3.4.23.15: renin
This is an abbreviated version!
For detailed information about renin, go to the full flat file.
Word Map on EC 3.4.23.15
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3.4.23.15
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hypertension
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aldosterone
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arterial
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urinary
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cardiovascular
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cardiac
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antihypertensive
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normotensive
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gastric
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glomerular
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natriuretic
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hemodynamic
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systolic
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diastolic
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sympathetic
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ras
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angiotensin-converting
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norepinephrine
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output
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adrenal
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blocker
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prostaglandin
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ventricular
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catecholamine
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diuretic
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creatinine
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hg
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electrolyte
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placebo
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vasopressin
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captopril
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vasodilator
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cortisol
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supine
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intrarenal
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renovascular
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conscious
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pressor
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posture
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acth
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noradrenaline
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losartan
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hypotensive
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mineralocorticoid
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vasoconstriction
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enalapril
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furosemide
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anp
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medicine
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macula
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pharmacology
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aceis
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diagnostics
- 3.4.23.15
- hypertension
- aldosterone
- arterial
- urinary
- cardiovascular
- cardiac
-
antihypertensive
-
normotensive
- gastric
- glomerular
-
natriuretic
-
hemodynamic
-
systolic
-
diastolic
-
sympathetic
- ras
-
angiotensin-converting
- norepinephrine
- output
- adrenal
-
blocker
- prostaglandin
- ventricular
- catecholamine
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diuretic
- creatinine
- hg
-
electrolyte
-
placebo
- vasopressin
- captopril
-
vasodilator
- cortisol
-
supine
-
intrarenal
-
renovascular
-
conscious
-
pressor
-
posture
- acth
- noradrenaline
- losartan
-
hypotensive
-
mineralocorticoid
-
vasoconstriction
- enalapril
- furosemide
- anp
- medicine
-
macula
- pharmacology
-
aceis
- diagnostics
Reaction
cleavage of Leu-/- bond in angiotensinogen to generate angiotensin I =
Synonyms
angiotensin-forming enzyme, angiotensinogenase, EC 3.4.4.15, EC 3.4.99.19, prorenin, REN, SVAP, SVAP A1, SVAP B1, SVAP B2, venom aspartic protease
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diagnostics
medicine
pharmacology
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comparison of active renin concentration and plasma renin activity for the diagnosis of primary hyperaldosteronism in patients with an adrenal mass, the ratio of plasma renin activity to plasma aldosterone concentration is a screening test for primary hyperaldosteronism
diagnostics
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the plasma aldosterone-to-renin ratio measuring plasma renin activity, PRA, is used for screening of primary aldosteronism
diagnostics
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the ratio of plasma aldosterone concentration to plasma renin activity is used for screening for primary aldosteronism in hypertension, development of a test method, overview
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depending on incubation conditions, circulating renin inhibitors interfere with the recognition of active renin molecules by the monoclonal antibodies used in commercial available assays. Careful considerations must therefore by given to the methodology used for quantifying immunoreactive plasma active renin when patients are treated with renin inhibitors, to avoid an overestimation of the magnitude of active renin release attributable to conformational changes in plasma prorenin
medicine
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hypertension is a pathophysiologically heterogeneous condition in which renin-angiotensin system activity is an important determinant of the blood pressure response to antihypertensive drug treatment. The pretreatment plasma renin activity level is a significant predictor of treatment efficacy despite the different experimental designs employed and the ethnically diverse populations evaluated. These observations support the case that pathophysiologic markers such as plasma renin activity should be incorporated into the design of studies that assess antihypertensive treatment strategies
medicine
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plasma active renin concentration is superior to plasma renin activity and a high plasma active renin concentration is an independent prognostic predictor in heart failure patients who are already receiving angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers
