angiotensin

(redirected from angiotensinogen)
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  • noun

Synonyms for angiotensin

any of several vasoconstrictor substances (trade name Hypertensin) that cause narrowing of blood vessels

References in periodicals archive ?
The formerly established determination of plasma renin activity (PRA), which measures the formation of AngI from the physiologic angiotensinogen pool, may be influenced by liver impairment, which often accompanies advanced heart failure (21, 22).
Bennett et al., "ACE, angiotensinogen and obesity: a potential pathway leading to hypertension," Journal of Human Hypertension, vol.
High levels of urine tubular biomarkers such as urine cystatin C, angiotensinogen, KIM-1, and NGAL presented more rapid decline in renal function among Thai patients with T2DM [16].
Angiotensinogen. The AGT is a glycoprotein and serine protease inhibitor that belongs to the superfamily of the inhibitory serpins.
Brasier, "Angiotensinogen gene activation by angiotensin II is mediated by the rel A (nuclear factor-kappaB p65) transcription factor: one mechanism for the renin angiotensin system positive feedback loop in hepatocytes," Molecular Endocrinology, vol.
If efficient suppression of renin is not done, angiotensinogen I production could be stimulated and, in salt-wasting CAH patients, AII synthesis could be increased.
Active vitamin D down-regulates renin expression by suppressing renin gene transcription [76]; it reduces urinary angiotensinogen and intrarenal RAAS blockade [77].
The AGT gene which encodes angiotensinogen was also highly expressed in the normal lung tissue, and its mRNA was nearly doubled in the lung tumor tissue (p < 0.05, corrected for multiple comparisons Table 2).
Angiotensinogen (AGT), the primary meg diator of the RAS, is a globular glycoprotein produced by the liver that is cleaved by renin to yield angiotensin I (ANG I).
This system is activated through the conversion of angiotensinogen to angiotensin (Ang I) by renin (12).
It produces hormones including the above-mentioned leptin and peptides like angiotensinogen, the only known precursor of Ang II--the main effector of the renin-angiotensin system (RAS).
Now we have consensus that splanchnic arterial vasodilatation resulting from excess of vasodilators in circulation in a patient with cirrhosis is the primary trigger for HRS.5 Many authorities now believe that this vasodilatation is a consequence of systemic spread of bacterial products following induction of inflammation by host micorbiota, resulting in endothelial injury more pronounced in splanchnic circulation.6 Splanchnic vasodilatation results in reduced effective circulatory volume with renal hypo-perfusion which is further augmented by renal arterial vasoconstriction due to sympathetic over-activity and excess angiotensinogen II levels.7
[12] Estrogen increases hepatic productions of angiotensinogen causing increased formation of the hormone angiotesin II, which causes elevated systolic blood pressure.
It is also significantly correlated with the duration of diabetes, glycemic control (HbA1c), and urinary interleukin-18 (IL-18: proinflammatory biomarker) and angiotensinogen (renin-angiotensin system biomarker), suggesting urinary NGAL as a useful noninvasive tool for the evaluation of renal involvement in diabetes [21,23, 25, 28, 29].
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