ISSN:1660-8151    

DOI:10.1159/000180507

出版商:S. Karger AG    

年代:1975

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000180508

出版商:S. Karger AG    

年代:1975

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000180509

出版商:S. Karger AG    

年代:1975

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000180510

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

This paper reviews the physiology of antidiuretic hormone, including the factors involving the formation, storage and release of the hormone, the metabolism of vasopressin and its physiologic and pharmacologic effects on water and electrolyte transport. The consequences of both deficiency and excess of the hormone are also discussed.

ISSN:1660-8151    

DOI:10.1159/000180511

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

The in vivo mechanisms whereby systemic α- and β-adrenergic stimulation exert opposing effects on renal water excretion are reviewed. An extrarenal mechanism is suggested since the effect of intravenous infusion of norepinephrine or isoproterenol on water excretion cannot be mimicked by the intrarenal administration of these agents. A role of vasopressin is implicated since neither man nor dog without a pituitary source of vasopressin demonstrate the same effect of catecholamines on water excretion as observed in intact man and dog. Evidence also is presented that systemic α- and β-adrenergic stimulation affect vasopressin release primarily by altering baroreceptor tone. The potential role of the autonomic nervous system in mediating other nonosmotic stimuli for vasopressin is discus

ISSN:1660-8151    

DOI:10.1159/000180512

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

This report reviews the interrelationship between the activity of the parathyroid glands and renal function. Among the topics discussed are: effects of parathyroid hormone on various aspects of renal function such as: (1) glomerular filtration rate and renal blood flow; (2) renal handling of phosphorus, calcium, magnesium, sodium and potassium; (3) renal production of 1,25-dihydroxycholecalciferol; (4) renal handling of bicarbonate and acid-base metabolism, and (5) mechanism of action of parathyroid hormone on the renal cell. Further topics include: renal metabolism of parathyroid hormone; the kidney in hyperparathyroidism, and effects of renal failure on structure and function of the parathyroid glands.

ISSN:1660-8151    

DOI:10.1159/000180513

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

Thyroid hormones affect both renal morphology and function. They are required for kidney growth and development, and thyroid deficiency results in decreased renal plasma flow and glomerular filtration rate and in impaired urinary concentration and dilution. Thyroid hormones also influence membrane transport and electrolyte metabolism, and alterations in mineral metabolism in hyperthyroidism frequently cause calcium nephropathy which affects renal function adversely. The kidney plays an important role in the peripheral metabolism of iodine and thyroid hormones, and thyroid function is altered in certain kidney diseases, particularly chronic renal failure. The pathogenesis of these alterations is currently under active investigation.

ISSN:1660-8151    

DOI:10.1159/000180514

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

Calcitonin, whatever its origin, produces a decrease in the renal tubular reabsorption of sodium, phosphate and calcium in man and in the rat. Renal receptors for calcitonin have been demonstrated in the membranes of rat tubular cells using 125I salmon calcitonin as a tracer. Hormone-receptor interaction initiates the activation of membrane adenyl cyclase. In the rat and in man, the kidney plays a major role in degradation of both human and salmon calcitonin. Plasma levels of immunoreactive calcitonin are high in chronic renal failure. The question of the physiological role of calcitonin on kidney function is still unsettled.

ISSN:1660-8151    

DOI:10.1159/000180515

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

We have presented a review of the interrelationship between the kidney and the adrenocortical steroids, aldosterone and cortisol, primarily in the regulation of water and electrolyte metabolism. The presentation is divided into three parts: (1) the influence of cortisol and aldosterone on renal structure and function; (2) the effect of kidney disease on secretion and metabolism of these steroids, and (3) the role of the kidneys in the plasma clearance of these steroids and their metabolites. There is no evidence that an excess or deficit of these steroids have a direct effect on renal structure, but both are necessary to maintain normal GFR and RPF. Glucocorticoids augment renal hemodynamics in pharmacologic doses. The phenomenon of ‘escape’ by the kidney from the sodium-retaining effect of adrenocortical steroids is discussed in detail, as well as the ability of glucocorticoid to antagonize the sodium retaining activity of any adrenal steroid of analogue with lesser glucocorticoid noperties. It is included that the impaired water dunesis of glycocorticoid deficiency is due to the absence of the permissive action of these steroids on the kidney, augmented at times by enhanced ADH secretion in response to sustained nonosmotic stimuli. The effect of gluco and mineralocorticoids on the renal excretion of divalentions and uric acid is also discussed. While progressive chronic renal failure (CRF) does not seem to significantly after the secretion or metabolism of cortisol it is possible that CRF causes a state of chronic hyperaldosteronism that is essential to maintain normal excretion (secretion) of potassium per nephron as renal mass progressively decreases. A direct or an indirect effect of potassium ion may be responsible for the hypersecretion or aldosterone rather than the renin-angiotensin sys

ISSN:1660-8151    

DOI:10.1159/000180516

出版商:S. Karger AG    

年代:1975

数据来源: Karger