Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renin-aldosterone profiling was used to classify patients with hypertension: 243 patients with essential hypertension were classified by renin-urinary sodium indexing; 107 were reclassified by response to administration of furosemide and intravenous saline; 45 were further classified by response to a low-sodium diet. Arbitrary "normal ranges" were determined in 89, 32, and 38 volunteers, respectively. Patients with low-renin apparently do not have "high-volume" hypertension. Rather, they show a primary renal abnormality in renin secretion and become relatively deficient in angiotensin II and aldosterone when they are subjected to diuresis. They can maintain aldosterone secretion under normal conditions because their adrenal aldosterone receptor is supersensitive to angiotensin II. No evidence of abnormal sympathetic neural activity was found among the renin subgroups. Renin-aldosterone profiling in current clinical practice seems useful mainly in the detection of patients with curable forms of secondary hypertension. Aldosterone/renin ratios may be particularly helpful in diagnosis when obtained after a patient has undergone expansion or contraction of his extracellular fluid volume.
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PMID:Renin-aldosterone profiling in hypertension. 33 42

The recognition of secondary causes of hypertension, such as renovascular disease and aldosteronism, can be enhanced by stimulation and suppression of the 2 limbs of the renin angiotensin system. Normal values have been established in unstimulated and stimulated conditions. Saline infusion suppresses plasma aldosterone normally. Patients with proved adenomas do no suppress renin and are outside the well established ranges of normal suppression. Likewise, furosemide will stimulate renin release. Patients with proved aldosteronism are outside the normal ranges of plasma renin activity. These maneuvers also are useful in discriminating renovascular hypertension, particularly when achieving differential renal venous collections under stimulated conditions (after furosemide and tilting). By stressing this system (with furosemide stimulation or saline suppression) one can discriminate better secondary hypertension by the failure to respond normally.
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PMID:Evaluation of patients for secondary hypertension. 39 53

To test whether central neurogenic factors participate in blood pressure elevation in primary hypertension, we studied the concentrations of: norepinephrine, epinephrine and dopamine-beta-hydroxylase (DBH) in cerebrospinal fluid (CSF); and norepinephrine, epinephrine, DBH and plasma renin activity (PRA) in plasma of 22 subjects (seven with primary hypertension, 11 normotensive patients with non-systemic neurological disorders, and four with secondary hypertension). Plasma and CSF norepinephrine (NE) were increased in primary hypertensives compared to normotensives. Cerebrospinal fluid norepinephrine was related to diastolic blood pressure, and systolic blood pressure when normotensive and primary hypertensives were taken together. The CSF norepinephrine of primary hypertensive patients was correlated with natural log PRA. The CSF norepinephrine was correlated inversely with age in primary hypertensive patients but not in the normotensive subjects. The low CSF norepinephrine and epinephrine, despite markedly increased plasma NE and epinephrine, in two patients with pheochromocytoma, indicate a blood-brain barrier for these neurohormones. The observations support the view that the central sympathetic nervous system is involved in the pathogenesis of primary hypertension, particularly in younger patients.
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PMID:Raised cerebrospinal fluid norepinephrine in some patients with primary hypertension. 39 37

Racial differences in prevalence of essential hypertension are well known. In order to explore these differences at an early age in terms of etiology, we investigated schoolchildren in an entire, biracial community. A sample of 278 children, stratified by diastolic (fourth-phase) blood pressure and specific for age, race, and sex, was reexamined 1--2 yr after initial observation for the following: (1) a physical examination and urinalysis to exclude secondary hypertension; (2) 24-hr urine sodium, potassium, plasma renin activity, and serum dopamine beta-hydroxylase; (3) 1-hr oral glucose tolerance test; and (4) heart rate and blood pressure at rest and under standarized physical stress. We found that 24-hr urine sodium was positively associated with blood pressure level as measured on the same day for the high blood pressure strata of black children. Urine potassium excretion was lower in blacks than in whites, although their intakes seemed equal. In the high blood pressure strata especially, black boys had lower renin activity than whites, and the resting-supine and stressed systolic blood pressures were higher in black boys than in any other group. In these black boys, resting and stressed systolic pressures were negatively related to plasma renin activity. On the other hand, dopamine beta-hydroxylase levels in white children were higher than in blacks for all blood pressure strata, and in the high blood pressure strata white children had higher 1-hr glucose levels and faster resting heart rates than black children. Different mechanisms may play a role in and contribute to the early stage of essential hypertension.
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PMID:Racial differences of parameters associated with blood pressure levels in children--the Bogalusa heart study. 51 82

Succinamyl-arg-val-tyr-val-his-pro-phenylglycine acetate (succinamyl1-val5-phenylglycine acetate3-A II), an analogue of angiotensin II, has a pressor effect upon patients suffering from primary and secondary hypertension regardless of prevailing plasma renin concentration. It stimulates the release of aldosterone, whereas plasma renin concentration is not influenced. It is concluded, that this new analogue is, as far as its effect upon blood pressure and release of aldosterone in man is concerned, an agonist of angiotensin II.
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PMID:Effect of an angiotensin II analogue upon blood pressure, plasma renin concentration and plasma aldosterone in hypertensive patients. 58 19

