Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

One of the most common and serious side effects of diuretic therapy is in increased urinary loss of K. Another, although less well publicized, side effect of diuretic therapy is excessive urinary loss of Mg. In examining the effects of diuretics on Mg and K metabolism, the following factors should be taken into account: site of action and duration of action of diuretics, duration of treatment and dosage used, concurrent drug therapy, underlying disease conditions and dietary intake of Mg. Diuretics acting in the proximal tubule tend to have only minor effects on Mg excretion. Loop-blocking diuretics, however, cause major urinary losses of Mg. The Mg-wasting effects of loop-blocking diuretics have been demonstrated in large numbers of experimental and clinical studies, and the findings are consistent with micropuncture studies in laboratory animals which indicate the loop of Henle as the major site of Mg reabsorption. The effects of thiazide diuretics on Mg excretion are less well established than those of loop-blocking diuretics. Experimental studies demonstrate that thiazides have little or no direct effect on Mg transport in the nephron. However, some clinical studies indicate that thiazide treatment may induce Mg loss. This may be secondary to alterations in the renin-angiotensin-aldosterone system and in the calcium and parathyroid hormone and may be contributed to by concurrent drug treatment and the underlying disease conditions. K-sparing diuretics are usually administered concomitantly with more potent diuretics to counteract diuretic-induced K depletion. These agents act in the late distal tubule and collecting duct. Evidence has accumulated in recent years indicating that these drugs may also exert some Mg-sparing properties. Experimental and clinical investigations from our own laboratories and from other investigators will be reviewed. In animal studies, a dose-response relationship has been established for the actions of amiloride in reducing fractional excretion of Mg and K during furosemide-induced diuresis. The effects of amiloride on Mg excretion are less than those on K excretion, and this is compatible with the different handling of K and Mg in the distal tubule and collecting duct. The effects of aldosterone antagonists on Mg excretion are less well established than those of amiloride. Some recent studies indicate that converting-enzyme inhibitors may also influence Mg and K metabolism. The Mg-sparing actions of drugs may have important therapeutic implications.
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PMID:Magnesium and potassium-sparing diuretics. 354 14

The natural course of renal function in patients with cirrhosis and ascites but without azotemia is unclear. Therefore, a prospective evaluation of 23 non-azotemic cirrhotic patients with ascites was carried out over a three-year interval. Assessment included evaluation of serum electrolyte values, liver function tests, plasma renin levels, and parathyroid hormone levels. Renal function was determined by measurement of clearances of water and solute excretion, and simultaneous clearances of para-amino hippurate, inulin, and creatinine. The initial mean glomerular filtration rate was 66 ml/minute, serum creatinine level was 1.1 mg/dl, and blood urea nitrogen value was 13 mg/dl. The glomerular filtration rate showed marked variability among patients. On the basis of initial glomerular filtration rate, the patients were divided into three groups. Group I consisted of patients with supranormal filtration rates (mean 183 ml/minute), Group II constituted patients with normal filtration rates (mean 92 ml/minute), and Group III comprised patients with severely impaired filtration rates (mean 32 ml/minute). The serum creatinine level was below 1.5 mg/dl in all three groups. Serial measurement of renal function was performed in 18 patients over a mean of 310 days (range four to 1,176 days). Eighty-six percent of patients studied from Groups I and II maintained a normal or supranormal glomerular filtration rate over one year. However, most patients in Group III showed a progressive decline in filtration rate, despite no change in serum creatinine value. Sixty-seven percent of Group III patients died over a mean of one year. The mean 24-hour solute excretion among Group III patients was only 263 mOsm per day, significantly less than the control value of 874 mOsm per day in other hospitalized non-cirrhotic patients. The serum creatinine level frequently failed to rise above normal even when the glomerular filtration rate was very low (less than 25 ml/minute), and creatinine clearance overestimated inulin clearance by a factor of two in Group III patients. However, the creatinine index was an aid in determining true glomerular filtration rate and may be a useful clinical test in the evaluation of renal insufficiency in cirrhotic patients with normal serum creatinine values. Many patients with cirrhosis and ascites will have a glomerular filtration rate of less than 60 ml/minute but a normal serum creatinine level. These patients may constitute a previously unrecognized large group.
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PMID:Unpredictability of clinical evaluation of renal function in cirrhosis. Prospective study. 357 63

