Dehydroepiandrosterone and dehydroepiandrosterone-sulfate content of the amniotic fluid]

Steroid hormone determinations have been performed in amniotic fluid obtained by amniocentesis in 16 to 20 weeks of pregnancy utilizing our radioimmunological methods. Sporadic estimations reported in the literature were completed with our results of dehydroepiandrosterone (D) and dehydroepiandrosterone sulphate (DS) measurements obtained in relatively great number of cases. The observations allowed the early diagnosis of placental sulphatase deficiency. Study of this enzymopathy suggested that, in addition to oestrogens and progesterone, D and DS may have per se biological-hormonal effects for maturation processes in the intrauterine life. Furthermore, a hypothesis has been outlined for prenatal differential diagnostics of the congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency.     

胎盘早剥的早期诊断(附67例临床分析)

目的:探讨发病诱因、临床表现和超声检查对胎盘早剥的诊断意义。方法:对2005年1月～2008年5月北京大学深圳医院收治的67例胎盘早剥患者资料进行回顾性分析。结果:胎盘早剥发生率为0.78%,妊娠期高血压疾病、胎膜早破为其重要诱因,主要临床表现为阴道出血、持续性下腹痛、血性羊水、胎心率异常或消失。胎盘早剥产前诊断率为67.16%,B超检出率为60.94%,新生儿窒息发生率为35.82%,围产儿死亡率为14.29%,产后出血、子宫胎盘卒中及DIC发生率分别为28.36%、16.42%和7.46%。其中Ⅱ、Ⅲ度胎盘早剥患者的临床表现、产前诊断率、母儿并发症发病率明显高于Ⅰ度胎盘早剥,其差异具有统计学意义(P<0.05);但胎盘早剥患者中B超对前、侧壁胎盘与后壁胎盘的产前诊断率比较差异无统计学意义(P>0.05)。结论:胎盘早剥严重威胁母儿生命,应结合诱因、临床表现以及B超等辅助检查全面考虑,尽早对其作出正确诊断和处理。     

Impact of CYP3A7*1C polymorphism on bone mineral content in postmenopausal women

INTRODUCTION: CYP3A7*1C polymorphism has been shown to be associated with lower levels of serum dehydroepiandrosterone sulphate in men. The age-related decline of dehydroepiandrosterone sulphate levels is believed to contribute to the development of osteoporosis. We hypothesized that CYP3A7*1C may lead to bone loss through decreased levels of dehydroepiandrosterone sulphate in postmenopausal women. PATIENTS AND METHODS: 319 postmenopausal women were studied and divided into two subgroups: 217 women with osteoporosis and 102 aged-matched women without osteoporosis. The CYP3A7*1C polymorphism was genotyped. Serum dehydroepiandrosterone sulphate levels and bone mineral density were measured. RESULTS: Homozygous CYP3A7*1C carriers had significantly lower bone mineral density at lumbar spine than that of wild type (T-score with CYP3A7*1C mutant type: -3.27 +/- 1.02, T-score with wild type: -1.35 +/- 1.53, p = 0.041) after adjusting for age and DHEAS levels. No association was found between genotypes and dehydroepiandrosterone sulphate levels. CONCLUSION: Our data suggest that CYP3A7 polymorphism might have an influence on bone mass at the lumbar spine independently of serum dehydroepiandrosterone sulphate concentrations.     

四氢生物喋呤负荷试验在高苯丙氨酸血症鉴别诊断中的临床应用

目的探讨四氢生物喋呤（BH4）负荷试验在高苯丙氨酸血症（HPA）鉴别诊断中的应用价值。方法自2008年1月-2010年6月,27例HPA患儿采用口服BH4（20 mg/kg）负荷试验。对其中血苯丙氨酸（Phe）浓度小于6 mg/dl患儿采用口服Phe-BH4联合负荷试验,结合尿喋呤分析、血红细胞二氢喋呤还原酶（DHPR）活性测定。结果 （1）在BH4负荷试验中,不同类型HPA患儿的血Phe浓度表现出各不相同的改变。27例HPA患儿中,共鉴别出5例BH4缺乏症,9例BH4反应性苯丙氨酸羟化酶（PAH）缺乏症,13例BH4无反应性苯丙氨酸羟化酶（PAH）缺乏症。（2）在22例中度苯丙酮尿症（PKU）患儿中,9例为BH4反应性PAH缺乏症。结论 BH4负荷试验在HPA早期鉴别诊断中十分重要,部分中度PKU对BH4有反应,可使用BH4替代治疗。     

