rhPTH(1-34)对成骨细胞增殖、Collagen I及Osterix mRNA表达的影响

目的 观察间歇给予重组人甲状旁腺激素(1-34)[rhPTH(1-34)]对体外成骨细胞增殖、I型胶原蛋白(CoHagen I)及Osterix mRNA表达的影响,初步探讨rhPTH(1-34)对体外成骨细胞的作用机制.方法 体外培养新生大鼠成骨细胞,间歇循环给予0、10-11、10-10、10-9、10-8、10-7 M rhPTH(1-34)干预,(24 h为一循环,前12h给药),共2次,用MTT法检测细胞的增殖;RT-PCR法半定量测定成骨细胞Collagen I、Ostefix mRNA的表达.结果 显示rhPTH(1-34)可明显促进成骨细胞的增殖(P<0.05),促进成骨细胞Collagen I和Ostefix mRNA表达(P<0.05),101-9 M增殖、表达最明显,呈剂量依赖关系.结论 rhPTH(1-34)可促进成骨细胞的增殖、分化,可能是通过Collagen I和Ostefix mRNA表达来调节.     

rhPTH（1-34）对成骨细胞增殖、CollagenⅠ及Osterix mRNA表达的影响

目的观察间歇给予重组人甲状旁腺激素(1-34)[rhPTH(1-34)]对体外成骨细胞增殖、Ⅰ型胶原蛋白(Collagen Ⅰ)及Osterix mRNA表达的影响,初步探讨rhPTH(1-34)对体外成骨细胞的作用机制。方法体外培养新生大鼠成骨细胞,间歇循环给予0、10-11、10-10、10-9、10-8、10-7M rhPTH(1-34)干预,(24 h为一循环,前12h给药),共2次,用MTT法检测细胞的增殖;RT-PCR法半定量测定成骨细胞Collagen Ⅰ、Osterix mRNA的表达。结果显示rhPTH(1-34)可明显促进成骨细胞的增殖(P<0.05),促进成骨细胞Collagen Ⅰ和Osterix mRNA表达(P<0.05),10-9 M增殖、表达最明显,呈剂量依赖关系。结论 rhPTH(1-34)可促进成骨细胞的增殖、分化,可能是通过Collagen Ⅰ和Osterix mRNA表达来调节。     

rhPTHl-34对成骨细胞增殖及BMP-7、BMP-9基因表达的影响

目的 研究重组人甲状旁腺激素1-34(rhPTH1-34)对成骨细胞增殖及BMP-7、BMP-9基因表达的影响.方法 通过不同剂量的重组人甲状旁腺素(rhPTH1-34)(0、10-11、10-10、10-9、10-8、10-7mol/L)间歇性(24 h/周期,前12 h rhPTH1-34干预)刺激体外培养的成骨细胞,用噻唑蓝(MTT)法检测细胞的增殖能力,RT-PCR法检测成骨细胞BMP-7、BMP-9基因的表达.结果 间歇性小剂量rhPTH1-34可明显促进成骨细胞的增殖能力及增强BMP-7、BMP-9基因的表达.结论 间歇性小剂量rhPTH1-34可促进成骨细胞增殖,可能与BMP-7、BMP-9基因表达相关.     

联合甲状旁腺激素和普萘洛尔对人成骨细胞增殖及OPG和RANKL mRNA表达的影响

目的 联合甲状旁腺激素(rhPTH 1-34)和普萘洛尔(PRO)处理体外培养的人松质骨源性成骨细胞(HOB),观察其对人成骨细胞增殖及骨保护素(OPO)和核因子KB受体活化因子配体(RANKL )基因表达的影响,探讨其对骨代谢影响的可能机制。方法 (1)以成人骼骨和股骨颈部松质骨为原料,分离培养原代人成骨细胞并对其鉴定。(2)以人成骨细胞为体外实验模型,固定浓度rhPTH1- 34 (50 ng/ml)和不同浓度PRO(0. 1μM,1μM,10μM)分别及联合刺激体外培养的人成骨细胞72 h后,采用CCK-8法检测细胞增殖能力,用实时荧光定量PCR法检测成骨细胞OPG和RANKL基因的表达。结果 rhPTH1-34和PRO单独给药均可促进成骨细胞增殖(P <0.05),在PRO 10μM时成骨细胞OPG基因的表达量增加(P<0.05),且大于RANKL基因的表达量;相反,联合rhPTH 1-34和PRO给药抑制成骨细胞增殖(P<0.05),并抑制成骨细胞OPG和RANKL基因的表达(P<0.05),且随着PRO浓度的增加,OPG和RANKL基因表达均呈下降趋势。结论 rhPTH1- 34和PRO单独给药均可促进成骨细胞增殖,而两者联合给药后却抑制了成骨细胞的增殖,可能是通过调控OPG和RANKL基因的表达来实现的。     

