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)

Glomeruli contain receptors for many hormones. Binding of angiotensin II (ANG II) or antidiuretic hormone (ADH) to glomerular mesangial cells elicits a contractile response. Other hormones induce synthesis of cyclic nucleotides (cAMP, cGMP). Glomeruli also synthesize several prostaglandins, renin, and ANG II. Micropuncture studies in Munich-Wistar rats have examined the effects of vasoactive drugs and hormones on the filtration process. Several vasodilators increase renal plasma flow in the dog and rat, but GFR remains relatively unchanged due to an offsetting fall in the ultrafiltration coefficient (Kf). Vasoconstrictor substances such as ANG II and norepinephrine cause declines in renal plasma flow and Kf, but GFR remains constant due to an increase in the transcapillary hydraulic pressure gradient. Antidiuretic peptides and parathyroid hormone also reduce Kf. Glomerular mesangial cells may regulate Kf by contracting and reducing glomerular capillary surface area. ANG II and ADH directly stimulate mesangial cell contraction in vitro. Other hormones appear to cause contraction by inducing local ANG II synthesis. These hormonal pathways are implicated in the pathogenesis of altered glomerular function in diverse forms of renal injury.
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PMID:Hormonal modulation of glomerular function. 629 13

Plasma adrenocorticotrophin (ACTH), cortisol and aldosterone increased during and after iv administration of calcium gluconate in 4 normal subjects, one patient with hypoparathyroidism and one patient with hypothyroidism. On the other hand, there was a decrease in plasma renin activity but only in the normal subjects. Plasma ACTH and cortisol responses to calcium were abolished whereas plasma aldosterone response persisted in 2 normal subjects pre-treated with dexamethasone. The results observed after calcium administration were compared to those observed after infusion of the solvent only in 6 normal subjects and 4 thyroidectomized patients who were studied twice at 3 day intervals. Plasma ACTH, cortisol and aldosterone were higher when calcium was administered. Plasma renin activity was not statistically different whether or not calcium had been injected in the subjects studied twice. These results demonstrate a direct effect of calcium on ACTH and aldosterone secretion which is not mediated by calcitonin and parathyroid hormone. The stimulatory effect of calcium on cortisol secretion depends on the increase in plasma ACTH.
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PMID:Effects of an acute calcium load on plasma ACTH, cortisol, aldosterone and renin activity in man. 632 May 69

A 53-year-old man with retinitis pigmentosa, who had two years' complaints of general malaise and muscle weakness, noticed occasional attacks of the cramps of the lower legs about three months prior to admission. At that time, hypocalcemia (7.6 mg/dl) and hyperphosphatemia (5.2 mg/dl) were pointed out. On admission, serum potassium was high-normal or high (4.4 - 4.9 mEq/l). Endocrinological studies revealed the findings of pseudohypoparathyroidism (PHP) type II, including a normal urinary cyclic AMP but blunted phosphaturic response to synthetic human parathyroid hormone (PTH), a high level of serum amino-terminal fragment of PTH with a low level of serum calcium and its ionized form, and a high-normal level of nephrogenous cyclic AMP. This patient also had selective hypoaldosteronism, as shown by intermittent hyperkalemia, low plasma and urinary levels of aldosterone and normal glucocorticoid levels. Plasma renin activity was normal but responded to a greater extent to furosemide plus upright posture. Plasma aldosterone was low and responded poorly to furosemide plus upright posture and graded angiotensin II infusions. The possible explanations for the association of PHP type II and selective hypoaldosteronism in this patient with retinitis pigmentosa are discussed.
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PMID:Pseudohypoparathyroidism (PHP) type II and selective hypoaldosteronism in a patient with retinitis pigmentosa. 632 73

A wide variety of pharmacologic agents have been implicated in a number of electrolyte disorders. The present review focuses on abnormalities of sodium, potassium, calcium, magnesium, and phosphate. Several mechanisms are involved in the pathogenesis of these disorders. These involve stimulation and modulation of other hormones (e.g., antidiuretic hormone, renin-angiotensin system, parathyroid hormone), damage to renal tubules, and, in some cases, a combination of factors. Recognition of these abnormalities is important because their presence may be life threatening or may aggravate the side effects of the drug itself.
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PMID:Drug-induced electrolyte disorders. 634 Oct 28

The ability of parathyroid hormone (PTH) to increase renin secretion was investigated in pentobarbital-anesthetized dogs. An intravenous infusion of bovine PTH 1-34, at the dose of 0.028 microgram/kg-1 min-1 increased renin secretion by 149% (501 +/- 105 to 1249 +/- 309 ng hr-1 min-1); renin secretion returned to control values during the recovery period. In order to determine whether PTH acted directly on the kidney to increase renin secretion, PTH was infused into the right renal artery at doses of 0.0014 to 0.0028 microgram/kg-1 min-1 and renin secretion from the right kidney was compared to that from the left (control) kidney. Renin secretion from the right (PTH-infused) kidney was not greater than control values for that kidney or different from the renin secretory rate of the left (control) kidney. In contrast, the excretion rates of both phosphate and sodium from the right kidney were greater than control values and from the excretion rates of the left kidney. These data suggest that PTH, while acting directly on the kidney to increase phosphate and sodium excretion, does not elevate renin secretion by a direct renal action.
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PMID:Effect of parathyroid hormone on renin secretion. 634

