Angiotensin (1-7)

Hersteller MedChem Express
Typ Inhibitors
Specific against other
Clon N/A
Menge 5mg
ArtNr HY-12403-5mg
eClass 6.1 30220300
eClass 9.0 32160605
Angiotensin-(1-7), Ang-(1-7)
H2O: >= 30.2 mg/mL
Biological Description
Angiotensin (1-7) inhibits purified canine angiotensin converting enzyme (ACE) activity with an IC50 of 0.65 uM.
IC50 & Target: IC50: 0.65 uM (ACE)[1]
In Vitro: Angiotensin 1-7 (Ang 1-7) acts as a local synergistic modulator of kinin-induced vasodilation by inhibiting ACE and releasing nitric oxide (NO). Angiotensin (1-7) augments the vasodilation induced by bradykinin (BK) in a concentration-dependent manner in rings preconstricted with the thromboxane analog U46619. The EC50 of BK (2.45+/-0.51 nM versus 0.37+/-0.08 nM) is shifted leftward by 6.6-fold in the presence of 2 uM concentration of Angiotensin (1-7). The BK-induced relaxation response is augmented by Angiotensin (1-7) (0.1 to 2 uM) in a dose-dependent manner. At a concentration of 2 uM Angiotensin (1-7), relaxation to BK is increased 92% compared to BK alone (41+/-4.4% versus 92+/-2.5%, P<0.01). Angiotensin (1-7) possesses novel biological functions that are distinct from Ang II. In contrast to Ang II, Angiotensin (1-7) is not a dipsogen or an aldosterone secretagogue, but similar to Ang II, it stimulates the release of vasopressin, prostaglandins, and NO. Angiotensin (1-7) counteracts several actions of Ang II. In both canine and porcine coronary arteries, Angiotensin (1-7) causes vasodilation, while Ang II divergently constricts the coronary arteries. Angiotensin (1-7) inhibits cultured vascular smooth muscle cell growth, whereas equal molar concentration of Ang II stimulates cell growth[1]. Angiotensin 1-7 (Ang 1-7) abrogates the methylglyoxal-modified albumin (MGA)-stimulated myofibroblast phenotype by inhibiting the chronic stimulation of the TGF-beta-ERK pathway in NRK-52E cells[2].
In Vivo: A seven fold decrease in the plasma level of Angiotensin 1-7 (Ang 1-7) is demonstrated in dextran sulfate sodium (DSS) treated mice compare to untreated (UT) group at day 7 post colitis induction. On the other hand, a significant increase in Ang 1-7 is observed in colon homogenates of DSS treated mice at day 7 (0.09 ng/mL) compare to UT mice (0.04 ng/mL)[3]. The ovariectomized (OV) female Wistar-rats receive estradiol (500 ug/kg/week) or vehicle for two weeks. The animals are anesthetized, cannulated, and the responses including mean arterial pressure, renal blood flow (RBF), and renal vascular resistance at the constant level of renal perfusion pressure to graded infusion of Angiotensin 1-7 (Ang 1-7) at 0, 100 and 300 ng/kg/min are determined in OV and OV estradiol-treated (OVE) rats, treated with vehicle or MasR antagonist; A779. RBF response to Ang 1-7 infusion increased dose-dependently in vehicle (Pdose<0.001) and A779-treated (Pdose<0.01) animals. However, when MasR is blocked, the RBF response to Ang 1-7 significantly increases in OV animals compare with OVE rats (P<0.05). When estradiol is limited by ovariectomy, A779 increases RBF response to Angiotensin (1-7) administration, while this response is attenuated in OVE animals[4].
Free  Sample
Available in quantities of 0, 5mg-1mg. Three different samples per customer per year!
Menge: 5mg
Lieferbar: In stock
Listenpreis: 108,93 €
Preis: 108,93 €


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