Lack of effects of 1,25- and 24,25-dihydroxyvitamin D on parathyroid hormone response to hypocalcemia in cattle

B. Voumard , U. Trechsel , J.A. Fischer , J.W. Blum
{"title":"Lack of effects of 1,25- and 24,25-dihydroxyvitamin D on parathyroid hormone response to hypocalcemia in cattle","authors":"B. Voumard ,&nbsp;U. Trechsel ,&nbsp;J.A. Fischer ,&nbsp;J.W. Blum","doi":"10.1016/0221-8747(84)90025-0","DOIUrl":null,"url":null,"abstract":"<div><p>Effects of 1,25(OH)<sub>2</sub>D<sub>3</sub> or 24,25(OH)<sub>2</sub>D<sub>3</sub> on plasma PTH were examined following induced hypocalcemia with EGTA. EGTA infusions caused an elevation of plasma PTH within 10 min. Sixty min after the start of EGTA infusions, 1,25(OH)<sub>2</sub>D<sub>3</sub> or 24,25(OH)<sub>2</sub>D<sub>3</sub> were IV administered. Transient (within 5 min) elevations in plasma PTH were observed in two of five animals following the administration of 1,25(OH)<sub>2</sub>D<sub>3</sub> or of 24,25(OH)<sub>2</sub>D<sub>3</sub>. Neither secosterol had an effect on the induced elevations in plasma PTH during the remaining 60 min of the EGTA infusions. Twenty-two hr following 24,25(OH)<sub>2</sub>D<sub>3</sub> administration, plasma PTH, ionized and total calcium, inorganic phosphate, and magnesium were normal, while plasma 24,25(OH)<sub>2</sub>D was elevated. The plasma PTH response to EGTA-induced hypocalcemia was not significantly altered from that observed prior to the administration of 24,25(OH)<sub>2</sub>D<sub>3</sub>. Animals, which were IV injected with 1,25(OH)<sub>2</sub>D<sub>3</sub> received the same amount IM 60 min later. Twenty-two h following IM 1,25(OH)<sub>2</sub>D<sub>3</sub>, plasma 1,25(OH)<sub>2</sub>D, ionized and total calcium, and plasma inorganic phosphate were elevated. Plasma PTH and magnesium were lowered. The PTH response to EGTA-induced hypocalcemia was significantly reduced in these animals. A similar reduction in the PTH response to induced hypocalcemia was observed in animals receiving 7 hr IV infusions of calcium chloride. The findings suggest that the blunted response was, in part, the consequence of the preceding hypercalcemia. These results indicate that 1,25(OH)<sub>2</sub>D<sub>3</sub> does not directly regulate plasma PTH secretion and that 24,25(OH)<sub>2</sub>D<sub>3</sub> has no effect on plasma PTH during induced hypocalcemia in the bovine species.</p></div>","PeriodicalId":79235,"journal":{"name":"Metabolic bone disease & related research","volume":"5 4","pages":"Pages 171-175"},"PeriodicalIF":0.0000,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0221-8747(84)90025-0","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Metabolic bone disease & related research","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0221874784900250","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 5

Abstract

Effects of 1,25(OH)2D3 or 24,25(OH)2D3 on plasma PTH were examined following induced hypocalcemia with EGTA. EGTA infusions caused an elevation of plasma PTH within 10 min. Sixty min after the start of EGTA infusions, 1,25(OH)2D3 or 24,25(OH)2D3 were IV administered. Transient (within 5 min) elevations in plasma PTH were observed in two of five animals following the administration of 1,25(OH)2D3 or of 24,25(OH)2D3. Neither secosterol had an effect on the induced elevations in plasma PTH during the remaining 60 min of the EGTA infusions. Twenty-two hr following 24,25(OH)2D3 administration, plasma PTH, ionized and total calcium, inorganic phosphate, and magnesium were normal, while plasma 24,25(OH)2D was elevated. The plasma PTH response to EGTA-induced hypocalcemia was not significantly altered from that observed prior to the administration of 24,25(OH)2D3. Animals, which were IV injected with 1,25(OH)2D3 received the same amount IM 60 min later. Twenty-two h following IM 1,25(OH)2D3, plasma 1,25(OH)2D, ionized and total calcium, and plasma inorganic phosphate were elevated. Plasma PTH and magnesium were lowered. The PTH response to EGTA-induced hypocalcemia was significantly reduced in these animals. A similar reduction in the PTH response to induced hypocalcemia was observed in animals receiving 7 hr IV infusions of calcium chloride. The findings suggest that the blunted response was, in part, the consequence of the preceding hypercalcemia. These results indicate that 1,25(OH)2D3 does not directly regulate plasma PTH secretion and that 24,25(OH)2D3 has no effect on plasma PTH during induced hypocalcemia in the bovine species.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
缺乏1,25-和24,25-二羟基维生素D对牛甲状旁腺激素对低钙血症反应的影响
1,25(OH)2D3或24,25(OH)2D3对EGTA诱导低钙血症后血浆甲状旁腺激素的影响。EGTA输注可在10分钟内引起血浆PTH升高。EGTA输注开始60分钟后,静脉给予1,25(OH)2D3或24,25(OH)2D3。在给予1,25(OH)2D3或24,25(OH)2D3后,5只动物中的2只观察到血浆甲状旁腺激素的短暂性(5分钟内)升高。在EGTA输注的剩余60分钟内,两种醇对血浆甲状旁腺激素的诱导升高均无影响。24,25(OH)2D3给药22小时后,血浆PTH、离子和总钙、无机磷酸盐、镁正常,而血浆24,25(OH)2D升高。血浆PTH对egta诱导的低钙血症的反应与服用24,25(OH)2D3之前的观察结果没有明显改变。动物静脉注射125 (OH)2D3, 60分钟后再注射等量的IM。注射1,25(OH)2D3后22 h,血浆1,25(OH)2D、游离钙和总钙、血浆无机磷酸盐升高。血浆甲状旁腺激素和镁降低。在这些动物中,甲状旁腺激素对egta诱导的低钙血症的反应显著降低。在接受7小时氯化钙静脉输注的动物中,观察到PTH对诱导低钙血症的反应也有类似的降低。研究结果表明,这种迟钝的反应部分是先前高钙血症的结果。这些结果表明,1,25(OH)2D3不直接调节血浆PTH分泌,24,25(OH)2D3对诱导低钙血症期间的血浆PTH没有影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Background review for the '2015 European guideline on the management of Chlamydia trachomatis infections'. Author index Keyword index Pathogenesis of osteopetrosis induced by rapid and slow onset plaque isolates of an avian osteopetrosis virus Dichloromethylene diphosphonate (Cl2MDP) reduces natural killer (NK) cell activity in mice
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1