盐酸二甲双胍对人成骨细胞增殖及Collagen I 、 LRP5 mRNA表达的影响

目的观察不同浓度二甲双胍对体外培养人成骨细胞增殖、Collagen I及LRP5mRNA表达的影响,探讨二甲双胍对成 骨细胞作用的可能机制。方法不同浓度二甲双胍(0、25、50、100、200 ^mo^L)刺激体外培养人成骨细胞72 h,采用CCK~8比 色法检测细胞增殖情况,用荧光定量RT~PCR法检测Collagen I、LRP5mRNA表达。结果显示二甲双胍可促进其增殖（P < 0.05),并促进成骨细胞CollagenI及LRP5mRNA表达（P <0.05),在200 pmoVL时增殖、表达最明显,呈剂量效应关系。结 论二甲双胍在一定浓度范围内可促进人成骨细胞增殖,可能通过Wnt/LRP5信号通路增强Collagen I及LRP5mRNA的表达 来调控。     

甲状旁腺激素联合辛伐他汀对成骨细胞分化及OPG和RANKL mRNA表达的影响

目的联合甲状旁腺激素(rhPTH1-34)和辛伐他汀(SIM)在体外对乳鼠颅盖骨成骨细胞分化及骨保护素(OPG)和核因子κB受体活化因子配体(RANKL)基因表达的影响。方法以乳鼠成骨细胞为体外试验模型,rhPTH1-34(10-9mol/L)联合不同浓度SIM(10-8、10-7、10-6mol/L)作用于体外培养的乳鼠成骨细胞,采用对硝基苯磷酸盐(PNPP)法测定碱性磷酸酶(ALP)活性;RT-PCR法测定OPG和RANKL基因的表达。结果 rhPTH1-34和SIM单独给药均可促进成骨细胞ALP活性及OPG基因、降低RANKL基因表达(P0.05);两者联合后与SIM单独作用组比较,ALP活性明显增加,并能协同促进OPG、降低RANKL基因表达(P0.05)。结论 rhPTH1-34和SIM联合应用对成骨细胞分化和代谢有协同作用。     

低能体外冲击波和低剂量间歇人重组甲状旁腺激素1-34刺激对体外培养大鼠成骨细胞增殖分化的影响

目的探讨低能体外冲击波（ESW）和低剂量间歇人重组甲状旁腺素1-34（rhPTH1-34）对体外培养大鼠成骨细胞（ROBs）增殖和成骨分化的影响。方法分别用不同次数的低能ESW刺激、不同浓度及作用方式的rhPTH1-34刺激，以及ESW和低剂量间歇性rhPTH1-34刺激共同作用于ROBs后，用细胞计数、MTY和流式细胞术细胞周期分析检测ROBs的增殖，用酶标仪检测ALP活性，用免疫组化检测I型胶原表达来观察ROBs成骨分化。结果60～150次0．18mJ／mm^2 ESW刺激、间歇性rhPTH1-34（1×10^-11和1×10^-10 mol／L）刺激以及ESW＋间歇性rhPTH1-34（1×10^-11mol／L）刺激均可显著促进体外培养ROBs细胞增殖和成骨分化（与对照组比较，P〈0．05）；其中60～150次ESW刺激＋间歇性rhPTH1-34（1×10^-11 mol／L）刺激各组作用最强。结论适当的ESW应力刺激和低剂量间歇性rhPTH1-34刺激可显著促进体外培养ROBs细胞增殖和成骨分化，两者联合应用作用最强。     