Two patients with both primary hyperparathyroidism and primary hyperaldosteronism are described. Each presented with high blood pressure and a history of renal calculi. Mild hypercalcaemia was associated with raised plasma parathyroid hormone concentrations and a parathyroid adenoma was excised from each. Both patients also had hypokalaemia, hyperaldosteronism and low plasma renin concentrations. Quadric analysis, adrenal vein plasma aldosterone concentrations, adrenal venography and CT scanning all suggested an adrenal adenoma in each patient. This suspicion was confirmed at operation in one patient; the other patient is unfit for adrenal surgery but her blood pressure and plasma potassium concentration have remained within the normal range during prolonged treatment with either spironolactone or amiloride. Because of this unusual association a search was made for parathyroid hormone excess in patients with primary hyperaldosteronism and for aldosterone excess in primary hyperparathyroidism. None was found.
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PMID:Primary hyperparathyroidism associated with primary hyperaldosteronism. 634 7

Renin secretion from the juxtaglomerular cell is controlled by numerous receptors, humoral agents, and ions. Recently, a stretch receptor hypothesis has been advanced to suggest that all of these diverse factors control renin secretion by a mechanism initiated by a fall in cytoplasmic Ca2+. This fall in Ca2+ may be achieved by lowering Ca2+ influx, raising Ca2+ efflux, or sequestering Ca2+ into cellular organelles and binding sites. The increased renin secretion observed with low arterial pressure, beta-adrenergic agonists, parathyroid hormone, glucagon, cyclic AMP, prostaglandins, low Ca2+ and Ca2+ ionophore, high Mg2+, and Na+ and Cl- may be explained in this context. On the other hand, the decreased renin secretion observed with high pressure, alpha-adrenergic agonists, some prostaglandins, angiotensin, vasopressin, and high K+ may be explained by a rise in cytoplasmic Ca2+ mediated by an opposite sequence of events. Recent observations suggest that the fall in cytoplasmic Ca2+ sets in motion the transport of renin from its site of storage (granules) or synthesis into the cytoplasmic space and finally across the plasma membrane. Thus although renin is stored in granules, its secretion occurs by a process quite different from exocytosis.
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PMID:Cellular mechanisms of renin secretion. 635 57

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions. Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and prostaglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by beta 1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II. Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified natriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide). Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure. Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion. Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected. The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.
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PMID:Endocrine physiology of electrolyte metabolism. 638 78

Drugs can interfere with the normal intake, elimination, regulation and total body distribution of electrolytes. These drug-induced abnormalities may be dramatic and life threatening, posing diagnostic and management problems to the physician who is not familiar with them. Serum potassium concentrations can be altered as potassium shifts between the tissue and plasma compartments secondary to drug actions. In addition, drugs have been shown to interfere with the normal physiological functioning of the kidney with respect to potassium homeostasis, as well as the renin-aldosterone axis. The regulation of serum sodium levels is integrally related to the regulation of total body water. Thus, drugs that alter the regulation of antidiuretic hormone secretion and its action on the kidney can result in large changes in serum sodium concentrations. Abnormal losses or intake of sodium related to drug use can also have profound effects in the plasma compartment. The normally fine regulation of serum calcium concentrations can be easily upset by pharmacological therapy at the level of parathyroid hormone secretion and action, bone metabolism or renal calcium excretion. Through awareness of these drug-induced changes in electrolytes and the mechanisms involved, subtle and often dangerous problems in clinical management can be handled rationally.
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PMID:Drug-induced electrolyte abnormalities. 675 89

Persistent hyperparathyroidism and its attendant hypercalcemia have been implicates as possible etiologic factors in posttransplant hypertension. To better define the role of parathyroid hormone (PTH) and calcium in posttransplant blood pressure homeostasis, we measured the acute response of blood pressure, ionized calcium (Ca++), plasma renin activity (PRA), and parathyroid hormone (PTH) to a 4-hr infusion of calcium (15 mg/kg) and an isoproterenol injection (0.15 mg SC) in seven normal subjects and 13 renal transplant (Tx) recipients with stable graft function and persistent hyperparathyroidism. Transient hypercalcemia produced a significant (p less than 0.01) increase in the systolic blood pressure (delta SBP) and suppression of PTH (p less than 0.001) in the posttransplant subjects. There was a significant (p less than 0.02) inverse correlation between changes (delta) in PTH and delta SBP in these subjects. There was no correlation between the delta SBP and either the change in Ca++ (delta Ca++) or the change in PRA (delta PRA) observed in the Tx recipients administered calcium. Following isoproterenol administration, SBP increased (p less than 0.01), PTH fell (p less than 0.05) and Ca++ was only minimally increased in the Tx recipients. A virtually identical, significant (p less than 0.05) inverse correlation existed between the delta PTH and delta SBP observed in the transplant subjects. Greater suppression of PTH was associated with a larger increase in systolic blood pressure. Transient hypercalcemia of comparable degree in normal subjects caused an insignificant increase in their blood pressure. The fact that PTH suppression in the normals was substantially (0.01) less (delta PTH -13 microliter/Eq/ml versus -65 microliter/Eq/ml in the transplant group) with a similar increase in serum calcium suggests that the blood pressure response to transient hypercalcemia is more dependent on PTH suppression than the level of ionized calcium. Plasma renin activity was unchanged during the blood pressure fluctuations induced by either the calcium or the isoproterenol administration to the normal subjects. Under the conditions of this study, endogenous parathyroid hormone has the characteristics of a vasodepressor hormone and may have a role in blood pressure regulation in transplant recipients with hyperparathyroidism. Since the vasodepressor effect can be dissociated from delta Ca+ and delta PRA, such a conclusion seems warranted. The implications of these findings for all subjects with renal disease requires further investigation.
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PMID:Parathyroid hormone: a determinant of posttransplant blood pressure regulation. 703 14


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