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H Rasmussen

Publications and source records attributed to H Rasmussen.

At least 343 records · Page 19Linked to original sources
PubMed1968

Thyrocalcitonin.

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Biological Assay↗
PubMed1968

Effect of dibutyryl cyclic adenosine 3',5'-monophosphate, theophylline, and other nucleotides upon calcium and phosphate metabolism.

The effect of dibutyryl cyclic adenosine 3',5'-monophosphate upon calcium and phosphate metabolism in thyroparathyroidectomized rats was undertaken in an effort to clarify the possible role of adenosine 3',5'-monophosphate (3',5' AMP) in parathyroid hormone action. The infusion of dibutyryl cyclic 3',5' AMP at a rate of 3 mg/hr into thyroparathyroidectomized rats leads to changes in calcium, phosphate, and hydroxyproline excretion, and calcium and phosphate concentrations in plasma that are qualitatively similar to those induced by parathyroid hormone given at a rate of 5 mug/hr. The effect of dibutyryl cyclic 3',5' AMP upon calcium and hydroxyproline mobilization from bone is blocked by thyrocalcitonin administration in the same way that thyrocalcitonin blocks PTH effects. Other closely related nucleotides do not act in the same way. These data indicate that dibutyryl cyclic 3',5' AMP produces effects similar to parathyroid hormone in thyroparathyroidectomized rats, and support the notion that 3',5' AMP is an intermediate in the mechanism of PTH action. However, the changes in magnesium and potassium excretion are different after dibutyryl cyclic 3',5' AMP infusion from those seen after PTH infusion. Also, theophylline was found to potentiate the action of smaller doses of dibutyryl 3',5' AMP, but not that of PTH.

Adenine Nucleotides↗
PubMed1967

Thyrocalcitonin and the response to parathyroid hormone.

1) In the absence of the thyroid gland, the infusion of parathyroid hormone leads to a prompt rise in plasma calcium and to prompt increase in the rate of excretion of calcium in the urine.2) In the presence of the thyroid gland, the parathyroid hormone-induced rise in plasma calcium is less marked; the rate of urinary calcium excretion falls initially and rises only after 20 to 30 hours of continuous parathyroid hormone infusion.3) The infusion of exogenous thyrocalcitonin along with the parathyroid hormone into a thyroparathyroidectomized animal leads to a pattern of response similar to that seen in the animal with an intact thyroid gland.4) Thyrocalcitonin has little apparent effect upon the immediate changes in renal function induced by parathyroid hormone.5) We conclude that bone is a major site of action of thyrocalcitonin and that it probably inhibits bone resorption.

Animals↗
PubMed1967

Thyrocalcitonin, EGTA, and urinary electrolyte excretion.

The infusion of thyrocalcitonin (TCT) into thyroparathyroidectomized rats, given either no exogenous parathyroid hormone or a constant infusion of this hormone, leads to a transient phosphaturia and a decreased excretion of urinary magnesium, calcium, and hydroxyproline without a change in glomerular filtration rate. The changes in phosphate excretion may be due to a direct effect of the hormone upon renal tubular function or they may be a consequence of the fall in plasma calcium brought about by the action of TCT upon bone. In support of this latter alternative is the fact that the infusion of sodium ethylenebis-oxyethylenenitrilotetraäcetic acid (EGTA, a specific chelator of calcium) also leads to phosphaturia presumably as a consequence of hypocalcemia. However, EGTA infusion leads to enhanced urinary hydroxyproline excretion and sustained phosphaturia. These latter observations are interpreted to mean that alterations in the local ionic environment of osteolytic cells lead to changes in their activity and constitute a local regulatory system whose activity is modulated by the hormones, thyrocalcitonin and parathyroid hormone.

Animals↗