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M Goligorsky

Publications and source records attributed to M Goligorsky.

6 recordsLinked to original sources
PubMed1986

Effects of parathyroid hormone on cytosolic calcium in renal proximal tubular primary cultures.

The effects of parathyroid hormone on the cytoplasmic Ca2+ concentration of canine renal proximal tubule cells grown in primary culture were determined using the fluorescent Ca2+ indicator quin 2. The cultured cells exhibited responses to hormones, enzyme activities, transport functions, and morphology characteristic of the proximal convoluted tubule. Parathyroid hormone stimulated an immediate rise in cytoplasmic Ca2+, both in suspended cells and cells studied as a monolayer on Nuclepore filters. The rise in cytoplasmic Ca2+ induced by the hormone was sustained for 15-30 min, was dose dependent, and was not mimicked by cyclic AMP. Removing Ca2+ from the extracellular media markedly decreased cytoplasmic Ca2+ and abolished the effects of parathyroid hormone on cytosolic Ca2+. 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate blocked the effects of the hormone on cytosolic Ca2+, but mitochondrial uncouplers failed to inhibit the effects of the hormone to increase cytoplasmic Ca2+. These studies support a role of Ca2+ in the activation of proximal renal tubule cells by parathyroid hormone.

Aminoquinolines↗
PubMed1984

Vascular hypersensitivity to noradrenaline: a possible mechanism of hypertension in rats with chronic uraemia.

Studies were performed to evaluate the mechanism involved in the hypertension of moderate renal failure in partially (five-sixth) nephrectomized rats. Cardiac index (CI) was studied by means of the microsphere technique, and systemic vascular resistance (SVR) calculated from the mean arterial resistance MAP/CI, in four groups of experimental animals: (A) partially nephrectomized rats; (B) group A rats chronically treated with the calcium channel blocker verapamil; (C) sham-operated rats; (D) sham-operated rats treated with verapamil. The results demonstrate a significant increase in MAP in group A rats, which was due to a 72% increase in SVR as compared with groups C and D. In group B rats, MAP decreased significantly owing to a marked decrease in SVR (40%) as compared with group A. However, MAP remained higher in group B than in group C. The vascular responsiveness to noradrenaline was studied in group A, group C and group A rats after parathyroidectomy (group A1). An increased pressor responsiveness to noradrenaline was indicated by a shift of the noradrenaline dose-response curve to the left in group A rats as compared with group C rats. This change was corrected after partial nephrectomy. We conclude that hypertension in nephrectomized rats is due to an increase in SVR, and that an increased pressor responsiveness to catecholamines may play a role in this phenomenon. Furthermore, verapamil reduced the hypertension, and parathyroidectomy improved the abnormal sensitivity to noradrenaline in group A rats. These results raise the possibility that an abnormality in calcium metabolism, possibly due to secondary hyperparathyroidism, may be implicated in the hypertension of mildly uraemic rats.

Animals↗
PubMed1984

Losses of 1,25- and 24,25-dihydroxycholecalciferol in the peritoneal fluid of patients treated with continuous ambulatory peritoneal dialysis.

We measured peritoneal losses of the active vitamin D metabolites 1,25(OH)2D3 and 24,25(OH)2D3 in patients receiving continuous ambulatory peritoneal dialysis (CAPD). The serum concentration of 24,25(OH)2D3 was considerably lower than in hemodialysis patients. The serum concentration of 1,25(OH)2D3 was undetectable and rose to levels similar to those in hemodialysis patients only after loading with much higher oral doses of 1-alpha-vitamin D3 than those received by hemodialysis patients. Losses of both metabolites in peritoneal fluid were considerable, averaging approximately 6-8% of the plasma pool per day. These losses lead to low serum levels of these active vitamin D metabolites in CAPD patients, which may be an important factor in exacerbating renal osteodystrophy. Our results indicate the need for increased replacement doses of vitamin D metabolites in CAPD patients.

24,25-Dihydroxyvitamin D 3↗