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An enzyme that catalyzes the coagulation of milk, obtained from the fourth stomach of calves and other young ruminants or from genetically engineered microorganisms and used in making cheeses and junkets. Also called chymosin.

American Heritage® Dictionary of the English Language, Fifth Edition. Copyright © 2016 by Houghton Mifflin Harcourt Publishing Company. Published by Houghton Mifflin Harcourt Publishing Company. All rights reserved.


(Biochemistry) an enzyme that occurs in gastric juice and is a constituent of rennet. It coagulates milk by converting caseinogen to casein. Also called: chymosin
[C20: from rennet + -in]
Collins English Dictionary – Complete and Unabridged, 12th Edition 2014 © HarperCollins Publishers 1991, 1994, 1998, 2000, 2003, 2006, 2007, 2009, 2011, 2014


(ˈrɛn ɪn)

a coagulating enzyme occurring in the gastric juice of the calf, forming the active principle of rennet and able to curdle milk.
[1895–1900; renn (et) + -in1]
Random House Kernerman Webster's College Dictionary, © 2010 K Dictionaries Ltd. Copyright 2005, 1997, 1991 by Random House, Inc. All rights reserved.
ThesaurusAntonymsRelated WordsSynonymsLegend:
Noun1.rennin - an enzyme that occurs in gastric juice; causes milk to coagulate
gastric acid, gastric juice - digestive secretions of the stomach glands consisting chiefly of hydrochloric acid and mucin and the enzymes pepsin and rennin and lipase
enzyme - any of several complex proteins that are produced by cells and act as catalysts in specific biochemical reactions
coagulase - an enzyme that induces coagulation
rennet - a substance that curdles milk in making cheese and junket
Based on WordNet 3.0, Farlex clipart collection. © 2003-2012 Princeton University, Farlex Inc.
References in periodicals archive ?
Achieving the best metabolic control (HbA1c <7%), treating hypertension (<130/80 mmHg or <125/75 mmHg if proteinuria >1.0 g/24 h and increased serum creatinine), using drugs with blockade effect on the rennin angiotensin aldosterone system and treating dyslipidaemia (LDL cholesterol <100 mg/dl) are effective strategies for preventing the development of microalbuminuria, in delaying the progression to more advanced stages of nephropathy and in reducing cardiovascular mortality in patients with type 1 and type 2 diabetes.
Decrease in blood volume is a powerful stimulus for rennin secretion (Hazon and Flik, 2002).
To this is added the well-recognized sequelae of heart failure like increased salt and water retention secondary to increased rennin and aldosterone production, impaired visceral, splanchnic and renal perfusion and increased catecholamine levels, which in time produce significant down regulation of beta receptors and diminished myocardial catecholamine stores.
This could be due to increased sympathetic activity or elevation of circulating catecholamine while other active hormone like rennin, angiotensin aldosterone also contribute, Rise in blood pressure due to stress leads to increased epinephrine secretion Rise in blood pressure is important sympatho-adrenal response to physiological stressful experience caused by premenstrual stress.
Human fetal kidney morphometry during gestation and the relationship between weight, kidney morphometry and plasma active rennin concentration as birth.
Several mechanism have been postulated for the effect of calcium on blood pressure, a low calcium intake increases blood pressure through stimulating rennin release, which in turn causes vasoconstriction, another possible mechanism is through lowering parathyroid release and intracellular calcium resulting in smooth muscle contractility.
Reports suggest that a positive relationship between plasma angiotensin level, plasma rennin activity, and plasma angiotensin converting enzyme with BMI exits in humans.
The plasma aldosterone level is normal or high, and plasma rennin activity (PRA) is low.
Plasma rennin was analysed on DIASORIN LIASONA(r) by sandwich chemiluminescence immunoassay and analysis of serum aldosterone was done by BIORAD PhD(tm) SYSTEM-enzyme-linked immunosorbent assay (ELISA).
It is well established that maternal diet induced-hypertension is related to mechanisms that include reduced nephron morphology and function, reduced glomerular filtration rate, dysfunction on the rennin angiotensin-aldosterone system (9), as well as sympathetic-respiratory dysfunctions (10).
Hypertension, associated with dyslipidemia, can be found in AAS users, and this can be a result of hyperactivation of adrenal cortex and rennin secretion increase (19).