性腺甾体激素对雌,雄大鼠下丘脑血管升压素mRNA水平的影响

实验用１０－１１周龄经阉割的雌、雄Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠进行。以３末端异羟基洋地黄毒甙标记的２６个碱基长的寡核苷酸作为检测探针,用核酸斑点杂交技术检测大鼠下丘脑血管升压素ｍＲＮＡ水平。在假手术对照组,雄性大鼠下丘脑ＡＶＰｍＲＮＡ水平经雌性大鼠高４５％（Ｐ〈０．０５）,血浆渗透压高于雌性大鼠（Ｐ〈０．０５）。摘除卵巢的大鼠下丘脑ＡＶＰｍＲＮＡ深恶痛绝经假手术组雌性大鼠高３０％（Ｐ〈０．０５     

束缚应激对大鼠下丘脑室旁核、视上核一氧化氮合酶活性的影响

目前已知下丘脑是应激反应的关键性调节中枢,下丘脑内一氧化氮是否参与应激反应尚未见报道。本文运用ＮＡＤＰＨ－ｄ酶组化技术和计算机图象分析方法,对束缚应激大鼠下丘脑室旁核（ＰＶＮ）和视上核（ＳＯＮ）一氧化氮合酶（ＮＯＳ）阳性神经元的相对切面面积和平均灰度进行了分析。结果显示,大鼠在急性束缚应激４小时后,其下丘脑ＰＶＮ和ＳＯＮ内的ＮＯＳ阳性神经元的平均灰度值与正常大鼠比较均明显降低（Ｐ＜０．００１）;ＳＯＮ的ＮＯＳ阳性神经元的相对切面面积明显大于正常大鼠（Ｐ＜０．００１）,但ＰＶＮ的ＮＯＳ阳性神经元的相对切面面积未见明显改变（Ｐ＞０．０５）。以上结果说明束缚应激使大鼠下丘脑ＰＶＮ和ＳＯＮ的ＮＯＳ活性增强     

大鼠排卵前促性腺激素释放激素释放过程中下丘脑前阿黑皮素基因表达和雌激素受体的水平

在大鼠动情前期促黄体生成激素峰形成前后测定了血清雌、孕激素水平变化、下丘脑正中隆起促黄体生成激素释放激素含量及弓状核区雌、孕激素受体密度改变和弓状核前阿黑皮素ｍＲＮＡ水平变化。结果表明：动情前期１４小时时血清雌激素水平开始升高（Ｐ＜００５）,于１６小时时达高峰。此时弓状核雌激素受体密度降低（Ｐ＜００５）,孕激素受体密度增加（Ｐ＜００５）,前阿黑皮素ｍＲＮＡ水平减少（Ｐ＜００５）。前阿黑皮素ｍＲＮＡ水平与血清雌激素及正中隆起的促性腺激素释放激素水平呈负相关（Ｐ值分别小于００１及００５）,与弓状核雌激素受体密度变化呈正相关（Ｐ＜００１）。提示弓状核的前阿黑皮素ｍＲＮＡ水平在此过程中可能受雌激素及其受体调控,下丘脑β内啡肽合成减少可能参与了排卵前促性腺激素释放激素／促黄体生成激素峰的形成。     