The effect of calcium supplementation on blood pressure was studied in three groups: eight normotensive subjects, 14 borderline essential hypertensive subjects, and 11 established essential hypertensive subjects (EEH). All subjects were outpatients and were given 6 g of calcium lactate (779 mg of elemental calcium) daily for 16 weeks. In EEH, systolic blood pressure was decreased significantly by 6 mmHg, but diastolic blood pressure was not decreased significantly (2 mmHg). In other groups, blood pressure was not reduced significantly. In all groups, urinary excretion of calcium was increased significantly but urinary excretion of other electrolytes, such as sodium, potassium and phosphate did not change. Serum electrolytes, various hormones, such as parathyroid hormone, 1-25(OH)2D3, 25OHD3, plasma renin activity, plasma aldosterone, plasma norepinephrine and epinephrine, and cardiac output did not change throughout this study. There were no adverse effects observed during this trial. From these results, it was concluded that daily administration of 6 g of calcium lactate produces a slight antihypertensive effect in EEH, and that this might be useful as a supplementary treatment for essential hypertension, especially in the aged.
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PMID:Effect of calcium supplementation on blood pressure in essential hypertensive subjects. 362 59

Calcium and magnesium metabolism was investigated in 10 hypertensive subjects with primary aldosteronism (seven adenomatous, three idiopathic). Serum levels of total calcium (9.03 +/- 0.2 mg/dl) and ionized calcium (2.06 +/- 0.06 meq/liter) were in the low-normal range, except for two patients who had levels of serum ionized calcium clearly above normal. Furthermore, both serum total (n = 6, p less than 0.01) and ionized calcium levels (n = 3) rose postoperatively in the patients who had an aldosterone-producing tumor removed. Dramatic elevations of parathyroid hormone levels (mean, 645 +/- 109 pgeq/liter; normal, less than 150 to 375 pgeq/liter) were seen in the majority of patients, including those two with frank ionized calcium elevations. Magnesium levels were within normal limits (2.07 +/- 0.07 meq/liter). These results indicate that parathyroid hypersecretion is a common feature of primary aldosteronism and also suggest a physiologic relationship between the activity of the renin-aldosterone system and parathyroid physiology. Sodium-volume expansion and negative calcium balance induced by aldosterone excess may predispose to hyperparathyroidism.
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PMID:Calcium metabolism and parathyroid function in primary aldosteronism. 388 68

Parathyroid hormone, thyrocalciotonin, testosterone, estradiol, aldosterone and renin activity of the blood plasma were radioimmunoassayed in 142 patients with neurological manifestations of lumbar osteochondritis. The blood levels of parathyroid hormone and, to a lesser degree, those of thyrocalciotonin were elevated. The levels depended on the severity and duration of the pain syndrome while thyrocalciotonin excretion depended on the degree of the degenerative dystrophic process in the spinal column. Prolonged pain syndrome was associated with an inhibited function of the gonads and the mineralocorticoid layer of the adrenals. A hypothesis is advanced, which explains the participation of the endocrine glands in the etiopathogenesis of lumbar osteochondritis and its neurological manifestations.
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PMID:[Role of various endocrine glands in the pathogenesis of the neurologic symptoms of lumbar osteochondrosis]. 389 Apr 27

The aging kidney suffers reduction both in mass and in glomerular filtration rate. These changes may be totally or partially due to atherosclerosis and hypertension, which reduce renal blood flow. Superimposed on these processes, and perhaps responsible for primary loss of renal mass irrespective of renal vascular disease, is glomerular damage and involution that is a consequence of adaptive increases in glomerular perfusion pressure that occurs as the number of nephrons decline with age. The data available at this time do not allow us to distinguish between these two potential mechanisms of renal senescence. The decline in GFR is in turn responsible for reduced renal acidification and the reduced renal clearance of drugs that are normally removed by the kidney. Certain renal functions, however, are depressed to a greater extent than is GFR. Both the ability to maximally dilute the urine and to maximally concentrate it are controlled by serum ADH concentrations and by the action of that hormone on the collecting duct. Aged rats do not maximally secrete ADH under conditions of dehydration and the effect of ADH on the kidney is also attenuated. Elderly humans also cannot maximally suppress ADH secretion when serum osmolality is reduced. Likewise, the renin-angiotensin-aldosterone axis is poorly responsive to volume depletion in aging subjects. As a result, elderly individuals cannot maximally retain sodium under conditions of plasma volume contraction out of proportion to reduction in GFR. The kidney is the site of vitamin D1 hydroxylation. Hydroxylation of vitamin D is reduced out of proportion to any reduction in GFR in the rat. There are no data as yet available on the effect of aging and the production of erythropoietin, a principal regulator of red blood cell mass. Neither are there data available on changes that might occur with advancing age in the ability of the aging kidney to metabolize various hormones, such as parathyroid hormone, glucagon, and insulin. The mechanisms and the full biochemical and physiologic consequences of renal senescence remain to be fully elucidated.
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PMID:The aging kidney. 391

