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)

We studied the effect of angiotensin II analogue (AII-A) and angiotensin I converting enzyme inhibitor (SQ 14,225) on blood pressure and the renin-angiotensin-aldosterone system in a patient with pseudo-Bartter's syndrome, who was a 26-year-old unmarried Japanese woman taking furosemide surreptitiously. The intravenous infusion of AII-A decreased blood pressure from 85/35 to 68/28 mmHg. This decrease in blood pressure was associated with an increment of plasma renin activity (PRA) and a decrement of plasma aldosterone concentration (PAC). Similarly, SQ 14,225 given orally decreased blood pressure to the same extent. An increment of PRA and a decrement of PAC were also observed. These results suggest that the renin-angiotensin system plays a considerable role in maintaining blood pressure in pseudo-Bartter's syndrome. Again, attention has to be paid to the possibility of surreptitious use of diuretics in an adult patient with persistent hypokalemic alkalosis, hyperactivity of the renin-angiotensin-aldosterone system and angiotensin II insensitivity simulating "true" Bartter's syndrome.
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PMID:Hypotensive response to angiotensin II analogue and angiotensin I converting enzyme inhibitor in pseudo-Bartter's syndrome. 627 3

A 24-yr-old woman with hypertension, hypokalemic alkalosis, low plasma renin and hypoaldosteronism was studied. Plasma aldosterone, renin and potassium returned to normal and blood pressure fell after sodium restriction or the administration of triamterene. Thiazide therapy also normalized her blood pressure while dexamethasone, spironolactone and furosemide did not improve her symptoms. Plasma aldosterone levels were low and responded poorly to a short term ACTH injection, but responded well to the maximal adrenal stimulation by ACTH-Z. Plasma levels of cortisol, corticosterone and deoxycorticosterone were within the normal range. Adrenal scintigram with 131I-adosterol and abdominal computed axial tomography did not reveal the presence of a sizeable adrenal tumor. In addition, the urinary kallikrein excretion was low after sodium restriction and showed no response to saline infusion. These findings suggest that the excessive secretion of unusual mineralocorticoids may not exist in this case. From these observations and the results of the therapeutic responses to the diuretic agents, we conclude that the primary cause of the disorder of this patient seems to be a renal defect in the distal tubule in handling sodium and potassium which is similar to that in Liddle's syndrome.
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PMID:Hypertension, hypokalemia and hypoaldosteronism with suppressed renin: a clinical study of a patient with Liddle's syndrome. 627 44

The principal side effects of the drug carbenoxolone (Biogastrone; 18 beta-glycyrrhetinic acid sodium hemisuccinate) are sodium retention, hypokalemic alkalosis, suppressed plasma renin, and hypertension. In previous animal studies, carbenoxolone appeared not to have intrinsic mineralocorticoid activity but, rather, to enhance aldosterone action by displacing it from nonspecific binding sites. We here report studies showing that carbenoxolone has demonstrable affinity for rat kidney mineralocorticoid receptors, intrinsic mineralocorticoid activity in the adrenalectomized rat at doses consistent with its receptor affinity, and, in addition, a powerful action of amplifying the electrolyte effects of near-maximal doses of aldosterone.
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PMID:The mechanism of mineralocorticoid action of carbenoxolone. 629 Jan 95

This is the first autopsy case of male 17 alpha-hydroxylase deficiency with malignant hypertension. The subject had hypertension, hypokalemic alkalosis, and pseudohermaphroditism. At age 21, 17 alpha-hydroxylase deficiency was diagnosed by low urinary excretion of 17-hydroxysteroids, low secretion rate of cortisol, and low plasma testosterone level in association with high urinary excretion of pregnanediol and high plasma progesterone and corticosterone. Urinary excretion of aldosterone and PRA were suppressed, and plasma ACTH was elevated. Hypertension and hypokalemic alkalosis were normalized with dexamethasone therapy. After missing 5 yr of follow-up, malignant hypertension developed, and PRA and aldosterone were elevated. Histological examination revealed some characteristic arteriolar lesions as in malignant nephrosclerosis. Juxtaglomerular hyperplasia and an increase of renin granules were observed, which reflected high PRA. Abnormal histological findings of endocrine organs were observed in the breast, the pituitary gland, the adrenal glands, and the testis.
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PMID:An autopsy case of 17 alpha-hydroxylase deficiency with malignant hypertension. 630 Jan 76

