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)

95 patients with essential uncomplicated hypertension were mostly submitted to measurement of plasma renin activity, plasma volume and exchangeable sodium. According to the results of the plasma renin activity, we noted variations in blood volume and exchangeable sodium in order to determine the best possible treatment based on these data. Single treatment, based either on diuretics or beta-blockaders was rarely sufficient to bring the blood pressure down to normal. Association of these two types of drug was often very useful. Finally, a critical study of these 3 parameters was made in an economic view of investigations of the blood pressure. The plasma volume seemed to us the most useful investigation, after which came the measurement of plasma renin activity. for the exchangeable sodium seemed of little interest.
Sem Hop 1977 May 23
PMID:[Measurement of plasma renin activity, blood volume and exchangeable sodium: an aid in the orientation of treatment of essential arterial hypertension]. 2 Jun 66

The concept of acute renal failure with anuria due to malignant nephro-angiosclerosis, is uncommon. We report two cases and compare them with others in the world literature. Knowledge of this disease entity is of triple interest: In diagnosis and classification in the field of acute vascular nephropathy with anuria. We cannot emphasise too much the interest of early renal biopsy after correction of abnormal blood pressure. In physiopathology, these malignant nephro-angioscleroses give rise to hypertension of pressor type with high renin levels. Finally therapeutic, for there exist drugs adapted to this type of hypertension. The association of acute renal failure and malignant nephro-angiosclerosis should be treated as an emergency, to avoid the passage to terminal and irreversible renal failure.
Sem Hop 1977 May 09
PMID:[Acute oligoanuric renal insufficiency in malignant nephroangiosclerosis]. 19 37

Primary hyperaldosteronism usually causes moderate hypertension. It is rare to note as in our two patients intermittent attacks of paroxysmal hypertension. The diagnosis of aldosteronism will be suspected on the finding of persistent hypokalemia with acidosis. It will be confirmed by laboratory examinations severe fall in plasma renin activity and rise in aldosterone in the adrenal veins. To determine the affected side, one may carry out adrenal phlebography which is a difficult technic, and/or a scan using iodine cholesterol which is benign and precise. Surgery with removal of the adenomatous hyperplasia in one case and of an adenoma in the other, gave one very good result.
Sem Hop 1978 Jan 09
PMID:[Primary hyperaldosteronism with paroxysmal arterial hypertension. Apropos of 2 operated cases]. 20 43

The authors report a case of horseshoe kidney responsible for hypertension through a one-sided renal dysplasia. The part of the renal malformation in the development of the hypertension is attested by the activities of renin from renal veins, by the isotopic nephrogram and by the disappearance of the hypertension following the heminephrectomy. The hypertension seems an exceptionnal complication of the horseshoe kidney, which can be surprising given the frequency of this malformation and associated urologic anomalies.
Sem Hop
PMID:[Horseshoe kidney and hypertension (author's transl)]. 21 4

After a minor abdominal traumatism, M. B., 53 years of age, presents a sudden and acute edematous syndrome. Cardiac, renal, hepatic, nutritional and thyroid etiologies ares rapidly eliminated. A cavography and lymphography reveal the integrity of the drainage pathways. The idiopatic cyclic edematous syndrome is therefore evoked by few clinical details (diurnal weight gain, diurnal oliguria...). Exploration of the renin - angiotensin - aldosterone system, the Landis test and the marked radioactive serum albumin test attest to the exaggeration of capillary permeability. Likewise, it was discovered in this patient, a Klinefelter syndrome which was, until now, unknown. This case poses interesting pathogenic problems since the idiopathic cyclic edematous syndrome is a predominantly feminine disease. Only a few cases were described in the masculine sex and, to our knowledge, this syndrome has never been associated with Klinefelter syndrome.
Sem Hop
PMID:[Idiopathic cyclic edema in Klinefelter syndrome (author's transl)]. 22 26

