Biomedical subjects
Publications and source records attributed to S C Kukreja.
Allotransplantation of fresh, 1 or 2 week cultured parathyroid glands from Wistar rats (AgB2) to Fischer rats (AgB1) resulted in prompt rejection of the transplant in the muscle site; whereas transplantation into the adrenal site offered slightly prolonged survival, suggesting that the latter is a privileged transplantation site.
Our previous in vitro and in vivo studies demonstrated that exogenous somatostatin inhibited secretion of both parathyroid hormone (PTH) and calcitonin (CT). This study evaluates the possible role of endogenous somatostatin in PTH and CT secretion. Rats receiving somatostatin antiserum i.v. had significantly greater circulating levels of serum immunoreactive PTH (iPTH) and CT (iCT) than rats receiving normal rabbit serum. In in vitro studies with bovine parathyroid tissue, the addition of somatostatin antiserum to the medium significantly increased PTH secretion from basal, low calcium-stimulated and high calcium-suppressed parathyroid tissue. These combined observations strongly suggest that endogenous somatostatin must have a suppressive effect on PTH and CT secretion. The in vitro observations with isolated parathyroid tissue suggest that somatostatin is synthesized by cells within this tissue. These data strongly suggest that somatostatin is a locally-synthesized hormone that has a role in modulation of both PTH and CT secretion.
This study evaluated the effect of somatostatin on immunoreactive parathyroid hormone (iPTH) and calcitonin (iCT) secretion in vivo in rats and monkeys and on iPTH secretion in vitro by normal bovine parathyroid tissue and by a human parathyroid adenoma. Somatostatin infusion promptly (within 0.5 h) suppressed both iPTH and iCT in both species studied in vivo, the suppression being progressive during the infusion period. In in vitro studies, somatostatin caused significant dose-related decreases in basal, low Ca-stimulated, and high Ca-suppressed PTH secretion from normal bovine parathyroid tissue and from basal and low Ca-stimulated PTH secretion from a human parathyroid adenoma. Therefore, somatostatin 1) suppresses both PTH and CT secretion in vivo; 2) acts directly on the parathyroid cell and presumably directly on the C-cell also; 3) acts upon normal and adenomatous parathyroid tissue; 4) suppresses basal, low Ca-stimulated and high Ca-suppressed PTH secretion; and 5) has a dose-related effect. The possible role of somatostatin in the physiological control of PTH and CT secretion (and therefore in Ca homeostasis), and in the pathogenesis of abnormalities of Ca homeostasis, requires further evaluation.
This study evaluated the effects of adrenergic agents on immunoreactive calcitonin (iCT) secretion in normal man, and compared the time course and magnitude of these adrenergic effects with those caused by modifying calcium (Ca) ion concentration. Ca infusion (15 mg Ca++/kg iv in 4 h) significantly increased plasma iCT within 1 h, reaching 140 +/- 8% of baseline at 4 h. EDTA (50 mg/kg iv in 2 h) significantly decreased plasma iCT within 15 min, with nadir value of 53 +/- 4.9% of baseline at 2 h. The beta-adrenergic agonist, isoproterenol, significantly increased plasma iCT with 5 min, reaching 136 +/- 5.9% of baseline at 30 min. The alpha-adrenergic antagonist, phentolamine, significantly increased iCT within 15 min, reaching 132 +/- 8.6% of baseline at 45 min. The beta-adrenergic antagonist, propranolol, significantly suppressed iCT with 15 min, reaching 51.8 +/-6.3% of baseline at 2 h. Therefore, 1) the adrenergic system (without induced change in serum Ca) can modify CT secretion to as great a degree as can change in Ca ion concentration induced by standard Ca and EDTA infusion tests and 2) even basal secretion of CT can be modified by adrenergic influences. These data strongly suggest 1) that the adrenergic system is an effective modifier of CT secretion and 2) that the adrenergic system, as well as Ca ion concentration, may play an improtant physiological role in control of CT secretion in man.
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During an episode of pneumonia and multiple pulmonary thromboembolic events, an adult male patient with sickle cell-C hemoglobinopathy developed a severe anemia associated with rapidly increasing splenic size and diminished splenic uptake of technetium Tc 99m sulfur colloid, indicating diminished splenic function due to hypersequestration, a rare and noteworthy phenomenon in adult patients with sickle cell-C disease.
In the rat, EDTA and isoproterenol stimulated PTH secretion, whereas high calcium and propranolol inhibited it. The stimulatory effects of EDTA and isoproterenol were still evident and unaltered in the presence of blocks induced by propranolol and high calcium, respectively. The findings suggest that: (i) both calcium and beta-adrenergic stimuli affect PTH secretion; and (ii) the two influences affect the PTH secretion by separate initial pathways.
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The role of adrenergic stimuli in the secretion of parathyroid hormone (PTH) in man was evaluated. Intradermal injections of isoproterenol, 0.15 mg, or epinephrine, 0.3 mg, caused significant prompt increases in serum PTH levels. These increases were not accompanied by any changes in serum calcium (Ca) during the period of observation. Phenylephrine, 1.5 mg, intradermally, did not cause any significant changes in serum PTH or serum Ca. Propranolol infusion alone significantly inhibited the basal secretion of PTH. This inhibition by propranolol was overcome by isoproterenol administration. The results indicate that 1) beta adrenergic agents increase PTH secretion whereas alpha adrenergic agents have no effect, 2) beta adrenergic stimuli probably play an important physiological role in basal PTH secretion in man.