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N Kugai

Publications and source records attributed to N Kugai.

70 records · Page 4Linked to original sources
PubMed1981

Evidence for acute inhibitory effects in vivo of 1 alpha-hydroxycholecalciferol on parathyroid hormone secretion in rats.

In an attempt to elucidate the influence of 1 alpha-hydroxycholecalciferol (1 alpha OHD3) on parathyroid hormone (PTH) secretion, sequential measurements were made of 1) serum calcium and urinary excretion of cAMP in conscious perfused rats, and 2) serum calcium in nephrectomized rats; also, the effects of a single iv injection of 1 alpha OHD3 on these parameters were examined. In conscious perfused rats, 6.25 micrograms/kg (15 nmol/kg) 1 alpha OHD3 reduced the urinary excretion of cAMP (approximately 40% of the initial value; P less than 0.05), which reached a level compatible with that of parathyroidectomized rats at 4 h; this fall was sustained for 24 h. Serum concentrations of calcium (total and ionized) did not change at 6 h, and increased at 24 h. In parathyroidectomized rats which were continuously infused with bovine PTH (0.75 U/h), the vitamin D preparation had no significant effect on the urinary excretion of cAMP. Nephrectomy, followed by an injection of the vehicle (0.05 ml 99.5% ethanol), induced a transient hypercalcemia (13.12 +/- 0.39 mg/dl at 6 h). This hypercalcemic response was prevented by prior parathyroidectomy. Injections of 1.25 and 6.25 micrograms/kg 1 alpha OHD3 caused a significant suppression of the hypercalcemia (P less than 0.05 and P less than 0.1, respectively) in the presence of parathyroid glands, whereas a dose-related hypercalcemic effect was observed in their absence. These results suggest that in rats, 1 alpha OHD3, either directly or most probably after conversion into 1 alpha, 25-dihydroxycholecalciferol, 1) acutely inhibits PTH secretion without causing a significant rise in serum calcium, and 2) suppresses PTH secretion in secondary hyperparathyroidism induced by nephrectomy.

Animals↗
PubMed1981

Inhibitory effects of 1 alpha, 25-dihydroxycholecalciferol on parathyroid hormone secretion in rats.

In an attempt to study the influence of vitamin D metabolites on PTH secretion, serum calcium and urinary excretion of cAMP were sequentially measured in conscious perfused rats, and the effects of a single iv injection of the metabolites on these parameters were examined. Four hours after the administration of 0.25 microgram/kg (0.6 nmol/kg, probably a physiological dose) of 1 alpha, 25-dihydroxycholecalciferol [1 alpha, 25 (OH)2D3], the urinary excretion of cAMP decreased to a level compatible with that of parathyroidectomized rats (approximately 60% of the initial value; P less than 0.05) and this level was sustained for nearly 24 h. Serum concentrations of calcium (total and ionized) did not change. In parathyroidectomized rats which were continuously infused with bovine PTH (1 U/h), the vitamin D metabolite had no significant effect on the urinary excretion of cAMP. 24 R, 25-dihydroxcholecalciferol (12.5 microgram/kg) had no significant effect either on the urinary excretion of cAMP or on serum calcium. These results suggest that in rats, a physiological dose of 1 alpha, 25(OH)2D3 inhibits PTH secretion without causing a significant rise iu serum calcium, reflecting a feed-back mechanism between active vitamin D metabolite, 1 alpha, 25(OH)2D3 and the parathyroid glands.

24,25-Dihydroxyvitamin D 3↗
PubMed1980

A case of primary hyperparathyroidism with low serum alkaline phosphatase levels.

A 23-year-old man with primary hyperparathyroidism which was typical except for reduced alkaline phosphatase activity is reported. Histological examination of surgical specimens revealed chief cell hyperplasia of the parathyroid glands. Systemic abnormalities of alkaline phosphatase were demonstrated, i.e., marked reduction of all isoenzymes and undetectable osseous enzyme in the serum, abnormal distribution of the enzyme in hepatocytes and diminished enzyme activities in leukocytes. In addition, diminished bone remodeling activity was revealed in a biopsy specimen of the rib. The association of hypophosphatasia is highly unlikely, because of normal urinary excretion of phosphoethanolamine, lack of osteomalacia, and no indication of an hereditary factor. The causal relationship between low remodeling activity and abnormalities in alkaline phosphatase was suggested.

Adult↗
PubMed1980

The renal parathyroid hormone receptor-adenylate cyclase system in vitro and in vivo.

High affinity parathyroid hormone (PTH) receptors in chicken renal plasma membranes were identified and quantitated using bPTH((1-34) labeled by electrolytic iodination and purified by a membrane absorption procedure. Parallel studies of PTH-receptor binding and activation of adenylate cyclase indicated that these activities were coupled. The PTH sensitivity of the renal receptor-adenylate cyclase system was similar in vivo and in vitro (Km congruent to 20 nM), whereas a 'physiologic' concentration of circulating bPTH (1-34) infused into thyroparathyroidectomized/ultimobranchial-ectomized chickens was estimated to be at least 40 times lower. Small increments in cellular cyclic AMP levels are apparently sufficient to mediate actions of PTH on the kidney.

