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J Clin Endocrinol Metab. 1983 Feb;56(2):397-400.
Cyproheptadine and mineralocorticoid effector mechanisms.

Armanini D, Goland GJ, Adam WR, Funder JW.

Cyproheptadine has recently been reported to blunt the furosemide-induced rise in PRA in normal subjects and to acutely lower plasma aldosterone levels in patients with hyperaldosteronism due to bilateral adrenal hyperplasia; both actions have tentatively been ascribed to the antiserotoninergic action of the drug. We here describe receptor studies showing cyproheptadine to occupy mineralocorticoid, but not glucocorticoid, receptors in rat and mouse kidney. On bioassay, cyproheptadine is a partial mineralocorticoid agonist/predominant antagonist.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6296186&dopt=Abstract




Klin Wochenschr. 1982 Aug 16;60(16):847-52.
Rapid increase of mineralocorticoids after furosemide in low-renin essential hypertension: evidence for 18-hydroxycorticosterone to be a better marker than aldosterone.

Witzgall H, Thayil G, Weber PC.

The response of plasma renin activity (PRA), plasma aldosterone, 18-hydroxycorticosterone (18-OH-B), 18-hydroxydeoxycorticosterone (18-OH-DOC) and corticosterone to furosemide were compared in 20 normal control subjects, 16 patients with normal-renin essential hypertension (NREH) and 12 patients with low-renin essential hypertension (LREH). Analyses were performed before medication, and 15 min (supine) and 120 min (active orthostasis) after IV administration of 40 mg furosemide. In normotensive subjects PRA increased 15 min after administration of furosemide from 0.8 +/- 0.4 ng AI/ml . h (SD) to 3.4 +/- 1.4 (P less than 0.01), plasma aldosterone from 109 +/- 28 pg/ml to 139 +/- 40 (less than 0.01) and 18-OH-B from 199 +/- 90 to 279 +/- 85 (P less than 0.01). In patients with NREH, PRA increased significantly less (P less than 0.01) and no significant increase of plasma aldosterone or 18-OH-B was found. PRA of patients with LREH (0.2 +/- 0.1 ng AI/ml . h) remained practically unchanged 15 min after furosemide administration, but in contrast to NREH aldosterone increased from 111 +/- 37 to 160 +/- 66 (P less than 0.05) and 18-OH-B from 162 +/- 101 to 261 +/- 71 pg/ml (P less than 0.01). The relative increase in plasma 18-OH-B was significantly greater in patients with LREH than in patients with NREH. The plasma levels of aldosterone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P less than 0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P less than 0.01) only at 120 min after furosemide erone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P less than 0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P less than 0.01) only at 120 min after furosemide erone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P less than 0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P less than 0.01) only at 120 min after furosemide administration combined with active orthostasis. In summary, our results support the concept that sensitivity of the mineralocorticoid-producing cells is enhanced in patients with LREH. Postfurosemide 18-OH-B seems to be a better marker of this phenomenon than aldosterone.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6752560&dopt=Abstract




Arch Dis Child. 1984 Sep;59(9):825-30.
Renal sodium handling in minimal change nephrotic syndrome.

Bohlin AB, Berg U.

Renal sodium handling was studied in 23 children at three different stages of the minimal change nephrotic syndrome--the oedema forming state, proteinuric steady state, and remission. Clearances of inulin and para-aminohippuric acid and urinary sodium excretion were determined basally, after intravenous infusion of isotonic saline and hyperoncotic albumin, and after furosemide injection. Absolute and fractional basal sodium excretion were significantly lower in oedema forming patients than in proteinuric patients in steady state, and non-proteinuric patients. In contrast to proteinuric patients in steady state and non-proteinuric patients, the oedema forming patients failed to respond to isotonic saline infusion with increased sodium excretion. After diuretic blockade with furosemide, the fractional sodium excretion of the oedema forming patients increased to values no different from those of the non-proteinuric patients, whereas the fractional sodium excretion of the steady state patients increased to significantly higher values. The plasma aldosterone concentration was within normal limits in 11 of 14 proteinuric patients, and did not correlate with the basal sodium excretion. Thus, sodium retention in the minimal change nephrotic syndrome was found only in oedema forming patients, and since this is not related to the plasma aldosterone concentration it may be caused by an intrarenal mechanism, probably sited in distal parts of the nephron.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6486860&dopt=Abstract












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