover Sprague–Dawley rats were maintained in collective cages in an appropriate room with controlled temperature and with a 12h light cycle. The vasorelaxant activity of Ang-(1–7) was measured in vessels with or without functional endothelium pre-contracted to the same tension level (approximately 1.5g of tension) with submaximal concentrations of phenylephrine (0.03–0.1μM). Ang-(1–7) was added in increasing cumulative concentrations once the response to phenylephrine had stabilized. In an attempt to determine which receptor is involved in the vasorelaxant effect of Ang-(1–7), experiments were performed in endothelium-containing vessels, in the presence of the Ang-(1–7) antagonists A-779 (0.1, 1.0 or 10μM) or (D-Pro⁷)-Angiotensin I/II (1-7) (0.1μM); the B2 receptor antagonist HOE 140 (1μM), the Ang II receptor antagonists CV11974 (0.01μM; AT1 antagonist) or PD123319 (1μM; AT2 antagonist). As a control, another vessel segment from each rat was simultaneously monitored for Ang-(1–7) effects alone. |
Dosage form | 0.1μM; 20min pre-incubation, vascular-bath perfusion |
Applications | (D-Pro⁷)-Angiotensin I/II (1-7) blocks an A-779-insensitive novel Ang-(1–7) receptor subtype and completely reverses the endothelium-dependent relaxation induced by Ang-(1–7) in isolated thoracic aortic rings from Sprague–Dawley rats. |
References: | |
Product Documents
Purity:98.68%Appearance:A solid
Chemical Properties
CAS No.
586962-44-9
Molecular Formula
C41H62N12O11
Molecular Weight
899.02
Solubility
1 mg/mL in Water
Storage
Store at -20°C
General tips
Select a suitable solvent according to the product solubility data. Once prepared, aliquot the stock solution to avoid repeated freeze-thaw cycles.
Use stock solutions within 6 months when stored at -80°C or within 1 month when stored at -20°C.
To improve solubility, warm the tube to 37°C and sonicate it for an appropriate period.
Use stock solutions within 6 months when stored at -80°C or within 1 month when stored at -20°C.
To improve solubility, warm the tube to 37°C and sonicate it for an appropriate period.
Shipping Condition
Evaluation samples are shipped with blue ice. Other available sizes are shipped at room temperature or with blue ice upon request.
CalculatorsMolarity / Dilution / Molecular Weight / Unit Conversion / In Vivo Formulation / Solubility
g/mol
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