Adenylyl Cyclases↗
PubMed1977

Oxidative response to aldosterone of pyridine nucleotide in rat kidney in situ.

In an attempt to elucidate early biochemical events in the action of aldosterone on rat kidney in situ, the response of the pyridine nucleotide oxidation-reduction state of surface cells was directly and continuously recorded with an organ-fluorometer. Intravenous administration of aldosterone induced a rapid (maximum response in 10 min) and dose-related (2.5-25 microng/100 g rat) oxidative response that was specific to aldosterone and to the kidney. The oxidative response was 1) detectable with minute dise (approximately 0.2 microng/100 g rat) of hormone: 2) reproduced by other mineralocorticoids; 3) enhanced by a maneuver for expanding the extracellular fluid compartment or by adrenalectomy; and 4) prevented by spironolactone, progesterone, actinomycin D, and cycloheximide. All of these data argue that the redox response is related to the subsequent changes in aldosteronemediated ion transport. Experiments with an uncoupler and with redox substrates showed that mitochondrial NADH was the major nucleotide pool responding to hormone. The oxidation was not accompanied by changes in the adenylate energy charge level of the whole organ. These observations support the view that aldosterone acts on energy metabolism of tubular cells before developing apparent cation transport effects.

Adenine Nucleotides↗
PubMed1977

A transient increase in renal clearance of phosphate in response to continuous infusion of salmon calcitonin in rats.

The effects of intravenous carrier-free salmon calcitonin on renal clearances of phosphate, calcium, magnesium, sodium and potassium were studied in male parathyroidectomized (PTX) and intact rats. Both natural and synthetic hormone, when infused at constant rates (0.005 approximately 0.5 MRC U/hr), produced a rapid increase (peaking at about 60-90 min) in phosphate clearance. However, the maximal increase was transient in nature in PTX rats. In intact rats, the phosphaturic response was somewhat more pronounced and the decline after the peak was rather modest. When a large amount (4 MRC U) of calcitonin was given in divided doses, the second dose produced a lesser extent of phosphaturia in both intact and PTX rats. The phosphaturic response was accompanied by an increase in sodium and potassium clearances in PTX rats and by an increase in potassium clearance in intact rats. A fall in the apparent clearance values for calcium and magnesium occurred and was maintained throughout the infusion period of hormone in both intact and PTX rats. In conclusion, PTX rats respond to the intravenous administration of salmon calcitonin with a transient phosphaturic response which is accompanied by parallel diuresis of sodium and potassium along with sustained retention of calcium and magnesium by the kidney.

Animals↗
PubMed1976

A transient increase in renal clearance of phosphate in response to continuous infusion of salmon calcitonin in rats.

The effects of intravenous carrier-free salmon calcitonin on renal clearances of phosphate, calcium, magnesium, sodium and potassium were studied in male parathyroid-ectomized (PTX) and intact rats. Both natural and synthetic hormone, when infused at constant rates (0.005 approximately 0.5 MRC U/hr), produced a rapid increase (peaking at about 60-90 min) in phosphate clearance. However, the maximal increase was transient in nature in PTX rats. In intact rats, the phosphaturic response was somewhat more pronounced and the decline after the peak was rather modest. When a large amount (4 MRC U) of calcitonin was given in divided doses, the second dose produced a lesser extent of phosphaturia in both intact and PTX rats. The phosphaturic response was accompanied by an increase in sodium and potassium clearances in PTX rats and by an increase in potassium clearance in intact rats. A fall in the apparent clearance values for calcium and magnesium occurred and was maintained throughout the infusion period of hormone in both intact and PTX rats. In conclusion, PTX rats respond to the intravenous administration of salmon calcitonin with a transient phosphaturic response which is accompanied by parallel diuresis of sodium and potassium along with sustained retention of calcium and magnesium by the kidney.

Animals↗
PubMedDate not supplied

Hypopituitarism associated with Cogan's syndrome; high-dose glucocorticoid therapy reverses pituitary swelling.

A 70-year-old woman with Cogan's syndrome first presented with central diabetes insipidus and then developed secondary hypothyroidism. Magnetic resonance imaging revealed a diffuse pituitary swelling without evidence of tumor. High-dose glucocorticoid therapy administered to treat Cogan's syndrome was very effective in suppressing the inflammatory process, and resulted in the reversal of the pituitary swelling and partial recovery of thyroid stimulating hormone secretion. This is the first case of hypopituitarism associated with Cogan's syndrome, a form of autoimmune vasculitis. The glucocorticoid-responsive pituitary lesion is best explained by autoimmune hypophysitis which shows pituitary swelling and is known to often associate with other autoimmune phenomena.

Aged↗