An analytical study of the renin-angiotensin-aldosterone system was made in 124 individuals with essential hypertension, aged from 25 to 55 years. The results obtained, with rigorous control to posture and sodium balance, indicate the existence of a number of subgroups of hypertensive subjects related to their renin activity and plasma aldosterone in the upright position. This classification thus makes possible comparison with patients suffering from secondary hypertension.
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PMID:[The renin-angiotensin-aldosterone system in hypertensive subjects. I-Analytical study of 124 patients (author's transl)]. 91 87

Renal artery stenosis, either fibromuscular or atheromatous, is probably the most common cause of secondary hypertension in man. Both of these diseases are active, ongoing processes that may be ameliorated but not cured by medical or surgical treatment. The clinical history and examination of the patient with hypertension may help differentiate renovascular hypertension from essential hypertension. The presence of a systolic-diastolic or continuous bruit is often an indicator of severe renal artery stenosis. Systemic hypertension is the physiologic consequence of significant renal artery stenosis. Knowledge of the basic concepts of the renin-angiotensin-aldosterone system, as has evolved from experimental models of renovascular hypertension, forms the basis for understanding the process of evaluation and treatment of such patients. The treatment of choice for the patient with severe hypertension and a functionally significant renovascular lesion is surgical--both in terms of successful treatment of hypertension and improved long-term prognosis. Diligent periodic reevaluation of these patients as well as those with less severe hypertension who are receiving medical treatment enables the physician to select the proper management that offers optimal control of patient blood pressure and avoids target-organ damage to the kidneys, central nervous system, or cardiovascular system.
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PMID:Management of the patient with renovascular hypertension. 92 May 87

Mineralocorticoids are out of the causes of secondary hypertension. Excess production of mineralocorticoids induces sodium and fluid retention, loss of potassium and metabolic alcalosis. The diagnosis of mineralocorticoid syndromes depends on the interpretation of the functional status of the renin-mineralocorticoid-system, which is in part responsible for the maintenance of normal blood pressure. The classical representative of this group is the syndrome of primary aldosteronism. Causes of mineralocorticoid syndromes associated with hypertension are: 1. autonomous production of mineralo-corticoids by an adrenal adenoma or by idiopathic bilateral adrenal hyperplasia; 2. deficiency of adrenal 17-alpha-hydroxylase or of 11-beta-hydroxylase; 3. secondary aldosteronism associated with primary reninism, or renal arterial stenosis; and 4. pseudo aldosteronism due to excessive ingestion of licorice. Malign or essential hypertension may also often be followed by secondary aldosteronism.
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PMID:[Mineralocorticoid syndromes and hypertension]. 96 85

Angiotensin-converting enzyme (ACE) inhibitors are now widely used as first-line treatment of essential hypertension. Their effectiveness is potentiated by a low-salt diet and, above all, by the simultaneous prescription of diuretics. When secondary hypertension is suspected, ACE inhibitors are a good pharmacological tool to study the renin-angiotensin system. Since activation of this system is the main mechanism responsible for renovascular hypertension, ACE inhibitors are very useful for diagnosis. Conversely, blood pressure is not influenced by ACE inhibitors in primary hyperaldosteronism because of the low plasma renin and angiotensin II levels. Pheochromocytoma activates the renin-angiotensin system, and ACE inhibitors combined with beta-blockers enable the hypertension to be controlled prior to surgical treatment of the tumour. Finally, ACE inhibitors can be used to explore the renin-angiotensin system in the experimental model of renovascular hypertension and therefore contribute to our knowledge of the complex pathophysiology of this most frequent type of secondary hypertension.
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PMID:[Usefulness of converting enzyme inhibitors in the diagnosis of arterial hypertension]. 129 39

Although essential arterial hypertension is believed to have a strong genetic predisposition, the gene(s) responsible are unknown. The mechanisms underlying the regulation of blood pressure and experimental studies place the renin gene among the main candidate genes that need to be tested in humans. We tested the hypothesis of a linkage between the renin gene and essential hypertension using the affected sib pair method. Siblings (133 subjects, 52.1 +/- 10.9 years) from 57 families were selected for sustained hypertension (160.7 +/- 22.9/99.5 +/- 12.8 mmHg with 80% of patients under antihypertensive treatment), of early onset (40.7 +/- 12.0 years), in the absence of obesity, diabetes mellitus, and secondary hypertension. Eight renin haplotypes were generated from three diallelic renin restriction fragment length polymorphisms (RFLPs) (TaqI, HinfI, HindIII) located throughout the renin gene. The allelic concordance between the sib pairs was analyzed by identity by state relationships for 98 sib pairs (41 for 41 couples, 39 for 13 trios, 18 for 3 quartets). Allelic frequencies in the 57 hypertensive probands were similar to those observed among 102 hypertensive subjects studied previously. Six of eight possible haplotypes were observed, the informativity of the marker corresponded to 70% of heterozygosity. Allelic concordance for all sib pairs according to sibship size was not significantly different from that expected under the hypothesis of no linkage (t = 0.52, P = 0.15) reflecting only a small excess of renin alleles shared by the hypertensive sibs (1.44 +/- 0.6 vs 1.36 +/- 0.6). Likewise the linkage hypothesis was unsupported by weighted estimates to correct for possible bias due to large sibship size. Thus, the sib pair analysis suggests that the renin gene does not have a frequent role in the pathogenesis of essential hypertension; further more powerful linkage studies or other approaches will be needed to detect contributions at the renin locus to the heritability of essential hypertension.
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PMID:Sib pair linkage analysis of renin gene haplotypes in human essential hypertension. 134 86


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