1983
DOI: 10.1007/bf00663903
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Mineralo- and glucocorticoid effects on renal excretion of electrolytes

Abstract: The acute effects of mineralo- and glucocorticoids on urinary electrolyte excretion were studied in the conscious, acutely potassium deprived, adrenalectomized rat. Sodium, potassium, and creatinine were measured in the urine excreted from 2.5 to 5.5 h after injection of one or more of the following steroids: aldosterone (Aldo), 9-alpha fluorocortisol (FC), deoxycorticosterone (DOC), dexamethasone (Dex), and spironolactone (Spiro). The hierarchy (a) for increasing creatinine excretion was Dex greater than FC g… Show more

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Cited by 54 publications
(33 citation statements)
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“…It was noted earlier that when aldosterone has been found in previously reported studies to cause an acute kaliuresis, it has usually been in the context of either some degree of sodium-loading (33,35,36), or of potassium-depletion (18,29,30). For example, one recent report (35) found an absence of kaliuresis after acute aldosterone administration in animals receiving minimal amounts of sodium during clearance studies, which contrasted with a kaliuretic response if sodium was provided freely during the study as well as in the 24-h-period before study.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…It was noted earlier that when aldosterone has been found in previously reported studies to cause an acute kaliuresis, it has usually been in the context of either some degree of sodium-loading (33,35,36), or of potassium-depletion (18,29,30). For example, one recent report (35) found an absence of kaliuresis after acute aldosterone administration in animals receiving minimal amounts of sodium during clearance studies, which contrasted with a kaliuretic response if sodium was provided freely during the study as well as in the 24-h-period before study.…”
Section: Discussionmentioning
confidence: 99%
“…Although this phenomenon has been repeatedly documented using clearance techniques (16)(17)(18)(19)(20)(21), only limited information is available on the specific effect of glucocorticoids on tubular transport function (14). In particular, it is unknown whether these agents stimulate tubular potassium secretion directly, or whether the observed kaliuresis is secondary to their marked stimulant effect on glomerular filtration, sodium excretion, and urinary flow rate.…”
mentioning
confidence: 99%
“…This concept of differences between Na C and K C effects was developed by Campen et al (1983), who distinguished between glucocorticoid-and mineralocorticoid-induced kaliuresis. In adrenalectomised animals treated subcutaneously at time 0 and 2 .…”
Section: G P Vinson Mislabelling Of Docmentioning
confidence: 99%
“…The relatively poor activity of DOC on kaliuresis was adduced by Campen et al (1983) as evidence that DOC is a partial glucocorticoid agonist. Whether or not they were right to ascribe its sodium effects to mineralocorticoid receptor (MR) activation alone, and potassium effects to both GR and MR mediation, the relatively poor effect of DOC on K C relative to Na C does not seem to be adequately accounted for.…”
Section: G P Vinson Mislabelling Of Docmentioning
confidence: 99%
“…Keeping with their physiologic function, GRs are differentially distributed www.intechopen.com along the kidney nephron. In vitro studies have implicated GRs in the regulation of ammoniagenesis, gluconeogenesis, GFR, Na-H exchange and Na-phosphate co-transport, all of which are proximal renal tubule processes (Baylis et al 1990;Boross et al 1986;Campen et al 1983;Freiberg et al 1982). Measurement of GRs in normal rat kidney cortical tubules enriched in proximal tubules yielded three to six fold higher GR content as compared to the distal tubules (Mishina et al 1981).…”
Section: Expression Of Gr In the Normal Kidneymentioning
confidence: 99%