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Qingda granule inhibits angiotensin Ⅱ induced VSMCs proliferation through MAPK and PI3K/AKT pathways.

08:00 EDT 18th March 2020 | BioPortfolio

Summary of "Qingda granule inhibits angiotensin Ⅱ induced VSMCs proliferation through MAPK and PI3K/AKT pathways."

The abnormal increase in vascular smooth muscle cell (VSMC) proliferation is widely accepted as the pivotal process in the vascular remodeling of hypertension. Qingda granule (QDG) is simplified from Qingxuan Jiangya Decoction (QXJYD) which has been in usage for a long time as a traditional Chinese medicine formula to treat hypertension based on the theory of traditional Chinese medicine. However, its underlying molecular mechanisms of action remain largely unknown.

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This article was published in the following journal.

Name: Journal of ethnopharmacology
ISSN: 1872-7573
Pages: 112767

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Medical and Biotech [MESH] Definitions

A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.

A decapeptide that is cleaved from precursor angiotensinogen by RENIN. Angiotensin I has limited biological activity. It is converted to angiotensin II, a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME.

An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.

A heptapeptide formed from ANGIOTENSIN II after the removal of an amino acid at the N-terminal by AMINOPEPTIDASE A. Angiotensin III has the same efficacy as ANGIOTENSIN II in promoting ALDOSTERONE secretion and modifying renal blood flow, but less vasopressor activity (about 40%).

An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR.

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