Administration of lithium chloride to rats injected intracerebrally with [3H]inositol led to time- and dose-dependent increases in levels of labeled inositol monophosphates in brain. Quantitative analysis of the inositol phosphates by ion chromatography revealed 37- and 20-fold increases in the mass of myo-inositol 1-phosphate and 4-phosphate, respectively, at 4 h intraperitoneal after injections of 6 mEq/kg of lithium chloride. Albeit to a much lesser extent, lithium administration also resulted in an increase in the level of myo-inositol, 1,4-bisphosphate in brain. The lithium-induced increase in content of labeled inositol monophosphates was marked by a concomitant decrease in content of labeled inositol, and after injections of high doses of lithium, e.g., 10 mEq/kg, this was followed by a general decrease in labeling of the inositol phospholipids. In general, animals injected with [3H]inositol but not lithium did not reveal obvious differences in labeling of inositol monophosphates on stimulation by mecamylamine or pilocarpine. However, when animals were injected with [3H]inositol and then lithium, there were large increases in the levels of labeled inositol monophosphates on administration of these compounds. Administration of atropine to the lithium-treated mice led to a partial reduction in the amount of labeled inositol monophosphates accumulated due to the administration of lithium alone. Furthermore, atropine was able to block the pilocarpine-induced increase in level of labeled inositol monophosphates. These results demonstrate the suitable use of the radiotracer technique together with lithium administration for assessing the effects of drugs and receptor agonists on the signaling system involving polyphosphoinositide turnover in brain.
. The calcium endocrine system of adolescent rhesus monkeys and controls before and after spaceflight. Am J Physiol Endocrinol Metab 282: E514-E521, 2002; 10.1152/ajpendo.00299.2001.-The calcium endocrine system of nonhuman primates can be influenced by chairing for safety and the weightless environment of spaceflight. The serum of two rhesus monkeys flown on the Bion 11 mission was assayed pre-and postflight for vitamin D metabolites, parathyroid hormone, calcitonin, parameters of calcium homeostasis, cortisol, and indexes of renal function. Results were compared with the same measures from five monkeys before and after chairing for a flight simulation study. Concentrations of 1,25-dihydroxyvitamin D were 72% lower after the flight than before, and more than after chairing on the ground (57%, P Ͻ 0.05). Decreases in parathyroid hormone did not reach significance. Calcitonin showed modest decreases postflight (P Ͻ 0.02). Overall, effects of spaceflight on the calcium endocrine system were similar to the effects of chairing on the ground, but were more pronounced. Reduced intestinal calcium absorption, losses in body weight, increases in cortisol, and higher postflight blood urea nitrogen were the changes in flight monkeys that distinguished them from the flight simulation study animals. rhesus monkey; 1,25-dihydroxyvitamin D EXPERIMENTS CONDUCTED on the Russian biosatellite missions have contributed a great deal of information on the effects of spaceflight on bone in the primate. Although each mission was limited to the participation of only two nonhuman primates in orbit for ϳ2 wk, the effects of microgravity on bone were evaluated by biopsies after the flight (38, 39). As well, exercise activity, which may confound the interpretation of bone responses, was controlled during the flight. Reduced mechanical stress is known to depress new bone formation in localized areas of the skeleton at any age (2) and to stimulate bone resorption in the mature skeleton (18,40). The role of the calcium endocrine system in this response of bone tissue has been studied through the analyses of blood samples acquired during ground-based simulations (2, 17, 40) and spaceflight (23, 30). Smith et. al (30) note in their detailed listing of human spaceflight results that the two major calcemic hormones, parathyroid hormone and 1,25-dihydroxyvitamin D, were suppressed and that calcitonin was unchanged. Decreases in parathyroid hormone are initiated by the release of calcium, not always detectable as an increase in serum, from an unloaded skeletal site. Suppressed parathyroid hormone would operate to reduce osteoclastic resorption and bone loss directly and indirectly by reduced intestinal absorption of calcium through decreases in the production of the vitamin D hormone. Collectively, these observations in humans place the calcium endocrine system in a role that responds to the biomechanical effects of weightlessness on bone that initiates increased resorption and decreased formation at different skeletal sites.In juvenile monkeys, pre...
High levels of salt promote urinary calcium (UCa) loss and have the potential to cause bone mineral deficits if intestinal Ca absorption does not compensate for these losses. To determine the effect of excess dietary salt on the osteopenia that follows skeletal unloading, we used a spaceflight model that unloads the hindlimbs of 200-g rats by tail suspension (S). Rats were studied for 2 wk on diets containing high salt (4 and 8%) and normal calcium (0.45%) and for 4 wk on diets containing 8% salt (HiNa) and 0.2% C (LoCa). Final body weights were 9-11% lower in S than in control rats (C) in both experiments, reflecting lower growth rates in S than in C during pair feeding. UCa represented 12% of dietary Ca on HiNa diets and was twofold higher in S than in C transiently during unloading. Net intestinal Ca absorption was consistently 11-18% lower in S than in C. Serum 1,25-dihydroxyvitamin D was unaffected by either LoCa or HiNa diets in S but was increased by LoCa and HiNa diets in C. Despite depressed intestinal Ca absorption in S and a sluggish response of the Ca endocrine system to HiNa diets, UCa loss did not appear to affect the osteopenia induced by unloading. Although any deficit in bone mineral content from HiNa diets may have been too small to detect or the duration of the study too short to manifest, there were clear differences in Ca metabolism from control levels in the response of the spaceflight model to HiNa diets, indicated by depression of intestinal Ca absorption and its regulatory hormone.
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