瘦素对成骨细胞增殖及CollagenⅠ和Cbfa1 mRNA表达的影响

目的研究瘦素在体外对原代培养乳鼠颅盖骨成骨细胞增殖及对CollagenⅠ(Ⅰ型胶原蛋白)和Cbfa1 mRNA表达的影响。方法培养乳鼠成骨细胞,以乳鼠成骨细胞为体外实验模型,采用MTT法检测不同浓度瘦素(0、40、80和160ng/ml)作用于成骨细胞后的增殖情况;通过RT-PCR方法检测不同浓度瘦素对CollagenⅠ和Cbfa1 mRNA的表达的影响。结果瘦素作用于成骨细胞后,可促进其增值,OD值显著增加(P0.01);瘦素增加CollagenⅠ和Cbfa1 mRNA的表达,呈剂量效应关系。结论瘦素促进成骨细胞增殖,同时通过调节CollagenⅠ和Cbfa1的表达,促进成骨细胞分化,进而促进骨形成。     

胰岛素样生长因子-1对甲状旁腺激素介导成骨细胞增殖及成骨活性的影响

目的：通过构建乳鼠颅盖骨成骨细胞分离培养与鉴定方法,研究胰岛素样生长因子－1（Insulin－like growth factor－1,IGF－1）及IGF－1联合重组人甲状旁腺激素1－34（recombinant human parathyroid hormone 1－34,rhPTH1－34）对成骨细胞增殖及I型胶原蛋白mRNA表达的影响。方法培养乳鼠成骨细胞,并观察其形态及功能,以原代培养乳鼠成骨细胞为实验模型,分空白组、PTH组、IGF－1组及不同浓度IGF－1作用的PTH介导的成骨细胞组（0、10、50、100 ng／L）。通过不同剂量的胰岛素样生长因子－1（0、10、50、100 ng／L）联合10－9 mol／L重组人甲状旁腺素刺激体外培养的成骨细胞,用噻唑蓝（ MTT）法检测细胞的增殖能力,RT－PCR法检测成骨细胞I型胶原蛋白mRNA的表达。结果 PTH和IGF－1均可促进成骨细胞增殖;IGF－1联合PTH可以促进成骨细胞增殖,且具有剂量依赖性。 PTH联合IGF－1使成骨细胞增殖能力增强、I型胶原蛋白mRNA表达增强。 IGF－1可以促进成骨细胞I型胶原蛋白mRNA的表达,且具有剂量依赖性。 IGF－1可以促进成骨细胞I型胶原蛋白mRNA的表达,且具有剂量依赖性。结论 PTH与IGF－1均可刺激成骨细胞增殖和分化,IGF－1可促进PTH对成骨细胞的分化、增殖。两者合用其作用增强,有协同促进作用。     

甲状旁腺素羧基端肽段的表达及其对大鼠成骨细胞增殖的影响

目的：探讨 rhPTH1～84、rhPTH37～84及 hPTH1～34对大鼠成骨细胞增殖的影响。方法分子生物学方法克隆表达 hPTH1～84、hPTH37～84重组蛋白。体外培养的大鼠成骨细胞给予不同浓度的 PTH 作用后,采用噻唑蓝（MTT）法检测细胞增殖。结果获得了浓度约为261．82 mg／L 的 rhPTH1～84和浓度为165．45 mg／L 的rhPTH37～84。10－10～10－7 mol／L 范围的 rhPTH1～84和 hPTH1～34促进大鼠成骨细胞的增殖;rhPTH37～84则抑制大鼠成骨细胞增殖。结论成功获得了高浓度高纯度的 rhPTH1～84及 rhPTH37～84。rhPTH37～84抑制细胞增殖,为进一步研究甲状旁腺激素及其羧基端肽段的功能奠定了基础。     

国产重组人甲状旁腺素(1-34)对绝经后骨质疏松症的治疗作用研究

目的评价国产重组人甲状旁腺素(1-34)治疗绝经后骨质疏松症的临床疗效和安全性。方法入选绝经后骨质疏松症患者37例,年龄64.2±8.1岁,采用自身前后对照试验设计,每日皮下注射重组人甲状旁腺素(1-34)20μg,同时口服钙尔奇D600 0.6g/d,试验时间6个月,观察患者治疗前后骨密度变化、骨折发生情况,以及血尿常规、肝肾功、电解质、心电图改变等。结果试验期间有1例脱落;经过6个月治疗后,患者L1骨密度增加23.2%(P<0.05),L2骨密度增加18.0%(P<0.05),L3骨密度增加12.5%(P<0.05),L4骨密度增加19.9%(P<0.05),腰椎平均骨密度增加17.8%(P<0.05),股骨颈骨密度增加2.2%(P>0.05),大粗隆骨密度降低6.0%(P>0.05),Wards区骨密度降低1.3%(P>0.05);试验期间新发骨折2例,1例右肱骨骨折,另1例腰椎压缩骨折,无其他严重不良事件发生。结论重组人甲状旁腺素(1-34)治疗绝经后骨质疏松症有效,对腰椎骨密度改善显著,不良反应较轻。     

