2. GPCR/G Protein
  3. Angiotensin Receptor
  4. A-779 TFA

A-779 TFA is a selective angiotensin-(1-7) (Ang-(1-7)) antagonist. A-779 TFA blocks Arachidonic acid release, bradykinin potentiation effects and hypotensive action. A-779 TFA exerts diuretic effects in non-pregnant rats, antidiuretic effects in late-pregnant rats, and also inhibits feed intake and water consumption in late-pregnant rats. A-779 TFA attenuates the regulatory effects of prostacyclin, nitric oxide and thromboxane A2 associated with angiotensin-(1-7). A-779 TFA can be used in studies related to hypertension.

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A-779 TFA

A-779 TFA Chemical Structure

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Description

A-779 TFA is a selective angiotensin-(1-7) (Ang-(1-7)) antagonist. A-779 TFA blocks Arachidonic acid release, bradykinin potentiation effects and hypotensive action. A-779 TFA exerts diuretic effects in non-pregnant rats, antidiuretic effects in late-pregnant rats, and also inhibits feed intake and water consumption in late-pregnant rats. A-779 TFA attenuates the regulatory effects of prostacyclin, nitric oxide and thromboxane A2 associated with angiotensin-(1-7). A-779 TFA can be used in studies related to hypertension[1][2][3][4].

In Vitro

A-779 (10-10 to 10-6 M) potently competes with 125I-Ang-(1-7) TFA for binding to Mas-transfected CHO cells, with an IC50 of 0.3 nM[2].
A-779 (10-8 M; 10 min pre-incubation followed by 15 min incubation with Ang-(1-7) at 37°C) TFA blocks the [3H]-arachidonic acid release induced by Ang-(1-7) (HY-12403) in Mas-transfected CHO and COS cells[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

A-779 TFA Related Antibodies
In Vivo

A-779 (24 μg/kg/h; intravenous injection; continuous infusion; 8 days) TFA significantly increases urine output by 126% in unmated female Sprague Dawley rats[1].
A-779 (24 μg/kg/h; intravenous injection; continuous infusion; from 8 days before pregnancy to gestational day 19) TFA significantly reduces feed consumption by 83% and urine output by 76% in late-pregnant Sprague Dawley rats, decreases water intake by 83% in mid-pregnancy and by 80% in late-pregnancy, with no impact on fetal outcomes[1].
Continuous intravenous infusion of A-779 TFA at a rate of 80 ng/min significantly attenuates the potentiating effect of Captopril (HY-B0368) on the hypotensive action of bradykinin in conscious male Wistar rats[3].
A-779 (48 µg/kg; intravenous injection; single administration; 100 pM; co-incubated with isolated aortic rings) TFA partially blocks the Ang-(1-7)-induced hypotensive response in male Dahl salt-sensitive rats with high salt-induced hypertension, and inhibits all Ang-(1-7)-mediated changes in the levels of vasodilatory/vasoconstrictive prostaglandins, nitric oxide, and cGMP[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Sprague Dawley (female, 9 weeks old)[1]
Dosage: 24 μg/kg/h
Administration: i.v.; continuous infusion; 8 days
Result: Increased urine volume by 126%.
Tended to decrease urinary osmolality.
Did not alter chow consumption and water intake relative to vehicle controls.
Animal Model: Sprague Dawley (female, originally 9 weeks old virgin, pregnant)[1]
Dosage: 24 μg/kg/h
Administration: i.v.; continuous infusion; 8 days pre-pregnancy through gestational day 19
Result: Decreased water consumption by 83% relative to vehicle controls in mid-pregnancy (gestational day 15).
Decreased chow consumption by 83%, decreased water consumption by 80%, and reduced urine volume by 76% relative to vehicle controls in late pregnancy (gestational day 19).
Tended to increase urinary osmolality in late pregnancy.
Had no significant effect on fluid/food intake-output balance, urinary sodium or potassium concentrations, maternal body weight, or fetal characteristics (body weight, length, number).
Animal Model: Wistar (male, 230-320 g)[3]
Dosage: 80 ng/min
Administration: i.v.; continuous infusion
Result: Produced a significant shift of the intravenous bradykinin dose-response curve, requiring approximately two-fold higher bradykinin doses to achieve the same hypotensive effect observed with captopril alone.
Significantly attenuated the captopril-induced potentiation of intra-arterial bradykinin's hypotensive effect.
Did not significantly alter bradykinin's hypotensive effect or baseline MAP when infused alone (without captopril).
Did not modify the pressor effect of angiotensin II.
Did not change captopril's inhibitory effect on angiotensin I's pressor response.
Did not alter the captopril-induced decrease in baseline MAP.
Animal Model: Dahl salt-sensitive (male, 4-5 weeks of age, high 8.0% NaCl salt diet for 2 weeks or low 0.3% NaCl salt diet)[4]
Dosage: 48 µg/kg (in vivo); 100 pmol (ex vivo tissue incubation)
Administration: i.v.; single dose (in vivo); incubated with isolated aortic rings (ex vivo)
Result: Blocked the maximal MAP reduction of -14 mm Hg induced by Ang-(1-7) in high salt diet rats, resulting in a significantly attenuated blood pressure decrease.
Prevented the Ang-(1-7)-induced increase in plasma 6-keto-PGF1α levels, maintaining levels near basal values.
Prevented the Ang-(1-7)-induced decrease in plasma TXB2 levels, maintaining levels near basal values.
Prevented the Ang-(1-7)-induced increase in plasma nitric oxide levels, maintaining levels near basal values.
Prevented the Ang-(1-7)-induced increase in aortic ring 6-keto-PGF1α levels (from 31 to 49 pg/mL/mg ring wt, maintained at 36 pg/mL/mg ring wt) and PGE2 levels (from basal 22 to Ang-(1-7)-induced 33 pg/mL/mg ring wt, maintained at 21 pg/mL/mg ring wt) in high salt diet rats.
Attenuated the Ang-(1-7)-induced decrease in aortic ring TXB2 levels (from basal 44 to Ang-(1-7)-induced 23 pg/mL/mg ring wt, increased to 37 pg/mL/mg ring wt) in high salt diet rats.
Prevented the Ang-(1-7)-induced increase in nitric oxide levels in aortic rings from both high and low salt diet rats.
Totally abolished the Ang-(1-7)-induced 52% increase in aortic ring cGMP levels (from basal 102 to Ang-(1-7)-induced 212 fmol/mg protein, maintained at 67 fmol/mg protein) in high salt diet rats.
Had no significant effect on MAP, plasma 6-keto-PGF1α, TXB2, nitric oxide, aortic ring 6-keto-PGF1α, PGE2, TXB2, nitric oxide, or cGMP levels compared to basal values in either diet group.
Molecular Weight

986.99

Formula

C41H61F3N12O13
Sequence

Asp-Arg-Val-Tyr-Ile-His-{d-Ala}
Sequence Shortening

DRVYIH-{d-Ala}
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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A-779 TFA Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

A-779A779A 779Angiotensin ReceptorMas-transfected CHO cellsWistar ratsarachidonic acidSprague Dawley ratsangiotensin-(1-7)bradykininvirgin ratsMas-transfected COS cellslate-gestation ratsMas protooncogene G protein-coupled receptorInhibitorinhibitorinhibit

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