粉防己碱抑制血管平滑肌细胞增殖及对HSP70和p53表达的影响

目的：观察粉防己碱（Ｔｅｔ）对ＶＳＭＣ增殖的作用及对热应激蛋白７０ｋｄ（ＨＳＰ７０）及其ｍＲＮＡ和抑癌基因ｐ５３ｍＲＮＡ的影响。方法：用内皮素建立培养的血管平滑肌细胞增殖模型。采用氚－胸腺嘧啶核苷（［３Ｈ］ＴｄＲ）掺入法流式细胞术,Ｗｅｓｔｅｒｎ及Ｎｏｒｔｈｅｒｎｂｌｏｔ杂交方法。结果：Ｔｅｔ能逆转内皮素所致的［３Ｈ］ＴｄＲ掺入量增多（Ｐ＜０．０１）,阻止血管平滑肌细胞由静止期（Ｇ０／Ｇ１期）进入ＤＮＡ合成期（Ｓ期）和有丝分裂期（Ｇ２／Ｍ期）,并能逆转内皮素引起的ＨＳＰ７０及ｍＲＮＡ表达增强（Ｐ＜０．０１或Ｐ＜０．０５）,ｐ５３抑癌基因ｍＲＮＡ表达减弱（Ｐ＜０．０５）。结论：Ｔｅｔ能抑制血管平滑肌细胞增殖,与ＨＳＰ７０及ｐ５３的调控有关     

心衰心脏收缩蛋白分子变化及与收缩力的关系

采用ＤＯＣＡ硅胶管皮下埋入法建立大鼠心衰模型,从基因转录水平检测正常与心衰大鼠心肌组织中心肌收缩蛋白分子基因α－ＭＨＣ、β－ＭＨＣ、α－ｃａｒｄｉａｃａｃｔｉｎ、α－ｓｋｅｌｅｔａｌａｃｔｉｎ表达的变化。结果显示：（１）心衰大鼠心肌收缩力指标ｄｐ／ｄｔｍａｘ较正常大鼠明显降低（下降２７．５１％,Ｐ＜０．０１）,（２）心衰大鼠与正常大鼠相比,心肌组织中α－ＭＨＣ基因表达水平显著下降（降低２１．４３％,Ｐ＜０．０５）,β－ＭＨＣ基因表达水平显著升高（升高６２．４３％,Ｐ＜０．０１）、α－ｃａｒｄｉａｃａｃｔｉｎ基因和α－ｓｋｅｌｅｔａｌａｃｔｉｎ基因表达水平未见明显改变,（３）α－ＭＨＣｍＲＮＡ的含量与心肌收缩力指标ｄｐ／ｄｔｍａｘ值之间存在正相关关系（ｒ＝０．４１４３,ｎ＝４３,Ｐ＜０．０５）,β－ＭＨＣｍＲＮＡ的含量与ｄｐ／ｄｔｍａｘ值之间存在负相关关系。（ｒ＝－０．３９０２,ｎ＝４３,Ｐ＜０．０５）。这提示：心肌组织中ＭＨＣ基因表达水平的改变是心衰时心肌收缩力降低的主要分子基础     

维生素A缺乏胎鼠作为先天性心脏病动物模型的实验研究

目的　探讨将维生素Ａ缺乏（ＶＡＤ）胎鼠作为先天性心脏病动物模型的可行性。方法取１１－１９ｄ不同胎龄正常及ＶＡＤ胎鼠心脏经石蜡包埋、切片及 ＨＥ染色观察其发育情况。结果 １．实验组饲料含维生素Ａ（ＶＡ）７μｇ／１００ｇ,经ＶＡＤ饮食喂养后实验组大鼠血清ＶＡ水平明显低于对照组［（０．１６８±０．０５９）μｍｏｌ／Ｌ Ｖｓ（２．１８±０．２３）μｍｏｌ／Ｌ,ｔ＝３２．８８, Ｐ＜０．００１］。 ２．大鼠死亡百分比：饲养于屏障系统的ＶＡＤ大鼠死亡百分比较饲养于开放系统中的要低４．６倍（１０％ Ｖｓ ４５．８３％．ｘ ２＝１６．６４, Ｐ＜０．００１）,对照组为０。 ３．实验组大鼠受孕百分比及每只孕鼠产仔数均低于对照组［５８．３３％ Ｖｓ ８１．５％, ｘ ２＝４．３７,Ｐ＜０．０５：（６．９７±２．７９） Ｖｓ（１３ ±１．０５）,ｔ＝７．１６, Ｐ＜０．００１］。 ４．经切片观察１１～１５ ｄ胎龄胎鼠实验组心脏出现明显发育延迟的占３６．６７％, １６～１９ ｄ胎龄胎鼠实验组心脏畸形占４１．４３％,血管异常占１８．５７％。结论ＶＡＤ胎鼠可用来作为先天性心脏病动物模型,但需改进饲养环境以减少异常死亡。     