rhPTH(1-34)对骨质疏松大鼠的作用及对sclerostin的影响

[目的]探讨人重组甲状旁腺素1-34(rhPTH1-34)对骨质疏松的治疗作用以及与血钙、磷代谢和生长因子的关系。[方法]用摘除大鼠双侧卵巢的方式制备骨质疏松模型,实验动物分为3个组:模型对照组(OVX组,摘除大鼠双侧卵巢不作任何处理);rhPTH1-34治疗组(PTH组,摘除大鼠双侧卵巢12周后用rhPTH1-34治疗8周);假手术组(sham组,仅切除卵巢周围的脂肪组织约3 g,术后12周纳入实验)。应用第4代双能X线骨密度仪测量大鼠股骨上段骨密度值(BMD);用ELISA法测定血清硬化蛋白(sclerostin)水平及骨钙素(BGP)浓度;用自动生化仪测定血清碱性磷酸酶(ALP)。[结果]rhPTH1-34治疗组、sham组均较OVX组股骨上段骨密度增高,组间比较差异有显著性(P<0.01)。rhPTH1-34治疗组血清BGP浓度值升高及sclerostin值降低,与OVX组比较差异有显著性(P<0.01)。各组血清钙、磷含量无明显变化,与OVX组比较差异无显著性,ALP值治疗组与OVX组无明显差异。[结论]rhPTH1-34能够预防股骨上段骨密度丢失,并且血清BGP浓度值升高及sclerostin值降...     

Comparison of bone formation responses to parathyroid hormone(1-34), (1-31), and (2-34) in mice

In this study we used a mouse model system to compare the in vivo effects of parathyroid hormone(1-34) [PTH(1-34)] with that of PTH(1-31) or PTH(2-34) analogs. Daily subcutaneous administration of PTH(1-34) for 15 days caused a dose-dependent increase in the serum osteocalcin level and bone extract alkaline phosphatase activity, markers of bone formation. PTH(2-34) was much less potent, whereas PTH(1-31) was equipotent in stimulating bone formation parameters in mice. PTH(1-34) caused significant increases in serum calcium (after 4 h) and tartrate-resistant acid phosphatase activity in bone extract (after 4 h), whereas PTH(2-34) and PTH(1-31) were less potent. Because PTH(1-31) caused a smaller increase in bone resorption parameters compared to PTH(1-34), despite similar effects on bone formation parameters, we evaluated the long-term anabolic effects of PTH(1-31) and PTH(1-34) in mice. Weekly evaluations of serum osteocalcin levels demonstrated that daily injections of PTH(1-34) and PTH(1-31) at 80 microg/kg body weight increased serum osteocalcin levels within 1 week of the start of treatment, which were maintained during the entire 22 week treatment. Assessment of bone density at the end of the treatment period with peripheral quantitated computed tomography (pQCT) revealed that PTH(1-34) caused a significantly greater increase in femoral bone density compared to PTH(1-31) at the middiaphysis (18% vs. 9% over vehicle control; p < 0.001). Both PTH(1-34) and PTH(1-31) increased periosteal circumference compared to vehicle (p < 0.01) without a significant difference between the two treatments. In contrast, PTH(1-34) caused a significantly greater reduction in endosteal circumference than PTH(1-31) (p < 0.001). Both analogs significantly increased maximum load and area of moment of inertia over the vehicle group. In conclusion, our findings suggest that PTH(1-34) and PTH(1-31) may exhibit different anabolic effects at the periosteum vs. endosteum in the long bones of mice.     