medicine
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renin angiotensin system inhibition improves diabetic nephropathy at several levels, independently of its effects on blood pressure and glycemic control, via mechanisms depending of renal oxidative stress
medicine
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in patients with biopsy-confirmed post-transplant glomerulonephritis, statins and renal reini-angiotensin system blockers prolong graft survival. The effect persists after adjustment for presentation with nephrotic syndrome, graft dysfunction, mean arterial pressure, immunosuppression enhancement with mycophenolate mofetil
medicine
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renin inhibition improves systemic insulin sensitivity, insulin metabolic signaling and glucose transport, along with normalization of angiotensin II, angiotensin type I receptor and mineralocorticoid receptor levels, oxidative stress markers, fibrosis and mitochondrial structural abnormalities
medicine
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blockade of renin activation is a therapeutic target to prevent glomerular injury and associated proteinuria
medicine
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direct renin inhibition with aliskiren represents an effective option for the long-term treatment of essential hypertension
medicine
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inhibition of the renin-angiotensin-aldosterone system plays a pivotal role in preventing and treating diabetic nephropathy. Inhibition of renin with aliskiren decreases blood pressure in patients with hypertension. Direct renin inhibition with aliskiren has antiproteinuric effects in type 2 diabetic patients with nephropathy and additive proteinuric effects when used in diabetic patients already treated with the maximal dose of angiotensin type 1 receptor blockers
medicine
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plasma renin activity is an independent predictor of morbidity and mortality in patients with hypertension
medicine
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renin inhibition is the preferred pharmacologic approach to blockade of the renin-angiotensin system. Renin inhibition offers substantial promise for cardioprotection and renoprotection
medicine
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renin inhibition with aliskiren is useful for antihypertensive treatment in patients with severe arterial hypertension, in patients with an already long-lasting course of disease, and in the presence of comorbidities such as diabetes mellitus
medicine
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renin-angiotensin system inhibition is used as treatment for the primary and secondary prevention of atrial fibrillation
medicine
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there is an association of polymorphisms of renin-angiotensin-aldosterone system genes with the risk of non-control of hypertension in angiotensin-converting enzyme inhibitor drugs-treated patients
the renin-angiotensin system is a potential target for lymphangioleiomyomatosis therapy
pharmacology
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after 12 weeks of treatment in patients with hypertension, aliskiren, atenolol and aliskiren/atenolol lower systolic and diastolic blood pressure from baseline by 14.3/11.3, 14.3/13.7 and 17.3/14.1 mmHg, respectively. Systolic blood pressure reductions with aliskiren/atenolol are significantly greater than those with aliskiren or atenolol alone, and diastolic blood pressure reductions are greater than with aliskiren alone. Diastolic blood pressure changes are larger with atenolol than with aliskiren. Aliskiren, atenolol and aliskiren/atenolol reduce geometric mean plasma renin activity from baseline by 65%, 52% and 61%, respectively. In patients with moderate or high baseline plasma renin activity, plasma renin activity is reduced to low levels at week 12 endpoint in a greater proportion of patients receiving aliskiren or aliskiren/atenolol than with atenolol. Aliskiren treatment is associated with numerically lower rates of adverse events and discontinuations due to adverse events compared with atenolol or combination treatment, and unlike atenolol is not associated with bradycardia
pharmacology
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aliskiren at the highest approved dose of 300 mg once daily for 7 days and a 4-fold higher dose has no effect on cardiac repolarization or conduction in healthy volunteers
pharmacology
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co-administration of aliskiren results in changes below 30% in pharmacokinetic parameters AUC and Cmax of digoxin, atorvastatin, o-hydroxyatorvastatin, and p-hydroxyatorvastatin, indicating no clinically significant interaction with P-glycoprotein or CYP3A4 substrates. Aliskiren AUC is significantly increased by coadministration with atorvastatin or ketoconazole
pharmacology
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detailed pharmacodynamic analysis of aliskiren in humans. Development of an integrated pharmacokinetik/pharmacodynamic model for aliskiren, including an empirical submodel to account for additional complexities arising from multiple dosing
pharmacology
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renal vasodilation in healthy people with renin inhibitor aliskiren exceeds responses seen with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. The effects are longer lasting and are associated with significant natriuresis. Aliskiren may provide more complete and more effective blockade of the renin-angiotensin system
pharmacology
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study on long-term safety, tolerability, and antihypertensive efficacy on Japanese patients with mild to moderate essential hypertension. Aliskiren alone or in combination with a diuretic or a calcium channel blocker is well tolerated. The incidence of suspected study-related adverse events was 25.3%. The overall responder efficacy was 73.3% at the endpoint. A clinically meaningful reduction of 17.6/12.8 m Hg from baseline was achieved in the mean sitting blood pressure at the endpoint
pharmacology
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treatment of Watanabe heritable hyperlipidemic rabbits with aliskiren or aliskiren plus valsartan leads to greater increases in plasma nitric oxide concentration in response to intra-aortic acetylcholine infusion than in control. Aliskiren plus valsartan treatment increases acetylcholine-induced nitric oxide by 6.2 nmol/l, which is significantly higher than with either aliskiren or valsartan alone. Vascular superoxide and peroxynitrite levels are both significantly higher in controls and significantly lower in the aliskiren plus valsartan group than in the aliskiren or valsartan group