Acute hypercalcemia in the conscious, unanesthetized rat, achieved by a 30-minute infusion of CaCl2 (serum calcium level, 12.8 +/- 0.6 mg/dl) resulted in significant elevation of mean arterial pressure (from 112 +/- 2 mm Hg to 129 +/- 3 mm Hg, p less than 0.001). This pressor response was associated with a significant increase in systemic vascular resistance, from 0.45 +/- 0.02 mm Hg/(ml/min)/kg body weight to 0.50 +/- 0.02 mm Hg/(ml/min)/kg body weight (p less than 0.05), but it caused no alteration in cardiac index. The pressor response to acute hypercalcemia does not appear to be mediated by vasopressor hormones or attenuated by vasodepressor hormones since inhibition of the renin-angiotensin system (nephrectomy), catecholamines (central and peripheral 6-hydroxydopamine), vasopressin (vascular antagonist), prostaglandins (indomethacin), and parathyroid hormone (parathyroidectomy) did not significantly alter the pressor response to infusion of CaCl2 in spite of similar serum calcium levels in all groups of animals. Rather, the pressor response to acute hypercalcemia seems to be mediated by a direct action of calcium ion on smooth muscle and perhaps myocardial cell contractility, since pretreatment with the calcium channel blockers verapamil or nifedipine blocked the pressor response to acute hypercalcemia.
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PMID:Mechanism of acute hypercalcemic hypertension in the conscious rat. 407 24

A case of pseudohypoparathyroidism (PHP) associated with several hormonal abnormalities in addition to parathyroid hormone (PTH) was reported. Several endocrinological examinations before and after treatment with 1 alpha-OH-D3 revealed abnormal thyroid stimulating hormone and prolactin responses to thyrotropin releasing hormone, abnormal plasma renin activity responses to renin stimulation test, and abnormal calcitonin responses to calcium infusion test. These abnormalities were not corrected when serum calcium levels returned to normal after therapy. From these results, it was suggested that in PHP resistance to multiple hormones that worked by stimulating adenylate cyclase might be the cause of these hormonal abnormalities, irrespective of serum calcium levels.
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PMID:A case of pseudohypoparathyroidism (PHP) associated with multiple hormonal abnormalities. 609 49

Through these actions on K+ balance, thiazide diuretics modify multiple endocrine systems. Potassium depletion likely contributes directly to disorders of carbohydrate metabolism, the renin-angiotensin-aldosterone axis, prostaglandin metabolism, and parathyroid hormone function. Besides these direct adverse effects on endocrine function, these disturbances likely contribute directly to the emergence of additional cardiovascular signs in subjects receiving long-term diuretic therapy.
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PMID:The impact of diuretics on potassium and glucose. 620 15

The levels of several hormones (ACTH, GH, TSH, FSH, LH, parathyroid hormone--PTH, insulin, thyroxine--T4, triiodothyronine--T3, cortisol, testosterone, aldosterone, renin), catecholamines (epinephrine, norepinephrine, dopamin), prostaglandins (F1 alpha, F2 alpha, A + E), electrolytes (Na, K, Ca, Mg), cAMP and glucose in blood were measured before and immediately after the examination in 15 male students aged 28 to 35 years. Simultaneously the blood pressure was measured and hemodynamic measures were registered with the aid of echocardiography. A remarkable increase of catecholamines, ACTH, renin, T3, PTH, cAMP, PG F1 alpha, PG F2 alpha and Ca was found before the examination together with the increase of blood pressure. After the examination the levels of catecholamines, renin, aldosterone, T3, PTH, GH, FSH, LH, testosterone, PG A + E, glucose and Ca were found to be increased, while these of insulin, Na, PG F1 alpha, PG F2 alpha were decreased. The decrease of blood pressure was also found.
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PMID:Changes of blood levels of several hormones, catecholamines, prostaglandins, electrolytes and cAMP in man during emotional stress. 624 18


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