四氢生物蝶呤缺乏症鉴别诊断的进展及发病率调查

目的 了解我国各省(市)、自治区对高苯丙氨酸血症(hyperphenylalaninemia,HPA)患儿进行四氢生物蝶呤缺乏症(tetrabydrobiopterin deficiency,BH4D)鉴别诊断的普及情况及BH4D的发病率.方法 选取1993--2007年接受BH4D鉴别诊断的1392例HPA患儿(门诊591例,递送标本801例)为研究对象.根据门诊及实验室资料统计BH4D鉴别诊断的病例数,探讨诊断标准,得出BH4D发病率及高发地区.结果 (1)近3年尿蝶呤谱分析及红细胞二氢蝶啶还原酶(dihydropteridine reductase,DHPR)活性测定的病例数明显递增,2005年2项试验的病例数分别为217例和198例,至2007年病例数分别达到511例和458例,病例总数约为2005年的2.3倍,覆盖全国29个省(市)、自治区;(2)尿生物蝶呤及生物蝶呤百分比是诊断6-丙酮酰四氢蝶呤合成酶缺乏症(6-pyruvcyl tetrahydropterinsynthase deficiency,PTPSD)的关键指标,96.83%(61/63)PTPSD患儿尿生物蝶呤百分比<5%[(1.41±1.10)%],生物蝶呤极低[(0.14±0.17)mmol/mol肌酐];四氢生物蝶呤(BH4)负荷试验2-6 h血苯丙氨酸浓度降至正常有助于诊断;DHPR活性降低是DHPR缺乏症的确诊方法 ;(3)1392例HPA患儿中PTPSD及DHPR缺乏症的发病率分别为8.41%(117/1392)和0.18%(2/1108);80%(8/10)的高发省(市)、自治区位于我国的华东及南部;上海PTPSD在HPA患儿及新生儿群体中发病率分别为10.81%(8/74)和0.007‰(8/1 121 429).结论 近3年我国大部分省(市)、自治区临床医生开展BH4D鉴别诊断的意识明显提高;BH4D在HPA患儿中的发病率至少为8.55%(119/1392),PTPSD占98.32%(117/119).     

Suppression of ovarian function by Microgynon 30 in day 1 and day 5 "starters"

The suppression of ovulation during the first treatment cycle with Microgynon 30 (150 micrograms levonorgestrel and 30 micrograms ethinyl oestradiol) for nine subjects starting the "pill" on day 1 of their cycle and five subjects on day 5 was investigated. Serum oestradiol and progesterone levels throughout the cycle and midcycle urinary LH levels were reliably suppressed in all day 1 "starters". Serum progesterone levels and urinary LH levels were also suppressed in day 5 "starters" but one subject produced oestradiol levels within the normal range of ovulatory cycles. Mean oestradiol levels of day 5 "starters" were found to be significantly higher than those of day 1 "starters" (p less than 0.05).     

Zinc supplementation alters thyroid hormone metabolism in disabled patients with zinc deficiency.

We examined zinc (Zn) status in relation to thyroid function in disabled persons, because the association between Zn deficiency and thyroid function remains controversial.

After measuring serum free 3,5,3′-triiodothyronine (T3) and free thyroxine (T4) in 134 persons, TSH-releasing hormone (TRH) injection test and estimation of Zn status were conducted in persons with low free T3.

Thirteen had low levels of serum free T3 and normal T4. Patients with elevated levels of serum 3,3′,5′-triiodothyronine (rT3) showed an enhanced reaction of serum thyrotropin (TSH) after TRH injection. Nine of 13 patients had mild to moderate Zn deficiency evaluated by body Zn clearance and increased urinary Zn excretion. After oral supplementation of Zn sulphate (4-10 mg/kg body weight) for 12 months, levels of serum free T3 and T3 normalized, serum rT3 decreased, and the TRH-induced TSH reaction normalized. Serum selenium concentration (Type 1 T4 deionidase contains selenium in the rat) was unchanged by Zn supplementation.

Zn may play a role in thyroid hormone metabolism in low T3 patients and may in part contribute to conversion of T4 to T3 in humans.     

