Renin

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Related to plasma renin activity: aldosterone

renin

[′rēn·ən]
(biochemistry)
A proteolytic enzyme produced in the afferent glomerular arteriole which reacts with the plasma component hypertensinogen to produce angiotensin II.

Renin

 

a proteolytic enzyme in vertebrates and humans. It is produced by specialized cells in the arteriole walls of renal glomeruli, from where it passes into the blood and lymph. Renin is one of the enzymes in the renin-angiotensin system. It acts on the specific glycoprotein angiotensinogen by breaking the bond between two leucine radicals. The resultant inactive decapeptide (angiotensin I) is enzymatically converted into the active hormone angiotensin II (hypertensin, or angiotonin). Enzymes resembling renin are found in the uterus, placenta, salivary glands, brain, and the walls of certain major arteries.

References in periodicals archive ?
Plasma renin activity and N-terminal pro-B-type natriuretic peptide levels in patients with recent, persistent and permanent AF Variables Controls Recent AF n=30 n=32 p *** PRA, ng/ml/h 0.
For typical samples, the correlation of the plasma renin activity results for the samples processed with and without neomycin was excellent (m = 1.
Whereas the plasma renin activity assay exploits the endogenous proteolytic activity of renin, unbiased and targeted proteomics assays use exogenous proteinases to degrade proteins into peptides, which then act as surrogates for the intact proteins.
Kodish ME, Katz FH Plasma renin concentration: comparison of angiotensinase inhibitors and correlation with plasma renin activity and aldosterone.
Plasma renin activity fell by an average of 54%-65%, compared with baseline, in patients who took any dosage of aliskiren (75, 150, or 300 mg/day) as monotherapy.
In a study of 120 consecutive patients with resistant hypertension (uncontrolled by three or more medications) and no dietary salt restriction, he and his colleagues prospectively evaluated plasma renin activity and 24-hour urinary aldosterone and sodium excretion.
We fully agree with their reservations on the use of commercial assays by inexperienced laboratories and their point that patient management decisions should not be based on a single measurement of the ratio of aldosterone to plasma renin activity (ARR).
Those persons with an occult adrenal mass and hypertension should have serum potassium, plasma aldosterone, and plasma renin activity measured to assess for primary aldosteronism.
Direct renin assay and plasma renin activity assay compared.
In addition to its greater BP control, aliskiren neutralized the ARB-induced compensatory rise in Plasma Renin Activity (PRA), a risk factor for end organ damage.
The ratio assumes that the plasma aldosterone level is linearly and positively dependent on plasma renin activity, so that as renin increases, so does aldosterone.
Removal of angiotensin II negative feedback on renin secretion leads to increased plasma renin activity.

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