The effects of 2 potassium-retaining diuretics on arterial pressure, intravascular volume, responses of the renin-angiotensin-aldosterone system, serum electrolytes, and renal function were compared by means of an 8-wk double-blind, crossover trial in 13 patients with "volume-dependent" essential hypertension. The fall in systolic, diastolic, and mean arterial pressures in the supine and erect positions (all p less than 0.005) induced by spironolactone was greater than that by triamterene. The pressure fall induced by spironolactone was also associated with a persistent contraction in plasma volume (p less than 0.05) and a secondary hyperaldosteronism that was not accompanied by hypokalemic alkalosis. The pressure fall induced by triamterene was not associated with reduced plasma volume, effect on plasma renin activity, or aldosterone excretion. Both drugs produced significant rises in blood urea nitrogen and creatinine levels that never exceeded normal limits.
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PMID:Spironolactone and triamterene in volume-dependent essential hypertension. 698 54

The effect of magnesium treatment on serum potassium and potassium balance was examined in three siblings with a recently described syndrome of hypokalemic alkalosis with renal tubulopathy. Oral magnesium supplementation for 11 days in the three siblings increased mean serum potassium from 2.7 +/- 0.1 meq/liter to 3.3 +/- 0.2 meq/liter (p less than 0.05). In addition, urinary and fecal potassium excretion decreased by about 11 meq/day. Magnesium chloride did not affect plasma renin activity while the patients were supine or upright. In contrast, mean supine plasma aldosterone concentration increased from 5.3 +/- 1.5 ng/dl to 13.2 +/- 4.1 ng/dl (p greater than 0.1) and mean upright plasma aldosterone concentration increased from 17.4 +/- 3.8 ng/dl to 66.1 +/- 7.3 ng/dl (p less than 0.01). These findings suggest that hypokalemia and potassium loss in this disorder may be caused by abnormal magnesium metabolism. The increase in plasma aldosterone concentration may have been caused by the positive potassium balance or a direct effect of magnesium on aldosterone secretion from the adrenal gland.
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PMID:Correction of hypokalemia by magnesium repletion in familial hypokalemic alkalosis with tubulopathy. 702 24

A 34-year-old female complaining of numbness and weakness of the extremities was examined. Consanguineous marriage was contracted between mother and father. She was of short stature (149 cm), and her blood pressure was normal (118/60 mmHg). Her serum potassium concentration had decreased to a level between 2.5 and 3.2 mEq/L, and hypokalemic alkalosis was present. Potassium clearance had increased and urinary concentrating capacity was impaired. Plasma renin activity was high at 25 ng/ml/hr but plasma aldosterone concentration was normal. Hypertensive response to angiotensin II (50 ng/kg/min) was weak but improved to nearly the normal value after the administration of indomethacin for 17 days at a dose of 50 mg/day. A slight elevation in blood pressure was observed during the infusion of norepinephrine (250 ng/kg/min). A decrease in blood pressure was observed during the infusion of 1-sarcosine, 8-isoleucine angiotensin II (600 ng/kg/min) with concomitant increase of plasma renin activity. Twenty-four hour urinary excretion of prostaglandin E decreased somewhat (225 approximately 252 ng/day), and hyperplasia of the juxtaglomerular cells and increased JG index were demonstrated in the biopsy specimens of the right kidney. From the findings, the present case were diagnosed as Bartter's syndrome. Although mild enlargement of the sella turcica was found in skull x-ray films, no abnormalities in pituitary function were demonstrated. Other unusual complications, i.e. hyperlipidemia (type II, beta-dominant) and abnormal configuration of peripheral erythrocytes, were demonstrated. Phospholipid composition of the erythrocyte membrane was normal. The fluidity of plasma VLDL examined by electron spin resonance was increased. Hypokalemia and hyperreninemia were improved through the administration of indomethacin. However, because of headache as an adverse effect, further administration could not be accepted. The patient's complaints were resolved by the rectal application of indomethacin with oral administrations of spironolactone and triamterene. Changes in serum lipid levels did not occur with the above mentioned treatment. alpha-tocopheryl nicotinate lowered the levels of serum lipids and normalized the configuration of peripheral erythrocytes. But increased fluidity of plasma VLDL remained, and phospholipid composition of erythrocyte membrane was also unchanged. The relationship between the rare complications mentioned above and the pathophysiology of Bartter's syndrome is still obscure.
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PMID:[A case with Bartter's syndrome associated with type II hyperlipidemia, increased fluidity of plasma VLDL and abnormal configuration of peripheral erythrocytes (author's transl)]. 704 42

