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Biomedical subjects

J B Field

Publications and source records attributed to J B Field.

At least 163 records · Page 9Linked to original sources
PubMed1972

Effects of long-acting thyroid stimulator on thyrotropin stimulation of adenyl cyclase activity in thyroid plasma membranes.

Both thyroid-stimulating hormone (TSH) and long-acting thyroid stimulator (LATS) stimulated adenyl cyclase activity in plasma membranes obtained from bovine thyroid glands. The stimulation induced by LATS was much less than that obtained with maximal amounts of TSH. LATS inhibited TSH stimulation of adenyl cyclase activity while an equivalent amount of normal human gamma-globulin did not influence basal or TSH-stimulated activity. The inhibition by LATS appeared to be noncompetitive and was greatest when the plasma membranes were initially exposed to LATS for 30 min at 0 degrees C before being incubated with TSH for 10 min at 37 degrees C. Inhibition could still be demonstrated when the plasma membranes were incubated for 30 min at 0 degrees C with TSH before the addition of LATS. Prolonging the period of incubation of plasma membranes with LATS from 30 to 60 min did not augment the stimulation of adenyl cyclase or increase the inhibition of the effect of TSH. Papain digests of LATS also increased adenyl cyclase activity of thyroid plasma membrane and inhibited the stimulation induced by TSH. The inhibitory effect of LATS was not completely specific for TSH and thyroid plasma membranes since glucagon stimulation of adenyl cyclase in hepatic plasma membranes was also inhibited, but to a lesser extent. In contrast to the results obtained with thyroid plasma membranes, LATS did not influence basal adenyl cyclase activity in hepatic plasma membranes. Furthermore equivalent amounts of normal human gamma-globulin also decreased glucagon stimulation of adenyl cyclase activity in plasma membranes obtained from liver. The present data suggest that LATS stimulation of adenyl cyclase in thyroid plasma membranes might be due to a change in the membrane configuration rather than binding to a specific receptor site. Such modification of the membrane structure could interfere with the binding of TSH to specific receptors or to the subsequent stimulation of adenyl cyclase. However, the results do not exclude the possibility that some component in the preparation other than LATS might be responsible for the inhibition of the stimulation by TSH.

Adenylyl Cyclases↗
PubMed1972

Effects of thyroid-stimulating hormone on adenyl cyclase activity and intermediary metabolism of "cold" thyroid nodules and normal human thyroid tissue.

"Cold" thyroid nodules do not concentrate (131)I before or after thyrotropin (TSH) administration. In an attempt to elucidate the reason for this TSH unresponsiveness, the effect of TSH in vitro on several metabolic parameters was studied in 11 "cold" thyroid adenomas, 2 medullary carcinomas, and in the surrounding normal thyroid tissue. Basal adenyl cyclase activity, glucose-1-(14)C oxidation, and (32)P incorporation into phospholipids were significantly greater in the adenomas than in the adjacent normal thyroid; basal cyclic 3',5'-adenosine monophosphate (cyclic AMP) concentration and adenine-(3)H incorporation into (3)H-labeled cyclic AMP were not different. In adenomas as well as normal thyroid, all parameters responded significantly to in vitro TSH stimulation. The response to TSH of adenyl cyclase activity and (32)P incorporation was enhanced in adenomas compared with that of the adjacent normal thyroid. These differences were not explained by an increased cellularity of the adenomas. Medullary carcinomas did not respond to TSH in any of the above parameters. The studies demonstrate an intact, TSH-responsive adenyl cyclase-cyclic AMP system in the adenomas and, accordingly, imply the presence of receptor sites for TSH on the cells of the adenoma. The failure of such nodules to concentrate (131)I may be owing to a subsequent impairment in the expression of cyclic AMP action on iodine metabolism.

Adenine↗
PubMed1972

Effect of prostaglandin E 1 on certain renal actions of parathyroid hormone.

Parathyroid hormone increased basal adenyl cyclase activity and that increase was inhibited by prostaglandin E(1) (PGE(1)). Tissue cyclic 3',5'-adenosine monophosphate (cyclic AMP) concentrations were increased by parathyroid hormone and that increase was likewise inhibited by PGE(1). Both parathyroid hormone and dibutyryl cyclic AMP increased (32)P incorporation into renal cortical phospholipids. PGE(1) diminished the effect of parathyroid hormone but not dibutyryl cyclic AMP to influence that parameter. PGE(1) likewise modulated the effect of parathyroid hormone but not dibutyryl cyclic AMP to decrease fractional phosphate reabsorption by the renal tubule. It is suggested that PGE(1) inhibits the effect of parathyroid hormone by decreasing its effect on adenyl cyclase. Such interaction may be important in modulating the intracellular action of parathyroid hormone on kidney cortex.

Adenylyl Cyclases↗
PubMed1971

"Essential" hypernatremia due to ineffective osmotic and intact volume regulation of vasopressin secretion.

A physiological explanation for sustained hyperosmolality was sought in a patient with histiocytosis. During 23 days of observation with only sodium intake regulated at 100 mEq daily, elevation (mean 310 mOsm/kg of water) and fluctuation (range 298-323) of the fasting plasma osmolality were recorded. The presence of endogenous vasopressin was indicated by the patient's ability to concentrate the urine to as high as 710 mOsm/kg of water with a creatinine clearance of 84 cc/min, and by dilution of the urine in response to alcohol. The failure of increasing fluid intake to as high as 6.2 liters daily to lower the plasma osmolality indicated that deficient fluid intake was not solely responsible for the elevated plasma osmolality. Hypertonic saline infusion during water diuresis resulted in the excretion of an increased volume of dilute urine. The water diuresis continued despite a rise in plasma osmolality from 287 to 339. An isotonic saline infusion initiated during hydropenia resulted in a water diuresis which continued despite a rise in the plasma osmolality from 303 to 320. Stable water diuresis induced during recumbency by either oral ingestion of water or intravenous infusion of normal saline was terminated by orthostasis and resumed with the return to the recumbent position. Antecedent alcohol ingestion blocked the antidiuresis of orthostasis. The data are interpreted as indicating impairment of the osmoreceptor mechanism as the primary cause of the hyperosmolar syndrome. They also indicate that vasopressin secretion was regulated primarily by changes in effective blood volume. Chlorpropamide was found to be an effective treatment for the syndrome.

Adult↗
PubMed1971

Effects of vasopressin and prostaglandin E 1 on the adenyl cyclase-cyclic 3',5'-adenosine monophosphate system of the renal medulla of the rat.

Vasopressin increased adenyl cyclase activity in homogenates of both inner and outer renal medulla of the rat. It also increased the concentration of cyclic 3',5'-adenosine monophosphate (AMP) in slices of both inner and outer medulla but not in renal cortex. In the inner medulla, a concentration of prostaglandin E(1) (PGE(1)), which was ineffective by itself significantly reduced the stimulation of adenyl cyclase activity and cyclic AMP concentration induced by vasopressin. These results are consistent with the hypothesis that PGE(1) can compete with vasopressin for adenyl cyclase-binding sites. However, the findings in the outer medulla suggest the situation is more complex. Although 10(-8) M PGE(1) had no effect by itself and inhibited the vasopressin-induced elevation of cyclic AMP, larger amounts of PGE(1) increased both adenyl cyclase activity and cyclic AMP levels. The maximum effect on the latter parameter was at least 6 times as great as that of maximum amounts of vasopressin.

Adenine Nucleotides↗