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)

A 26-year-old female with Bartter's syndrome associated with Graves' disease is reported. This patient had a history of Graves' disease from the age of 22 and anti-thyroid drug (Methimazole) had been administered for 2 years. Thyroid function returned to normal but general fatigue and polyuria continued. Hypokalemia was diagnosed at 25 years of age and she was referred to our hospital for evaluation. Blood pressure was normal and laboratory data revealed normal thyroid function, hypokalemic alkalosis, high plasma renin activity and high plasma aldosterone concentration. She showed normal pressor sensitivity to norepinephrine infusion, grossly diminished pressor sensitivity to exogenous angiotensin II infusion compared with the normal. A renal biopsy specimen showed juxtaglomerular cell hyperplasia. Electron microscopy confirmed lacis cell (agranular cell) proliferation.
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PMID:Bartter's syndrome--case report. 15 51

The pathogenesis of the increased operative risk in elderly patients is unknown. From a theoretical point of view, a change in endocrine-metabolic response might be involved. In the present study, a battery of hormonal and metabolic variables were measured in eight young and eight elderly healthy males undergoing elective inguinal hernial repair under general anesthesia. Blood was drawn before induction of anesthesia, at skin incision, and one, two, and six hours after skin incision. The findings were: 1) Plasma cortisol increase was significantly higher in elderly than in young controls. 2) Plasma renin level was lower in old age, but renin-aldosterone and electrolyte response patterns were alike in the two groups. 3) Thyroid parameters, in terms of serum T4, serum T3, serum rT3, and T3-resin uptake, responded normally to surgery and showed no age-related differences. 4) The hyperglycemic response was not significantly influenced by age indicating unchanged glycoregulatory mechanisms also verified by determinations of plasma catecholamines, cAMP, and insulin. 5) Blood lymphocyte count was constantly lower in elderly than in young and decreased with time, but the age-related difference was not significant. 6) Blood polymorphonuclear leukocytes showed an increase of the same magnitude in both age groups, although at a significantly slower rate in the elderly. It is concluded that age affects some aspects of the initial endocrine-metabolic response to surgery.
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PMID:Influence of age on the endocrine-metabolic response to surgery. 51 78

The effect of thyroid hormone on renin productiona and release by rat kidney slices was studied. Rat kidney slices were incubated in Warburg flasks containing Krebs-Ringer-Phosphate- Glucose- Dextran solution at 37 C for 5 hours. Renin content, renin released into the incubation media and oxygen consumption were measured. Kidney slices actively secreted renin. Kidney slices of hyperthyroid rats released more renin, and kidney slices of hypothyroid rats released less renin than normal kidneys (p less than 0.001). The addition of 1-thyroxine to the incubation medium increased significantly (p less than 0.001) renin release by kidney slices from normal and hypothyroid rats. Thyroid hormone affects renin release through a mechanism independent of the ouabain-sensitive sodium pump and protein synthesis, since ouabain and cycloheximide did not modify renin release or production. The results of this study suggest that thyroid hormone plays a role in renin release from the juxtaglomerular cells.
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PMID:The effect of thyroid hormone on renin production and release by rat kidney slices. 61 72

By studying the metabolic values of a nondiabetic and diabetic uremic population we demonstrated the following: 1. Insulin is higher in diabetic than nondiabetic uremic patients. A slight arteriovenous difference across the dialyzer membrane suggests that insulin is dialyzable in small amounts in man. 2. C-peptides are highest in nondiabetics, lower in maturity onset diabetics, and lowest in juvenile diabetics. 3. Growth hormone is higher in diabetics than nondiabetics, decreased in both groups during hemodialysis, and returns to pre-dialysis levels 2 hrs after the completion of dialysis treatment. 4. Plasma triglycerides are elevated in both popualtions during the fasting state anddrop during hemodialysis, rising slowly towards the end of hemodialysis. 5. The majority of diabetics on hemodialysis have low renin levels and do not respond to volume reduction. In the high renin diabetics and high and low renin nondiabetics the plasma renin levels rise in response to volume reduction during hemodialysis. Renin is not dialyzable in man. 6. Thyroid function tests show that diabetic and nondiabetic patients have measurements in the low normal range. Our results reveal significant information concerning metabolic changes which take place in diabetic and nondiabetic uremic patients on hemodialysis and helps to characterize these populations. This report may have implications in better understanding the nature of the problems encountered in these populations and in their management (Table III).
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PMID:Metabolic changes in diabetic uremic patients on hemodialysis. 95 59

