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Biomedical subjects

R Ardaillou

Publications and source records attributed to R Ardaillou.

At least 181 records · Page 10Linked to original sources

Effects of furosemide-induced plasma volume reduction on plasma antidiuretic hormone in normal and hypertensive subjects.

Plasma antidiuretic hormone (ADH) was measured before and after furosemide administration in hypertensive patients (essential benign hypertensions with low plasma renin activity) and in normal subjects. Furosemide-induced reduction of plasma volume was about 10% after 2 hours. In normal subjects, plasma ADH rose progressively till the end of the study (1.5 pg/ml per hour corresponding to about 3 pg/ml per liter of plasma water lost) whereas it remained unchanged in hypertensive patients. There was an early increase of plasma renin activity (PRA) in normal subjects followed by a progressive fall. PRA response was blunted in hypertensive patients. These results show that volume-dependent ADH secretion is inhibited in patients with essential benign hypertension.

Adult↗

Altered PGE2 production by glomeruli and papilla of rats with hereditary diabetes insipidus.

PGE2 synthesis rate was studied in vitro in isolated glomeruli and in papillary homogenates prepared from kidneys of Brattleboro rats with hereditary diabetes insipidus (DI) (no ADH) and of Brattleboro heterozygous control rats. Incubations were carried out in isotonic buffer at 37 degrees C in the presence or absence of arachidonic acid for 15, 30, 60 and 90 min. PGE2 production was measured in the supernatant by specific radioimmunoassay. Results were compared by analysis of variance. PGE2 production was significantly decreased in the papilla (p < 0.01) and increased in the glomeruli (p < 0.01) of DI rats compared to controls. Stimulation by arachidonic acid was similar in both groups. Chronic ADH deficiency thus modifies the ability of the kidney to produce PGE2 in vitro. The opposite effects observed in glomeruli and papilla suggest a different hormonal control of PGE2 synthesis in both tissues.

Animals↗

Effects of calcitonin on basal and thyrotropin-releasing hormone-stimulated prolactin secretion in man.

Plasma PRL fell in nine healthy subjects and four patients with hyperprolactinemia after iv administration of salmon calcitonin (CT). The maximum fall was observed 30--60 min after the infusion. There was no change in the plasma concentrations of the other anterior pituitary hormones tested (GH, FSH, LH, and TSH). In five healthy subjects, TRH was injected 60 min after the CT infusion. This protocol was repeated in the same subjects at 3-day intervals, except CT was not administered. Plasma PRL before TRH injection was clearly lower when CT had been administered. Plasma concentrations of the other anterior pituitary hormones did not change. PRL and TSH responses to TRH were markedly inhibited when CT had been previously infused. These observations are in agreement with preceeding studies showing a similar effect of CT on the plasma concentration of various other polypeptide hormones. This general effect of CT could be attributed to a change in intracellular calcium of the secreting cells.

Adenoma↗

[The effect of inhibition of angiotensin II synthesis on the response of plasma antidiuretic hormone (ADH) to the osmotic and volume-dependent stimuli in uremic patients (author's transl)].

The effect of inhibition of angiotensin II synthesis by captopril on the response of plasma ADH to the osmotic and volume-dependent stimuli has been studied in 15 uremic patients. Captopril administration had no effect either on basal plasma ADH or on plasma ADH response to the osmotic stimulus. Time-course of plasma ADH following hypertonic saline administration and sensitivity of the response (increase of plasma ADH related to increase of plasma sodium) were not modified. On the contrary, the response of plasma ADH to the volume-dependent stimulus induced by hemofiltration was markedly blunted by captopril administration. The sensitivity estimated from the slope of the regression line relating plasma ADH to the cumulated lost volume was clearly diminished. These results suggest that angiotensin II mediates ADH response only to the volume-dependent stimulus.

Adult↗

Prostaglandin synthesis by isolated rat renal glomeruli.

The PGE2, PGF2 alpha and 6-keto-PGF1 alpha contents of the incubation medium of glomeruli isolated from rat kidney were measured at different times with or without addition of arachidonic acid. These prostaglandins accumulated progressively with time and reached equilibrium after 60--120 min incubation. Synthesis of the 3 prostaglandins was inhibited when indomethacin was added whereas it was markedly enhanced, mainly for PGE2, at increasing doses of arachidonic acid. Plateaus were reached above 5 micrograms/ml and concentrations corresponding to 50% of the maximum values were 2 micrograms/ml for PGE2 and PGF2 alpha, and 0.8 microgram/ml for 6-keto-PGF1 alpha. There were strictly linear relationships between PGE2 or PGF2 alpha productions and the concentration of glomerular protein. PGE2 and PGF2 alpha synthesis with or without arachidonic acid were maximum at 30--37 degrees C. PGE2 glomerular content was almost undetectable initially and increased with time. These data demonstrate that PGE2, PGF2 alpha and PGI2, in order of decreasing abundance, are synthesized by the glomerular cells and suggest that PGE2 and PGI2-sensitive glomerular adenylate cyclase activities and PGE2-sensitive renin synthesis may be stimulated by prostaglandins formed in the glomeruli themselves.

Animals↗