Studies on the electrolyte metabolism and the renin-angiotensin-aldosterone system were made in a 47-year-old female patient with factitious Bartter's syndrome induced by surreptitious use of furosemide. The diagnosis was confirmed later by detection of the diuretic in the urine. In metabolic studies patient exhibited abnormalities similar to those reported in Bartter's syndrome; viz, hypokalemic alkalosis, blunted response to exogenous angiotensin II, which reverted to normal by volume expansion with an albumin solution, and diminished fractional free water clearance per fractional distal sodium delivery. The above data, along with the known pharmacological effects of furosemide, suggest that the abnormality in Na+ or Cl- reabsorption in the ascending limb of Henle's loop is a primary cause of Bartter's syndrome.
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PMID:Factitious Bartter's syndrome induced by surreptitious intake of furosemide. 718 84

We had a 20-year-old male patient of secondary aldosteronism similar to Bartter's syndrome, which had proved to be evident after the remission of nephrotic syndrome. In the patient, hypokalemic alkalosis and hyperreninemic hyperaldosteronemia were observed, although the blood pressure was normal. Hyperplasia of juxtaglomerular cells was observed and no abnormalities indicating either glomerulonephritis or renal artery stenosis were found; the pressor response to intravenously infused angiotensin (ang) II was markedly decreased; urinary prostaglandin (PG) E2, kallikrein and kinin excretion were elevated. The inhibition of PG synthesis with indomethacin decreased renal PG production and partially corrected both hypokalemia and pressor responsiveness to ang II. Thus, this case is considered to be a case of Bartter's syndrome. Contrary to the previously reported observations, the effective fractional chloride reabsorption rate in the renal distal tubules was normal (> 80%) and not changed by PG inhibition. Plasma atrial natriuretic peptide level was normal. An interaction between renin-angiotensin and PG systems appears to play a prior role in this case. To explain the pathophysiology, we have hypothesized an abnormal function of ang II receptor signal transduction which excessively stimulates PLA2, resulting in overproduction of PG synthesis in tissues.
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PMID:A case of secondary aldosteronism similar to Bartter's syndrome with no abnormality in renal chloride reabsorption. 769 92

In a 56-year-old normotensive white male subject with a 12-year history of hypokalemic alkalosis, hyperreninemia, and aldosteronism, the diagnosis of Bartter's syndrome was established on the basis of an impaired maximal renal diluting capacity and decreased distal fractional chloride absorption [CH2O/(CH2O+CCl)]. Negative urine analysis for diuretics suggested that this renal tubular defect was not secondary to diuretic (ab)use. In this normotensive patient with hyperreninemia and secondary aldosteronism, significant cardiovascular remodeling could be observed. Thus, in spite of normal arterial blood pressure and normal left ventricular systolic function (ejection fraction > 70%), impaired left ventricular diastolic function was observed using pulsed-wave Doppler echocardiography. Moreover, duplex analysis of the common carotid artery revealed significant intima-media hypertrophy with an average intima-media diameter of 0.9 mm (normal < or = 0.6 mm). Also, forearm venous occlusion plethysmography revealed an abnormally high minimal forearm vascular resistance following a 10-min period of forearm ischemia handgrip exercise suggesting remodeling within the peripheral arterioles. Thus, in a patient with Bartter's syndrome and activated neurohormonal systems such as the renin-angiotensin system, cardiac and vascular remodeling can be observed in the absence of hypertension. In analogy to the results of experimental studies showing that angiotensin II and noradrenaline act as growth factors on cardiac and vascular cells, cardiovascular remodeling present in our patient with Bartter's syndrome may be explained by increased activity of angiotensin II and/or noradrenaline.
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PMID:Evidence for cardiovascular remodeling in a patient with Bartter's syndrome. 789 15


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