A 62-year-old man with pneumonia and left flank pain had a clinical syndrome of hyponatremia, hypotension, dehydration, and high urinary sodium excretion in the presence of a normal glomerular filtration rate. The plasma level of antidiuretic hormone was relatively high despite decreased serum osmolality. Thyroid function and excretion of glucocorticoid and sex steroids were normal. The serum aldosterone level was very low despite elevated plasma renin activity. Angiotensin II failed to stimulate any secretion of aldosterone, despite the occurrence of a progressive rise in blood pressure. On the other hand, rapid ACTH administration increased both serum aldosterone and cortisol. The patient showed no effective response to increased salt intake, but large doses of mineralocorticoid resulted in a normal serum sodium level without dehydration. Subsequently, he suffered cardiac arrest secondary to ventricular tachycardia. Postmortem examination showed well differentiated adenocarcinoma in the left pleura and an intact, histologically normal adrenal zona glomerulosa and kidney. This is the first reported case of a critically ill patient with hyponatremia caused by hyperreninemic hypoaldosteronism possibly due to angiotensin II insensitivity and tubular unresponsiveness to mineralocorticoid.
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PMID:Hyponatremia and hyperreninemic hypoaldosteronism in a critically ill patient: combination of insensitivity to angiotensin II and tubular unresponsiveness to mineralocorticoid. 217 79

The effect of thyroxine (T4) replacement on the increased renal beta-adrenergic receptor number and the increased beta-adrenergic dipsogenic responsiveness of fasted rats was studied in male Sprague-Dawley rats. Food deprivation significantly decreased serum thyroxine (T4) and triiodothyronine (T3) levels, increased the dipsogenic response to isoproterenol, and elevated renal beta-adrenergic receptor concentration. Daily administration of T4 (40 micrograms/kg) to food-deprived rats restored serum thyroid levels to normal. Thyroxine replacement also reduced the increased beta-adrenergic dipsogenic responsiveness in the food-deprived rats to control levels. In addition, daily administration of thyroxine reduced the beta-adrenergic receptor concentration in renal cortices to that observed in controls. Thyroid treatment tended to decrease the isoproterenol-induced renin release in food-deprived rats and increase the response in the control rats. These results suggest that the relative hypothyroid state observed in the food-deprived rat may be responsible for the increased concentration of renal beta-receptors and the associated activation of the renin-angiotensin system, which may be partially responsible for the observed increased dipsogenic response induced by isoproterenol. Collectively, the data reaffirm the interaction of thyroid hormone and beta-adrenergic responsiveness, although it is of interest that, in regard to renal beta-receptors, the concentrations are decreased to normal by thyroid treatment, whereas previous studies in hypothyroid rats demonstrate an increase to normal of cardiac beta-receptors. This would suggest thyroid hormone may normalize a response in an opposite direction depending on the direction of the disturbance.
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PMID:Thyroxine, renal beta-adrenergic receptors, and dipsogenesis in food-deprived rats. 282 30

Continuous ambulatory peritoneal dialysis for end-stage renal failure was first described in 1976. The purpose of the present study was to establish the value of this method in a group of eight patients with various renal diseases who were controlled monthly for one year. Main benefit was correction of anemia, better control of calcium and phosphate, and excellent blood pressure control. Hyperlipoproteinemia was observed in all patients, as was an increase in plasma renin activity and aldosterone. Thyroid values were in the low normal range. A low incidence of peritonitis was observed and cases of peritonitis were treated on an ambulatory basis. The results suggest that more patients could be included in this new treatment for end-stage renal disease.
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PMID:[Chronic ambulatory peritoneal dialysis]. 702 96