6-丙酮酰四氢蝶呤合成酶缺乏致四氢生物蝶呤缺乏症的诊断及1种新突变的发现

目的探讨6-丙酮酰四氢蝶呤合成酶（PTPS）缺乏所致四氢生物蝶呤缺乏症（BH4D）的诊断及其基因突变特点,为开展BH4D的基因诊断提供依据。方法（1）归纳、总结临床症状、体征,复检血苯丙氨酸（Phe）浓度;（2）进行Phe（100mg／kg）＋四氢生物蝶呤（BH4）（20mg／kg）负荷试验、尿蝶呤谱分析、红细胞二氢蝶呤还原酶（DHPR）活性测定;（3）采用PCR．限制性片段长度多态性（PCR-RFLP）及常规基因测序法进行PTPS基因突变检测,分析基因型与临床表型的关系。结果（1）患儿男,出生72h后经新生儿疾病筛查检出其Phe浓度为176．1μmoL／L,生后20d复查仅出现肌张力稍低下、皮肤稍白,复检其Phe浓度升高至222．6μmoL／L;（2）负荷试验前血Phe浓度271．2μmol／L,Phe负荷3h上升至756．0μmol／L,BH4负荷6h血Phe浓度迅速降至283．2μmol／L;（3）尿新蝶呤为2．95mmol／molCr,生物蝶呤为0．08mmol／molCr,生物蝶呤百分比为2．64％;（4）DHPR活性1．71nmol／（min·5mm disc）,为正常对照的45％,排除DHPR缺乏症;（5）患儿PTPS基因突变类型为c．259C〉T（P87S）及IVS1-129A〉G,IVS1-129A〉G突变是首次报道的新突变,筛查50例正常儿童未检测到该突变。结论（1）BH4负荷6h后血Phe浓度下降迅速,尿生物蝶呤明显降低,B％持续〈10％,DHPR活性正常是6-丙酮酰四氢蝶呤合成酶缺乏症（PTPSD）的确诊依据;（2）P87S为中国人PTPS的热点突变,采用PCR—RFLP方法对热点突变进行快速筛查可提高基因诊断效率;（3）IVS1—129A〉G可能是PTPS基因新的致病突变。     

Low birth weight, adrenal and sex hormones and their correlation with carbohydrate metabolism and cardiovascular physiology, investigated in young adulthood]

It is known that the prevalence of cardiovascular diseases, hypertension, noninsulin dependent diabetes mellitus and dyslipidemia in the late adulthood are in connection with intrauterine retardation, characterized by low birth weight. One possible explanation of this phenomenon is the abnormality of hypothalamus-hypophysis-adrenal cortex axis due to the accelerated growth. The authors investigated the steroid levels of young adults; whom birth weight were under 2500 g, and examined the relationship between hormone levels and some parameters of glucose metabolism and cardiovascular system. 75 subjects (43 female and 32 male patients, mean age: 19.6 and 19.8 years, respectively; range 18-22 ys) with low birth weight and without any sign of chronic disease, and 30 healthy, age-matched controls with normal birth weight were investigated. The basal serum cortisol, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEAS), androstenedione (AD), 17-hydroxyprogesterone (17OHP), estradiol (OE), sex-hormone binding globulin (SHBG), FSH, LH and insulin levels were determined. Moreover, oral glucose tolerance test with 75 g glucose (OGTT), impedance cardiography as well as ambulatory blood pressure monitoring were done by all subjects. In both sexes in subjects with low birth weight the mean serum cortisol level was significantly higher, than in the normal controls. In female patients the serum DHEA, DHEAS, AD, and 17OHP levels were significantly higher than in the controls. Moreover, among these females a relationship was found between the elevations of adrenal and gonadal steroids and hyperinsulinemia, characterized by increased insulin response during OGTT. In male subjects a significant correlation was found between serum cortisol levels and systolic blood pressure and heart rate. In females there was a positive relationship between serum DHEA and heart rate. Summarized, the basic abnormality in patients with low birth weight seems to be a relative hypercortisolism, and in females because of hyperinsulinemia exists a mild hyperandrogenism as well. The hypercortisolism may cause cardiovascular abnormalities in males directly, while in females indirectly through the hyperinsulinemia and hyperandrogenism. These subtle abnormalities can be detected when no clinical signs present themselves, in young adulthood, giving the opportunity of taking preventive actions.     