Separate binding sites for intact PTH 1-84 and synthetic PTH 1-34 in canine kidney

Summary The present studies examine the characteristics of parathyroid hormone (PTH) receptor binding in canine basolateral renal cortical membranes using iodinated preparations of intact bovine PTH 1-84 and [Nle⁸, Nle¹⁸, Tyr³⁴] bPTH 1-34 amide. A solid phase lactoperoxidase technique was used to iodinate the bPTH 1-84. The PTH 1-34 analog was iodinated using chloramine T. Both radioligands were purified by reverse phase high pressure liquid chromatography (HPLC). Specific binding of¹²⁵I PTH 1-84 reached equilibrium at 3 hours whereas binding of the¹²⁵I PTH 1-84 analog reached equilibrium at 45 minutes. Excess bPTH 1-84 resulted in complete inhibition of binding of¹²⁵I bPTH 1-84, whereas 22±1.6% of the bound radioligand remained bound in the presence of excess synthetic bPTH 1-34. These data suggested the possibility of a binding site for the carboxy-terminal region of intact PTH, or binding sites selective for intact hormone. Therefore, additional studies were performed with PTH fragments, PTH 28-53, PTH 35-84, and PTH 53-84. In contrast to previous studies in other systems, these fragments did not result in significant displacement of¹²⁵I PTH 1-84. Analysis of binding of¹²⁵I PTH 1-84 and¹²⁵I [Nle⁸, Nle¹⁸, Tyr³⁴] PTH 1-34 amide, using LIGAND, both indicated a single site model with similar affinities. Thus, the data are consistent either with multiple receptors with similar affinities or a second binding site for bPTH 1-84 on the same receptor. In the canine kidney membranes, bPTH 1-84 and synthetic bPTH 1-34 were equipotent in activating adenylate, although the dose-response curve for bPTH 1-84 was shifted slightly to the right (Kact 2 nm for synthetic bPTH 1-34 versus 5 nm for bPTH 1-84). The present studies suggest that there are binding sites in canine kidney which are selective for the intact hormone and support the existence of more than one class of PTH receptors or a second binding site for intact PTH on a single PTH receptor.     

Comparison of Hypotensive Response following Intravenous Injection of Parathyroid Hormone 1-84 and 1-34 in Conscious Rats

Activation of parathyroid hormone 1 (PTH-1) receptors on vascular smooth muscle cells causes relaxation and decreases blood pressure in rats and humans. However, when PTH(1-84) and PTH(1-34) were injected in anesthetized rats, PTH(1-34) produced a greater decrease in blood pressure. This study quantified the dose-response relationship of the hypotensive response to intravenously injected PTH(1-84) and PTH(1-34) in conscious rats and assessed the role that the C-terminal region of PTH(1-84) played in the differences. Mean arterial pressure (MAP) decreased rapidly following injection of both peptides (0–100 nmol/kg) and reached a nadir at 1–2 minutes before increasing at a rate that was dose- and time-dependent. PTH(1-34) produced a greater hypotensive effect than PTH(1-84) at most doses tested and was significantly different from PTH(1-84) at 1–10 nmol/kg. The greatest difference in MAP decrease between PTH(1-84) and PTH(1-34) (24 and 35 mm Hg, respectively) occurred at 10 nmol/kg. Median effective dose (ED₅₀) values for PTH(1–84) and PTH(1-34) were significantly different (5.9 and 1.3 nmol/kg, respectively). The C-terminal PTH fragments PTH(7–84), PTH(39–84), and PTH(53–84) did not affect MAP when injected alone (10 nmol/kg), nor did they influence the hypotensive response when given at a 10–fold molar excess in combination with PTH(1-84) or PTH(1-34) (1.4 nmol/kg). In conclusion, PTH(1-84) is a less potent but, because it induced the same maximum response, not a less efficacious hypotensive agent than PTH(1-34) when administered by bolus intravenous injection in conscious rats. We found no evidence to support the concept that the C-terminal region of PTH is responsible for this difference in potency.     

Natriuresis and cyclic GMP stimulation by parathyroid hormone 1-34 in man

Synthetic human parathyroid hormone (PTH 1-34) was infused into seven healthy adults and their renal responsiveness examined. Blood and urine were collected at time zero and at 30 and 60 min after the infusion of PTH 1-34 (15μg in 50 ml of glucose solution infused in 10 min). A highly significant and parallel rise in both cyclic GMP and sodium excretion was found. No variation in blood atrial natriuretic factor concentration could be detected thereby suggesting that cyclic GMP is directly stimulated by PTH 1-34 and may play a role in the natriuretic effect of PTH.     