Thyroid dysfunction produces marked cardiovascular responses; the renin-angiotensin system (RAS) is important in control of the cardiovascular system. We have measured changes in the plasma RAS and in angiotensin II (AT) receptors in experimentally hyperthyroid, euthyroid, or hypothyroid rats. Hyperthyroidism activated the plasma RAS, increasing plasma angiotensinogen by 85% after 7-day triiodothyronine (T3) treatment, plasma renin activity (PRA) by 47% and concentration by 52%, and plasma AT by 1.250%. Hypothyroidism reduced plasma angiotensinogen by 71%, PRA by 73%, and plasma AT by 81% without altering plasma renin concentration (PRC). Plasma aldosterone was reduced by 39% in hyperthyroid rats and by 95% in hypothyroid rats. AT receptors were characterized in heart, liver, adrenal gland, and kidney. Cardiac, liver, and kidney AT receptor densities increased in hyperthyroidism by 73, 113, and 75%, respectively; adrenal gland receptor density decreased by 39%. Similar results were observed in hypothyroidism except that adrenal gland receptor density was markedly increased by 205%. AT receptor subtypes were characterized in ventricular homogenates by the selective antagonist losartan. Hyperthyroidism markedly increased AT2-subtype density by 204% in left ventricle, and by 304% in right ventricle and decreased AT1-subtype density by 38% and 31% in left and right ventricles, respectively. AT2-subtype density increased by 168% in hypothyroid rats; AT1-subtype density was unchanged. Thyroid dysfunction causes significant changes in the RAS and in AT receptor density, especially of the AT2 subtype. Although a physiological function has not yet been reported for AT2 receptors, our results suggest that selective AT2-receptor antagonists may prove therapeutically useful in treatment of cardiovascular disease in thyroid dysfunction.
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PMID:Renin-angiotensin system in thyroid dysfunction in rats. 750 37

The endocrine response to stress is complex. Elevations in the serum concentrations of the "classic" stress hormones, epinephrine and cortisol, occur following many kinds of physiologic challenge and are accompanied by elevations in corticotropin, GH, and glucagon levels. These changes are probably responsible for the hyperglycemia and hypercatabolism common to most critical illness. If volume depletion is present, vasopressin, renin, and aldosterone secretion are also likely to be stimulated. These hormones, if present in excess, may produce fluid retention and hyponatremia. In some critically ill patients, there is a dissociation of renin and aldosterone production called hyperreninemic hypoaldosteronism, but the clinical importance of this syndrome is poorly understood. Thyroid hormone metabolism is commonly affected by critical illness, which results in characteristic abnormalities of thyroid function testing known as the euthyroid sick syndrome. The reproductive axis is exquisitely sensitive to physiologic stress; hypogonadotropic hypogonadism is a common finding in critical illness. The ongoing challenge to the clinician is to determine whether seemingly abnormal hormone measurements in critically ill patients reflect an appropriate homeostatic response to severe illness or, instead, whether they denote an independent metabolic disorder that might actually cause or contribute to the patient's unstable condition. In view of the exceedingly complex (and poorly understood) interactions involved in the human response to a severe illness, a thoughtful approach to the whole patient is essential and far preferable to indiscriminate hormone testing. Such testing, at best, may be uninterpretable in light of the clinical circumstances or, at worst, may lead to therapeutic misadventures.
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PMID:The endocrine response to critical illness. 780 93

We examined a Turkish kindred with a unique form of autosomal dominant hypertension that cosegregates 100% with brachydactyly and maps to chromosome 12p. Affected adults were 10 to 15 cm shorter than unaffected people; however, their body mass index (27 kg/m2) was not different. Blood pressure increased steeply with age in the affected people so that by age 40 years, they had a mean blood pressure of 140 mm Hg, compared with 92 mm Hg in unaffected individuals. Complete clinical, roentgenographic, and laboratory evaluation was performed in 6 subjects, including 24-hour blood pressure measurements and humoral determinations before and after volume expansion with 2 L normal saline over 4 hours followed by volume contraction on the following day with a 20-mmol sodium diet and 40 mg furosemide at 8 AM, noon, and 4 PM. Two affected men aged 46 and 31 years; 3 affected women aged 40, 31, and 30 years; and 1 unaffected man aged 29 years were studied. Systolic pressures ranged from 170 to 250 mm Hg, and diastolic pressures ranged from 100 to 150 mm Hg in affected people; the unaffected man had a blood pressure of 120/70 mm Hg. Thyroid, adrenal, and renal functions were normal; electrolyte and acid-base statuses were normal. Calcium and phosphate homeostasis was normal. Day-night circadian blood pressure rhythm was preserved. The subjects were not salt sensitive; renin, aldosterone, and catecholamine values reacted appropriately to volume expansion and contraction. Affected people had mild cardiac hypertrophy and increased radial artery wall thickness. Fibroblasts from affected people grew more rapidly in culture than from unaffected people. We conclude that this novel form of inherited hypertension resembles essential hypertension.
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PMID:Autosomal dominant hypertension and brachydactyly in a Turkish kindred resembles essential hypertension. 895 1


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