静脉盐水负荷试验在原发性醛固酮增多症诊断中的价值

目的探讨静脉盐水负荷试验在原发性醛固酮增多症诊断中的应用价值。方法选择2006-2010年临床诊断为原发性醛固酮增多症的患者47例,行静脉盐水负荷试验并同时检测其血、尿醛固酮及血钾等生化指标。以30例原发性高血压患者作为对照组。结果与对照组比较,原发性醛固酮增多症患者静脉盐水负荷试验前、后血醛固酮水平、24h尿醛固酮排量显著升高,血钾水平明显下降;原发性醛固酮增多症患者血醛固酮的抑制率[(13.3±5.6)%]和受抑制患者的比例(4.3%)明显低于对照组[分别为(78.0±12.5)%和(93.3%)],该试验对原发性醛固酮增多症诊断的敏感性和特异性分别为95.7%(45/47)和93.3%(28/30)。结论静脉盐水负荷试验是一项安全可靠的原发性醛固酮增多症确诊方法,其敏感性和特异性均较高。     

Selenium (selenate) transport by human placental brush border membrane vesicles

1. Selenate uptake by human placental brush-border-membrane vesicles was studied in order to establish whether this anion shares a pathway with sulphate. 2. Selenate uptake was found to be saturable with respect to medium selenate and was inhibited by the anion exchange inhibitor 4,4'-diisothiocyano-stilbene-2,2'-disulphonate (DIDS). 3. Anions which have a similar tetrahedral shape to selenate, e.g. chromate, molybdate, tungstate and sulphate, were effective inhibitors of selenate uptake when added to the incubation medium. 4. Sulphate inhibited selenate influx in a dose-dependent fashion; moreover sulphate was found to be a competitive inhibitor of selenate uptake. 5. It is concluded that selenate and sulphate share a pathway for transport in the human placental microvillus membrane.     

Effect of dietary picolinic acid on the metabolism of exogenous and endogenous zinc in the rat

The excretion of 65Zn was compared by metabolic balance studies in adult male rats fed purified diets containing 0.8 mmol Zn/kg diet, with and without 40 mmol picolinic acid per kilogram diet, after single intragastric (i.g.) and intraperitoneal (i.p.) doses of the isotope. In a third experiment picolinic acid was introduced for 3 d into the diet of rats prelabeled with 65Zn. The urinary excretion of total zinc was increased by the ingestion of picolinic acid in all three experiments. The urinary and fecal outputs of 65Zn were both consistently greater in picolinic acid-fed rats than in the corresponding control animals. This was particularly marked after i.p. injection of the tracer, and the specific activities of urine and feces from the treated rats were both increased. When picolinic acid was introduced into the diet of prelabeled rats there was a delay of 24 h in the urinary response and 48 h in the fecal response. The residual 65Zn levels were reduced in several tissues from the picolinic acid-fed rats, especially after i.p. administration of the isotope. These observations indicate that dietary picolinic acid increases the turnover of endogenous zinc in addition to enhancing the absorption and excretion of ingested metal, and this has implications for its use in cases of zinc deficiency.     

血液检验仪在诊断和鉴别诊断贫血中的应用价值

目的:探讨血液检验仪在诊断和鉴别诊断贫血中的价值。方法:选择2018年8月~2019年10月来本院治疗的100例贫血患者作为观察组,并挑选同期90例健康体检者作为对照组,所有人员接受血液检测,对比检测结果。结果:对比再生障碍性贫血组,与对照组的MCV、MCH、RDW水平比较,无统计学意义(P>0.05),而RBC、Hb水平都低于对照组,且Hb低于缺铁性贫血组(P<0.05);缺铁性贫血组RDW水平高于对照组,而其RBC、Hb、MCV、MCH水平都显著下降(P<0.05);巨幼细胞性贫血组MCV、MCH、RDW水平都高于对照组,而RBC、Hb都低于对照组(P<0.05)。结论:血液检验仪可以较好检验贫血患者RBC、Hb水平,并依据RDW、MCV、MCH水平变化鉴别诊断贫血。     

Maternal vitamin D deficiency influences long-chain polyunsaturated fatty acids and pregnancy outcome in association with alterations in one-carbon metabolism