人主动脉硫酸乙酰肝素蛋白聚糖对培养的人血管壁细胞生长的作用

通过培养的人主动脉平滑肌细胞（ｈＡＳＭＣ）及脐静脉内皮细胞（ｈＵＶＥＣ）,应用３Ｈ－ＴｄＲ参入、Ｎｏｒｔｈｅｒｎｂｌｏｔ分析、逆转录多聚酶链反应（ＲＴ－ＰＣＲ）、放射免疫分析（ＲＩＡ）、和紫外比色法等技术观察了人主动脉中硫酸乙酰肝素蛋白聚糖（ＨＳＰＧ）对ｈＡＳＭＣ和ｈＵＶＥＣＤＮＡ合成的作用及对血小板源生长因子（ＰＤＧＦ）、ＰＤＧＦ受体、转化生长因子β（ＴＧＦ－β）、内皮素－１（ＥＴ－１）或碱性成纤维细胞生长因子（ｂＦＧＦ）基因表达和肾素－血管紧张系统（ＲＡＳ）的影响,结果显示,ＨＳＰＧ明显抑制培养的ｈＡＳＭＣ基础的ＤＮＡ合成（ｃｐｍ值为：１０３８５±３２６３ｖｓ,２５５４１±６４２１,Ｐ＜０．０１）及外源性ＰＤＧＦ诱导的ＤＮＡ合成（ｃｐｍ值为：９８７８±１９４７ｖｓ．１３４８１±４４ｌ０,Ｐ＜０．０５）;抑制ＰＤＧＦＡ链、ＴＧＦ－Ｂｐ和ＥＴ－１ｍＲＮＡ表达,提高ＰＤＧＦａ和β受体ｍＲＮＡ的表达;显著降低ｈＡＳＭＣ培养液中血管紧张素Ⅱ（ＡｎｇⅡ）的浓度和血管紧张素转换酶（ＡＣＥ）的活性,推测ＨＳＰＧ抑制ＰＤＧＦＡ链、ＴＧＦ－β及ＥＴ－１ｍＲＮＡ表达,降低ＡＣＥ活性及ＡｎｇⅡ浓度是其抑制ｈＡＳＭＣ增殖的重要机     

电磁脉冲对大鼠学习和脑内神经递质的影响

探讨电磁脉冲（ＥＭＰ）对大鼠神经系统的效应。实验采用Ｗｉｓｔａｒ大鼠,ＥＭＰ辐照后不同时间用Ｙ－型迷宫测其学习能力,高效液相色谱法检测脑不同部位的神经递质含量。与假照射组（对照组）相比,照后三天内各测定组大鼠学习能力降低（Ｐ＜０．０５）,其中照射后第１天组的海马内５－羟色胺（５－ＨＴ）和多巴酸（ＤＯＰＡＣ）含量升高（Ｐ＜０．０５）,下丘脑多巴胺（Ｄｏｐａｍｉｎｅ）含量升高（Ｐ＜０．０５）,肾上腺素（Ａｄｒ）含量降低;照后２天组海马Ａｄｒ含量降低（Ｐ＜０．０５）,海马５－ＨＴ含量升高（Ｐ＜０．０５）;照后３天组海马内Ａｄｒ含量降低（Ｐ＜０．０５）。ＥＭＰ能够改变大鼠不同脑区神经递质的含量,降低大鼠学习能力     