Polypeptides are endogenous agents, involved in the regulation of many physiologic functions and the pathogenesis of several diseases. Polypeptide antagonists form a group of new chemical entities which may provide valid therapeutic agents. Some polypeptides (angiotensin, kinins) are released through the action of proteolytic enzymes (renin, kallikreins) and act as hormones or autacoids; others (substance P, neurotensin) are synthetized by nervous cells to serve as neurotransmitters or neuromodulators. The main homeostatic role of the renin-angiotensin system is to uphold high systemic arterial blood pressure. Overproduction of renin and insufficient checking of renin secretion are among the most common causes of arterial hypertension. Several forms of arterial hypertension (neurovascular, idiopathic) benefit from a reduction in renin-angiotensin system activity. This is achieved either through decreasing renin secretion, by inhibiting conversion of angiotensin I into angiotensin II, or through blocking the peripheral actions (at the receptor sites) of angiotensin II. Renin secretion is very significantly reduced by beta-blocking agents (propranolol); conversion of angiotensin I into angiotensin II is inhibited by teprotide, captopril and their derivatives; peripheral actions of angiotensin II are blocked by saralasin. Bradykinin and related agents produce vasodilation, increase vascular permeability and stimulate pain fibers. Kinins thus reproduce the cardinal features of inflammation and are held to be mediators of the inflammatory reaction. The substance P neuropeptide is found in the brain and bowel; it may act as a transmitter of the sensation of pain at the spinal cord and central nervous system sites. Among other effects outside of the brain, substance P is a potent vasodilator and inhibits renin secretion. Neurotensin is a neuropeptide which produces hypothermia, muscular relaxation and analgesia. Outside of the brain, this peptide is involved in the regulation of gastric secretion, intestinal motility and insulin and glucagon secretion. The vasoactive intestinal peptide, found in certain cholinergic nerve endings, is a large peptide which inhibits gastric secretion, intestinal motility and vascular tone.
Sem Hop 1984 Mar 29
PMID:[Polypeptides and antagonists]. 620 6

29 patients were treated between 1972-77 for arterial hypertension; all patients were on OC (oral contraception). Careful investigation of these patients revealed that only in some had hypertension been caused by OC treatment, which goes against the commonly held opinion that arterial hypertension in OC patients is always caused by hormonal treatment. At least 3 conditions must be satisfied in order to incriminate the responsibility of OC in inducing hypertension: 1) normal blood pressure prior to OC treatment; 2) normalization of blood pressure within 3 months after discontinuation of OC use; and 3) no other etiology of hypertension. Arterial hypertension seems to be caused by the synthetic estrogen component of OCs; the mechanism of action is still not clear, although it has been demonstrated that it does stimulate the renin-angiotensin-aldosterone system.
Sem Hop
PMID:[Hypertension and oral contraceptive therapy (author's transl)]. 625 32

Three cases of post-renal contusion hypertension are reported. The treatment was conservative in the three cases, and we think it had no incidence on return to normal arterial pressure. There was a good correlation between arterial pressure and renal vein renin activity.
Sem Hop 1982 Jan 07
PMID:[Three cases of regressive hypertension after renal trauma. (author's transl)]. 627 44

Ten patients with primary hyperaldosteronism resulting from a functioning adrenocortical adenoma were studied. The high incidence of hypertension and/or renal disease in the families of these patients suggests that hereditary factors play a part in the genesis of aldosteronomas. In patients with hypertension and hypokalemia the diagnosis of primary hyperaldosteronism is established by measurements of serum renin activity and serum aldosterone concentrations under normal conditions and during pharmacodynamic tests. The adenoma is demonstrated by radioactive iodocholesterol scintigraphy and computerized tomography. In nearly two-thirds of the patients, unilateral adrenalectomy is followed by complete definitive recovery.
Sem Hop 1982 Jun 24
PMID:[A review of ten cases of aldosteronoma. Diagnostic and therapeutic conclusions (author's transl)]. 628 23

A new case of analbuminemia in a fifty-four-year-old French woman is described. The patient was admitted to a hospital cardiology department for thoracic pain. Consanguinity between the patient's parents was established. Proteins were studied both during the acute phase and the subsequent remission. Total serum protein concentrations were stable, around 5.3 g. Hypoalbuminemia was compensated initially by alpha-2-globulins and subsequently by beta globulins. Increases in serum cholesterol and serum beta lipoproteins were recorded. Hydroelectrolytic balance was normal. Orthostatic renin and aldosterone release was significantly increased, denoting response to lowered hydrostatic pressure. A minor increase in serum thyroxin was recorded, probably because of the increase in thyroxin binding globulin.
Sem Hop 1983 Jan 13
PMID:[Biological study of a case of analbuminemia]. 630 Oct 31


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