Preeclampsia is a pregnancy-specific disorder, leading to maternal and infant morbidity and mortality. Abnormal placentation has been reported in preeclampsia. Nutrients like vitamin D and long-chain polyunsaturated fatty acids (LCPUFA) are known to play a role in placental development. In an animal model, we have previously demonstrated that maternal vitamin D deficiency increases the thromboxane/prostacyclin ratio and contributes to inflammation and vasoconstriction. We hypothesize that maternal vitamin D status influences placental LCPUFA metabolism through alterations in one carbon metabolism in women with preeclampsia. To test this hypothesis, we recruited 69 normotensive control (NC) women and 50 women with preeclampsia. Women with preeclampsia had lower placental protein and mRNA levels of cystathionine-β-synthase (CBS), higher plasma malondialdehyde (MDA) levels and higher levels of arachidonic acid (AA) and total omega-6 fatty acids in the placenta. Women with preeclampsia also demonstrated higher placental mRNA levels of cyclooxygenase-2 (COX-2) as compared to NC women. Maternal 25(OH)D levels were negatively associated with maternal plasma MDA levels. Placental vitamin D receptor (VDR) levels were positively associated with CBS while maternal MDA levels were positively associated with serum levels of thromboxane-B2 (TXB2) levels. Our findings indicate that vitamin D deficiency increases oxidative stress through alterations in one carbon metabolism to influence pro-inflammatory omega-6 metabolic pathway in the placenta. This study demonstrates a possible mechanism through which vitamin D deficiency can result in an imbalance in the LCPUFA metabolites and contribute to placental inflammation and endothelial dysfunction in preeclampsia.     

尿微量蛋白联合尿酶对高血压早期肾损害的诊断价值

目的探讨高血压早期肾损害的诊断标准。方法对50名健康者（对照组）和50例高血压患者（试验组）采用免疫散射比浊法检测尿转铁蛋白（TRF），终点法测微量白蛋白（mALB），免疫透射比浊法测定尿视黄醇结合蛋白（RBP），速率法测定尿N-乙酰氨基葡萄糖苷酶（NAG），酶法测定尿肌酐（Cr）。比较两组实验室指标结果。结果对照组：尿TRF／Cr为0．05±0．03mg／mmol，mALB为3．61±2．46mg／L，RBP／Cr为7．46±5．02ug／mmol，NAG／Cr为0．52±0．46U／mmol。试验组的TRF／Cr、mALB、RBP／Cr和NAG／Cr值较对照组的增高有统计学意义（P＜0．01）；两项指标联合检测，其阳性率分别为：TRF＋mALB：62％，TRF＋NAG：54％，mALB＋NAG：44％，TRF、mALB和NAG3项指标联合检测可使阳性率提高到78％，大大提高了阳性检出率。结论联合检测尿TRF、mALB及NAG是诊断高血压早期肾损害较灵敏的实验室指标。     

1例生物素酶缺乏症患儿的临床分析

目的 探讨生物素酶缺乏症患儿的临床特征、诊断与治疗的方法 .方法 运用血串联质谱、尿有机酸分析、医学外显子高通量测序等检查技术,对1例因"间断抽搐1月余,咳嗽20余天,反应差3天"于2019年5月入住空军军医大学第一附属医院的小婴儿进行筛查和诊断,分析其临床表现、实验室检查结果 及诊疗情况.结果 血串联质谱分析示:3-...     

Antenatally determined nephro-urological anomalies: correctness of diagnosis and influence on management

On the basis of the experience of 52 antenatal diagnoses of foetal urinary tract abnormalities we discuss the influence of these diagnoses on antenatal and postnatal management. A correct diagnosis was established in only 34 of the 52 cases (65%). Therefore, in utero intervention should be used with utmost restrictiveness. Moreover, the antenatal diagnosis is usually not made in the first half of the pregnancy (which most authors consider necessary) and the benefits of prenatal intervention are not yet established. The data emphasize the importance of a thorough postnatal investigation and, necessary, early treatment before severe infections may occur. Antenatal ultrasound can make an important contribution to the prevention of kidney damage.     