CCK-8对癫痫发作大鼠脑内SOD和MDA的影响

目的和方法：采用核团微量注射、光化学分析等实验方法,观察大鼠脑内ＳＯＤ和ＭＤＡ在ＣＣＫ－８调节癫痫发作中的变化。结果：①与下沉大鼠比较,遗传性听源性癫痫易感大鼠皮层、海马、下丘脑及垂体内ＳＯＤＦ活性、ＭＤＡ含量无显著差异（Ｐ＞０．０５）;②大鼠癫痫发作后,上述区域内ＳＯＤ活性明显降低（Ｐ＜０．０５）,而ＭＤＡ含量明显增加（Ｐ＜０．０５）,若癫痫发作次数增加,该变化愈显著（Ｐ＜０．０１）;③大鼠海马     

海马胆囊收缩素对大鼠癫痫发作的影响及其机制

目的和方法：采用原位杂交技术,观察遗传性听源性癫痫易感大鼠海马内ＣＣＫｍＲＮＡ表达的改变及少我注射ＣＣＫ３及其受体阻断剂对大鼠癫痫发作的影响。结果：（１）癫痫发作大鼠海马内ＣＣＫｍＲＮＡ表达明显增强（Ｐ〈０．０５－０．０１）,但癫痫反复发作的大嫌海马内ＣＣＫｍＲＮＡ表达的较癫痫发作一次大鼠明显减少（Ｐ〈０．０５）,海马ＣＡ主射Ｌ３６５后,ＣＣＫ８压抑癫痫发作的作用消失（Ｐ〈０．０１）。结论：ＣＣＫ     

Vasopressin V1a, V1b and V2 receptors mRNA in the kidney and heart of the renin transgenic TGR(mRen2)27 and Sprague Dawley rats.

Vasopressin plays significant role in regulation of blood pressure by means of V1 and V2 receptors, however regulation of synthesis of these receptors in hypertension is only poorly recognized. The purpose of the present study was to compare expression of V1a, V1b and V2 vasopressin (R) mRNA in the renal cortex, renal medulla and the heart of hypertensive renin transgenic TGR(mRen2)27 rats (TGR) and of their parent normotensive Sprague Dawley (SD) strain. The study was performed on 12 weeks old TGR and SD rats. Competitive PCR method was used for quantitative analysis of V1a, V1b and V2 receptors mRNA in fragments of renal cortex, renal medulla and apex of the left ventricle of the heart. In both strains expression of V1aR and V2R mRNA was significantly greater in the renal medulla than in the renal cortex. In the renal medulla but not in the cortex expression of V1aR mRNA was significantly greater in TGR than in SD rats. V2R mRNA expression was similar in the renal cortex and renal medulla of both strains. V1aR mRNA was well expressed in the heart of SD and TGR rats, however there was no significant difference between these two strains. V2R mRNA was not present in the heart. V1bR mRNa could not be detected either in the kidney or in the heart. The results provide evidence for specific increase of expression of V1a receptors mRNA in the renal medulla of TGR rats.     

3H]desGly-NH2(9)-d(CH2)5[D-Ileu2,Ileu4]AVP: an AVP V2 receptor antagonist radioligand

Binding characteristics of the selective V₂ antagonist radioligand [³H]desGly-NH₂⁹-d(CH₂)₅[D-Ileu²,Ileu⁴]AVP to rat kidney were determined. Binding was specific, saturable and reversible. The peptide bound to a single class of high-affinity binding sites with B_max 69.4±6.8 fmol/mg protein and K_D 2.8±0.3 nM. AVP and other related peptides displaced [³H]desGly-NH₂⁹-d(CH₂)₅[D-Ileu²,Ileu⁴]AVP binding. The order of potency of inhibition was desamino-D-AVP > AVP > d(CH₂)₅[D-Ileu²,Ileu⁴]AVP > oxytocin > d(CH₂)₃[Tyr(Me)²]AVP > d(CH₂)₅[sarcosine⁷]AVP, which is typical of a selective V₂ radioligand. Autoradiographic localization of [³H]desGly-NH₂⁹-d(CH₂)₅[D-Ileu²,Ileu⁴]AVP binding sites in kidney showed dense binding in the inner and outer medulla with less binding in the cortex, which is consistent with known renal V₂ receptor distribution.     

