期刊
CELL BIOCHEMISTRY AND FUNCTION
卷 34, 期 2, 页码 52-62出版社
WILEY-BLACKWELL
DOI: 10.1002/cbf.3164
关键词
parathyroid hormone; bone blood flow; nitric oxide; vasodilation; cortical bone
资金
- Arthritis Research UK
- BBSRC [BB/I014608/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/I014608/1] Funding Source: researchfish
- Versus Arthritis [20581] Funding Source: researchfish
There is strong evidence that vasodilatory nitric oxide (NO) donors have anabolic effects on bone in humans. Parathyroid hormone (PTH), the only osteoanabolic drug currently approved, is also a vasodilator. We investigated whether the NO synthase inhibitor L-NAME might alter the effect of PTH on bone by blocking its vasodilatory effect. BALB/c mice received 28 daily injections of PTH[1-34] (80 mu g/kg/day) or L-NAME (30mg/kg/day), alone or in combination. Hindlimb blood perfusion was measured by laser Doppler imaging. Bone architecture, turnover and mechanical properties in the femur were analysed respectively by micro-CT, histomorphometry and three-point bending. PTH increased hindlimb blood flow by >30% within 10min of injection (P<0.001). Co-treatment with L-NAME blocked the action of PTH on blood flow, whereas L-NAME alone had no effect. PTH treatment increased femoral cortical bone volume and formation rate by 20% and 110%, respectively (P<0.001). PTH had no effect on trabecular bone volume in the femoral metaphysis although trabecular thickness and number were increased and decreased by 25%, respectively. Co-treatment with L-NAME restricted the PTH-stimulated increase in cortical bone formation but had no clear-cut effects in trabecular bone. Co-treatment with L-NAME did not affect the mechanical strength in femurs induced by iPTH. These results suggest that NO-mediated vasorelaxation plays partly a role in the anabolic action of PTH on cortical bone. Copyright (c) 2016 John Wiley & Sons, Ltd.
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