胱抑素联合尿微量白蛋白肌酐比值在60例糖尿病早期肾损害中的应用

目的：分析血清胱抑素C（Cys-C）、尿微量白蛋白/肌酐比值（mAlb/Cr）联合检测在糖尿病患者早期肾损伤的诊断中的应用。方法：选取60例糖尿病患者（研究组）与60例健康体检者（对照组）,分别使用免疫透射比浊法、散射比浊法、苦味酸动力学法测定两组的Cys-C、尿微量白蛋白、肌酐水平。结果：研究组Cys-C、mAlb/Cr值分别是（1.43±0.43）mg/L、（12.57±8.13）mg/mmol,均明显高于对照组（P〈0.05）;研究组Cys-C水平〉1.4 mg/L者16例,阳性率为26.7%,mAlb/Cr水平〉3 mg/mmol者19例,阳性率为31.7%;两项指标联合检测结果高于正常范围共22例,联合检测阳性率为36.7%,高于两项指标单独检测（P〈0.05）;本组实际肾损伤22例,联合检测准确率100%。结论：Cys-C、mAlb/Cr比值联合检测可明显提升糖尿病早期肾损伤诊断准确度与敏感度。     

Recommended dose for repair of serum vitamin A levels in patients with HIV infection/AIDS may be insufficient because of high urinary losses

OBJECTIVE: Retinol deficiency is quite frequent in the population of human immunodeficiency virus (HIV)-infected individuals. Serum retinol levels of less than 1.05 micromol/L determine a 3.5 to five times higher death risk. However, studies evaluating the efficacy of retinol supplementation in HIV-seropositive individuals have reported conflicting results. The World Health Organization recommends the treatment of vitamin A deficiency in seropositive individuals in the same manner as for seronegative individuals, but clinical studies proving the efficacy of this scheme are lacking. The proposal of the present study was to assess the efficacy of supplementation with high retinol doses in HIV-infected patients with vitamin A deficiency. METHODS: Twenty-five adult HIV-seropositive individuals were monitored over a period of 9 months, with determination of serum and urinary retinol every 3 months. The subjects received retinol palmitate doses ranging from 300,000 IU to 600,000 IU. Patients whose retinol levels were higher than 1.60 micromol/L were only observed. RESULTS: Eighteen patients received supplementation during clinical monitoring. The dose of 600,000 IU induced a significant mean increase in serum levels of 0.47 micromol/L (P = 0.049) within a period of three months. Those who received 300,000 IU presented a mean increase of 0.29 micromol/L. In contrast, the patients who did not receive replacement therapy presented a significant decrease (P = 0.017) in serum retinol levels, with initial and final values of 1.77 micromol/L and 1.55 micromol/L. The individuals with the worst response to supplementation presented a higher urinary loss of retinol at the beginning of the study. Even with a mean retinol supplementation of 771,428 IU during the study period, six patients had marginal serum retinol levels at the end of the study. CONCLUSION: We conclude that, in view of the high urinary loss of this nutrient, there is the need to redefine the ideal dose for the treatment of HIV-infected individuals.     

Protein restriction during pregnancy induces hypertension in adult female rat offspring--influence of oestradiol

We previously reported that gestational dietary protein restriction in rats causes sex-related differences in development of blood pressure (BP) in the offspring, which is more pronounced in males than in females. As such effects may depend on sex hormones, we investigated the role of oestradiol in the development of hypertension in female offspring of protein-restricted dams. Female offspring of pregnant rats fed normal (20?%) or protein-restricted (6?%) casein diets throughout pregnancy were kept either intact, ovariectomised or ovariectomised with oestradiol supplementation. BP, Plasma oestradiol and testosterone levels, and vascular oestrogen receptor (ER) were examined. BP was significantly higher and plasma oestradiol levels were significantly lower (?-?34?%) in intact protein-restricted female offspring compared to corresponding controls. Further decrease in oestradiol levels by ovariectomy exacerbated hypertension in the protein-restricted females, with an earlier onset and more prominent elevation in BP compared to controls. Oestradiol supplementation in ovariectomised protein-restricted females significantly reversed ovariectomy-induced hypertension but did not normalise BP to control levels. The hypertensive protein-restricted females have reduced vascular ERα expression that was unaffected by ovariectomy or oestradiol replacement. In addition, testosterone levels were significantly higher by 2·4-, 3·4- and 2·8-fold in intact, ovariectomised and oestradiol-replaced protein-restricted females compared to corresponding controls. The present data show that: (1) hypertension in protein-restricted adult female offspring is associated with reduced plasma oestradiol levels; (2) oestradiol protects and limits the severity of hypertension in protein-restricted females and contributes to sexual dimorphism; (3) oestradiol replacement fails to completely reverse hypertension, which may be related to limited availability of vascular ERα receptors and/or increased circulating testosterone levels.