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Sympathectomy alters bone architecture in adult growing rats

โœ Scribed by F. Pagani; V. Sibilia; F. Cavani; M. Ferretti; L. Bertoni; C. Palumbo; N. Lattuada; E. De Luca; A. Rubinacci; F. Guidobono


Book ID
102302937
Publisher
John Wiley and Sons
Year
2008
Tongue
English
Weight
192 KB
Volume
104
Category
Article
ISSN
0730-2312

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โœฆ Synopsis


Abstract

Sympathetic nervous system (SNS) fibres and ฮฑโ€ and ฮฒโ€receptors are present in bone, indicating that the SNS may participate in bone metabolism. The importance of these observations is controversial because stimulation or inhibition of the SNS has had various effects upon both anabolic and catabolic activity in this tissue. In this study we evaluated the effects of pharmacological sympathectomy, using chronic treatment of maturing male rats with 40 mg of guanethidine/kg i.p., upon various parameters in bone. Double labelling with tetracycline injection was also performed 20 and 2 days before sacrifice. Bone mass, mineral content, density and histomorphometric characteristics in different skeletal regions were determined. Bone metabolic markers included urinary deoxypyridinoline and serum osteocalcin measurements. Guanethidine significantly reduced the accretion of lumbar vertebral bone and of mineral content and density, compared to controls. Femoral bone mineral content and density were also significantly reduced, compared to controls. Histomorphometric analyses indicated these effects were related to a reduction of cortical bone and mineral apposition rate at femoral diaphysials level. Both markers of bone metabolism were reduced in controls as they approached maturity. Guanethidine significantly decreased serum osteocalcin compared to controls, while urinary deoxypyridinoline was unchanged. These data indicate that guanethidineโ€induced sympathectomy caused a negative balance of bone metabolism, leading to decreased mass by regulating deposition rather than resorption during modeling and remodeling of bone. J. Cell. Biochem. 104: 2155โ€“2164, 2008. ยฉ 2008 Wileyโ€Liss, Inc.


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