Detection of bikunin mRNA in limited portions of rat brain.

Tissue distribution of bikunin mRNA, which encodes a Kunitz-type serine protease inhibitor of the inter-alpha-inhibitor family (IalphaI), was studied in rats and mice by the reverse-transcripsion polymerase chain reaction (RT-PCR). We found that the liver as well as other tissues, such as the kidney, testis and adrenal gland, expressed bikunin mRNA. Although signals of bikunin mRNA were faint in the whole brain of rats and mice, distinct signals were found in limited portions of rat brain, such as the hippocampus, cerebral cortex and pituitary, but undetectable in cerebellum, medulla oblongata, hypothalamus, striatum, midbrain and choroid plexus. In three distinct types of cells, such as neurons, astrocytes and meningeal cells, in primary cultures isolated from the cerebral cortex and meninges of 1-day-old newborn rats, only neurons positively expressed bikunin mRNA. These results suggest that, in addition to peripheral tissues, neurons in the hippocampus and cerebral cortex produce bikunin, suggesting a potential role of bikunin/IalphaI family in these brain regions.     

Mitochondrial respiration in heart, liver, and kidney of copper-deficient rats

Morphological observations in some tissues indicate that dietary copper deficiency results in structural damage to mitochondria. The purpose of this study was to determine whether mitochondrial function is impaired as well. Male, weanling Sprague-Dawley rats were fed diets deficient or sufficient in copper for 4 weeks. Mitochondria were isolated from heart, liver, kidney cortex, and kidney medulla. P/O ratio, state 3 and state 4 respiration rates (oxygen consumed in the presence and absence of ADP, respectively), and acceptor control index (ratio of state 3:state 4) were determined using succinate or pyruvate/malate as substrate. State 3 respiration rate in mitochondria from copper-deficient hearts and livers was lower than in mitochondria from copper-sufficient hearts. Copper deficiency reduced the state 4 respiration rate only in cardiac mitochondria. Neither respiration rate was affected by copper deficiency in mitochondria from kidney medulla or cortex. P/O ratio was not significantly affected by copper deficiency in any tissue examined. Acceptor control index was reduced only in liver mitochondria. The observed decreases in respiration rates are consistent with decreased cytochrome c oxidase activity, shown by others to occur in mitochondria isolated from hearts and livers of copper-deficient rats.     

自发性高血压大鼠心脏与红细胞L-Arg转运的改变

研究自发性高血压大鼠 (spontaneouslyhypertensiverats ,SHR)心脏L 精氨酸 /一氧化氮 (L Arg/NO)系统的改变及其与红细胞L Arg转运的关系。检测 12周龄 (W)、16W、captopril治疗 4周后的 16WSHR (SHR C)及同龄Wistar Kyoto (WKY)大鼠心脏的L Arg转运、tNOS活性、NO 2 NO 3 和cGMP含量以及红细胞L Arg转运的改变。结果显示 ,SHR心室肌组织L Arg高亲和转运成分的最大转运速率 (Vmax)及低亲和转运成分的米氏常数 (Km)均明显低于WKY大鼠 ;但高亲和转运成分的Km 值和低亲和转运成分的Vmax则无明显改变 ;SHR C组的改变基本同 12W组。心肌组织tNOS活性的变化无统计学意义。NO 2 NO 3 及cGMP含量则分别较WKY组降低 2 4 6 %、19 8% (P >0 0 5 ,P <0 0 5 ,12W组 ) ,5 2 5 %、6 0 4% (P <0 0 1,P <0 0 1,16W组 )和 14 8%、2 3 % (P >0 0 5 ,P <0 0 5 ,SHR C组 )。tNOS活性、cGMP含量与LVW/BW呈负相关 ,r=0 45 0 7,P =0 0 5 (NOS) ,r=0 6 898,P <0 0 1(cGMP)。红细胞L Arg转运的改变与心脏一致 ,且其Vmax与心肌组织高亲和转运成分的Vmax呈正相关 ,r=0 5 6 0 6 ,P =0 0 1;与LVW /BW呈负相关 ,r=- 0 6 2 31,P <0 0 1。以上结果表明 ,SHR心室肌组织L Arg/NO系统活动被抑制 ,其抑制程度与心肌肥厚     