Safety and Efficacy of PTH 1-34 and 1-84 Therapy in Chronic Hypoparathyroidism: A Meta-Analysis of Prospective Trials

Hypoparathyroidism is the only endocrine deficiency for which hormone replacement therapy is not the standard of care. Although conventional treatments may control hypocalcaemia, other complications such as hyperphosphatemia, kidney stones, peripheral calcifications, and bone disease remain unmet needs. This meta-analysis (PROSPERO registration number CRD42019126881) aims to evaluate and compare the efficacy and safety of PTH₁₋₃₄ and PTH₁₋₈₄ in restoring calcium metabolism in chronic hypoparathyroidism. EMBASE, PubMed, and CENTRAL databases were searched for randomized clinical trials or prospective studies published between January 1996 and March 2021. English-language trials reporting data on replacement with PTH₁₋₃₄ or PTH₁₋₈₄ in chronic hypoparathyroidism were selected. Three authors extracted outcomes, one author performed quality control, all assessed the risk of biases. Overall, data from 25 studies on 588 patients were analyzed. PTH therapy had a neutral effect on calcium levels, while lowering serum phosphate (−0.21 mmol/L; 95% confidence interval [CI], −0.31 to −0.11 mmol/L; p < 0.001) and urinary calcium excretion (−1.21 mmol/24 h; 95% CI, −2.03 to −0.41 mmol/24 h; p = 0.003). Calcium phosphate product decreased under PTH₁₋₈₄ therapy only. Both treatments enabled a significant reduction in calcium and calcitriol supplementation. PTH therapy increased bone turnover markers and lumbar spine mineral density. Quality of life improved and there was no difference in the safety profile between PTH and conventionally treated patients. Results for most outcomes were similar for the two treatments. Limitations of the study included considerable population overlap between the reports, incomplete data, and heterogeneity in the protocol design. In conclusion, the meta-analysis of data from the largest collection to date of hypoparathyroid patients shows that PTH therapy is safe, well-tolerated, and effective in normalizing serum phosphate and urinary calcium excretion, as well as enabling a reduction in calcium and vitamin D use and improving quality of life. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).     

Differential effects of intermittent PTH(1-34) and PTH(7-34) on bone microarchitecture and aortic calcification in experimental renal failure

PTH(1-84) and PTH(7-84) are elevated in chronic kidney disease (CKD). These peptides, as their shorter analogs PTH(1-34) and PTH(7-34) both promote PTH receptor (PTH1R) internalization but only PTH(1-34) and PTH(1-84) activate the receptor. Here, we examined the effects of intermittent administration of PTH(1-34) and PTH(7-34) on mineral ion metabolism, bone architecture, and vascular calcification in rats with experimental CKD. CKD with or without parathyroidectomy (PTX) was established by 5/6 nephrectomy (NPX) in rats. Animals were divided into 4 groups: Sham PTX+ sham NPX (Sham); PTX+ sham NPX (PTX); Sham PTX+NPX (NPX); PTX+NPX (PTX/NPX). Rats were treated with single daily doses of 40 microg/kg PTH(1-34), PTH(7-34), or vehicle. Creatinine was higher in NPX and Ca lower in PTX and PTX/NPX groups than in Sham or NPX rats. Plasma phosphate was higher in PTX, NPX and PTX/NPX than in Sham rats. PTH(1-34) was more hypercalcemic than PTH(7-34) in PTX rats. Fractional bone volume in rats treated with PTH(1-34) increased significantly in all groups compared to that of vehicle treatment. In addition, trabecular number, thickness and volumetric bone density increased in rats treated with PTH(1-34). In contrast, PTH(1-34) diminished vascular calcification. Bone and renal PTH1R mRNA expression was reduced as much or more in PTX/NPX rats as in NPX alone, whereas PTH(7-34) had no effect on PTH1R expression. Renal but not bone PTH1R mRNA increased in response to PTH(1-34). These findings suggest that PTH(1-34) exerts greater hypercalcemic and anabolic effects in parathyroidectomized and/or nephrectomized rats than does PTH(7-34). There was no evidence for significant bone or vascular actions of PTH(7-34). We conclude that PTH(1-34) protects against vascular calcification and bone demineralization in experimental renal failure.