Differential regulation of central vasopressin receptors in transgenic rats with low brain angiotensinogen

The consequences of permanent alteration to the brain renin-angiotensin system (RAS) on central vasopressinergic system was studied in transgenic rats with low brain angiotensinogen [TGR(ASrAOGEN)]. Levels of vasopressin (AVP) and V1a receptor mRNAs were measured by ribonuclease protection assay (RPA) and AVP by radioimmunoassay (RIA). AVP (100 pmol/50 nl) was microinjected into the nucleus tractus solitarii (NTS) of urethane-anesthetized TGR(ASrAOGEN) and Sprague-Dawley (SD) rats and the mean arterial pressure (MAP) and heart rate (HR) baroreflex induced by phenylephrine were evaluated. AVP but not its mRNA levels were significantly lower in the hypothalamus and hypophysis of TGR(ASrAOGEN) rats. Brainstem V1a mRNA levels were significantly higher in TGR(ASrAOGEN) in comparison to SD rats (5.2+/-0.4% vs. 3.3+/-0.2% of beta-actin mRNA, P<0.05). In contrast, the hypothalamic V1a mRNA levels in TGR(ASrAOGEN) were not different from those found in SD rats. AVP microinjections induced a greater decrease in MAP in TGR(ASrAOGEN) in comparison with SD rats (-19.9+/-5.2 vs. -7.5+/-0.7 mm Hg, P<0.01). The significantly higher baroreflex sensitivity observed in TGR compared to that of SD rats was normalized after AVP microinjection. The increased brainstem V1a mRNA levels and sensitivity to AVP in TGR(ASrAOGEN) rats indicates a functional upregulation of AVP receptors in the NTS. The fact that the hypothalamic V1a mRNA levels are not altered indicates that these receptors are differentially regulated in different brain regions. This study demonstrates that a permanent deficit in brain angiotensinogen synthesis can alter the functionality of central vasopressinergic system.     

Enhanced binding of 3H-arginine8-vasopressin in the Brattleboro rat

Specific binding sites for 3[H]-arginine8-vasopressin (AVP) were characterized using membrane preparations of liver, renal medulla and brain (septal) tissue of heterozygous (HE) and homozygous (HO) Brattleboro (BB) rats. Measurement of binding sites indicated that significantly greater numbers of AVP receptors are present in the liver and septum of HO-BB rats. Similar numbers of AVP receptors were present in renal medullary tissue from HO-BB and HE-BB rats. Higher equilibrium dissociation constants were measured in the HO-BB septal tissue indicating a lower affinity of the brain receptor for 3[H]-AVP than in heterozygotes. No significant differences in AVP receptor affinity were noted in liver or kidney tissue. It is concluded that "up-regulation" of AVP receptor number and, in the brain, alterations in AVP receptor affinity may occur in the absence of endogenous AVP.     

Alteration of renal adrenomedullin and its receptor system in the severely hypertensive rat: effect of diuretic

OBJECTIVE: We investigated the pathophysiological role of the renal adrenomedullin (AM) system, including the ligand, receptor, and amidating activity, in severe hypertensive rats. METHOD: We studied three groups: control Wistar Kyoto rats (WKY), spontaneously hypertensive stroke-prone rats (SHR-SP), and diuretic-treated SHR-SP. We measured AM-mature, active form, and AM-total (active form+inactive form) in plasma and renal tissues, and mRNA levels of AM and AM receptor system components such as calcitonin receptor-like receptor (CRLR), receptor activity-modifying protein (RAMP) 2, and RAMP3 in renal tissues. RESULTS: SHR-SP had higher blood pressure, plasma neurohumoral factors, and lower renal function than WKY. SHR-SP had higher AM-mature and AM-total levels in plasma and renal tissues than WKY. Although the plasma AM-mature/AM-total ratio was similar in the two groups, AM-mature/AM-total ratio in renal tissues was higher in SHR-SP than in WKY. In addition, mRNA levels of AM in the renal cortex and medulla and the mRNA levels of CRLR, RAMP2, and RAMP3 in the renal cortex were higher in SHR-SP than in WKY. Chronic diuretic treatment decreased blood pressure and improved kidney function and neurohumoral factors, with reductions in plasma and renal AM system. CONCLUSION: Upregulation of circulating and renal AM system may modulate pathophysiology in SHR-SP.     

Postmortem biochemical indices of antemortem hemorrhagic shock

The purpose of this study was to determine if the perturbations in two glycolytic metabolites that occur during hemorrhagic shock can be used as discriminatory postmortem indicators of death resulting from severe hemorrhagic shock. Two groups of male albino Sprague-Dawley rats were hemorrhaged by withdrawing either 40% (Group I) or 45% (Group II) of the total blood volume. Glycogen and lactate concentrations were determined at 0 and 48 hr postmortem in the following tissues and organs: diaphragm, heart, liver, kidney cortex, and kidney medulla. The differences in lactate and glycogen in Group I at 0 hr were not significantly different from the nonhemorrhaged controls, with the exception of the lower liver glycogen concentration (58% of control). In Group II glycogen concentration was significantly reduced at 0 hr in the diaphragm (70% of control), liver (37%), and kidney medulla (55%). Lactate concentration was higher in all tissues examined by 270-640%; within 48 hr all tissues for both control and hemorrhaged animals had declined to baseline levels of glycogen concentration, whereas lactate levels had increased as much as 34-fold. There were no highly significant differences in glycogen at 48 hr between the control and hemorrhaged groups. In Group II the lactates were similar for both the control and hemorrhaged animals with the exception of the higher concentrations in the kidney cortex (54%) and medulla (41%). It was concluded from these findings that although significant metabolic perturbations are present at the time of death due to hemorrhage these differences do not persist up to 48 hr postmortem, with the possible exception of the kidney lactate concentrations.     

Calcium-binding protein regucalcin mRNA expression in the kidney cortex is suppressed by saline ingestion in rats

The effect of adrenalectomy (ADX) or saline ingestion, which is a hypertensive factor, on the expression of calcium-binding protein regucalcin mRNA in the kidney cortex of rats was investigated. The change of regucalcin mRNA levels was analyzed by Northern blotting using rat liver regucalcin complementary DNA (0.9 kb of open-reading frame). Regucalcin mRNA was expressed in the kidney cortex but not the medulla. Rats were adrenalectomized, and 48 h later they were sacrificed. ADX caused a reduction of regucalcin mRNA levels in the kidney cortex, suggesting that adrenal glands participate in the regulation of the mRNA expression. This reduction was not restored by the subcutaneous administration of dexamethasone with an effective dose (1 mg/kg body weight), which can stimulate kidney regucalcin mRNA expression. Regucalcin mRNA levels in the kidney cortex of rats were markedly suppressed by the ingestion of saline for 7 days. The ADX-induced decrease of renal cortex regucalcin mRNA levels was not appreciably restored by saline ingestion. Moreover, regucalcin mRNA levels in the kidney cortex of spontaneous hypertensive rats (SHR) were clearly decreased as compared with that of control (Wistar-Kyoto) rats. Meanwhile, calcium content in the kidney cortex was not significantly decreased by ADX or saline ingestion. The present study suggests that the expression of regucalcin mRNA in the kidney cortex of rats is suppressed by saline administration.