The Response of Vasopressin and Blood Pressure to Hemorrhage in Shr and Wky Rats

The effects of hemorrhage on plasma vasopressin levels and blood pressure were examined in conscious, age-matched spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. Graded hemorrhage was produced by bleeding the rats at 10 min intervals over a total period of 65 min, to produce cumulative blood losses equivalent to 0.5, 1.0, 1.5, 2.0 and 3.0% of body weight in each animal. Hemorrhage progressively lowered blood pressure and increased plasma vasopressin levels in both SHR and WKY. At cumulative reductions in blood volume equivalent to 1.0 to 3.0% of body weight, there were greater reductions in arterial pressure and greater increases in plasma vasopressin concentrations in SHR than WKY. Basal blood volume in SHR was 10% lower than in WKY. In SHR, the greater vasopressin response to hemorrhage may have been due in part to the greater fall in arterial pressure. Although the lower blood volume may have contributed to the latter, derangements in baroreceptor function may also have been important.     

导入人内皮型一氧化氮合酶基因对高盐饮食大鼠的血压及肾脏功能的影响

目的研究人内皮型一氧化氮合酶(eNOS)基因导入对高盐饮食诱导的高血压大鼠的降压作用和对肾功能的保护作用。方法选取8周龄雄性SD大鼠18只随机分成3组,其中2组以高盐(8%氯化钠)饲料喂养,一组以正常饮食喂养;6周后高盐组形成高血压动物模型,再经尾静脉分别注射含人eNOScDNA的重组质粒(pcDNA3.1-eNOS)和对照质粒(pcDNA3.1),然后监测血压,收集尿液以测定尿微量白蛋白,处死动物后测定人eNOS基因在各主要器官的表达;并采用Western-Blot的方法检测了肾脏和主动脉组织的血管紧张素Ⅱ1型受体(AT1R)蛋白表达情况。结果静脉注射人eNOS基因的重组质粒后第7天高盐饮食大鼠的血压出现明显下降6.2mmHg,实验结束时,最大降压效应达到15.4mmHg,实验组动物血压降低的同时,尿微量白蛋白亦出现显著下降;而且发现人eNOS基因的导入下调了AT1R的表达。整个实验过程动物并未出现因为质粒载体注入和表达所引起的严重不良反应。结论人eNOS基因的导入可能有助于降低血压,并预防高血压所导致的肾功能损害,为临床应用eNOS基因治疗并发肾功能损害的原发性高血压提供了可能。     

Gender Differences in Phagocytic Responses in the Blood and Liver, and the Generation of Cytokine-Induced Neutrophil Chemoattractant in the Liver of Acutely Ethanol-Intoxicated Rats

Phagocytosis by circulating and liver-recruited polymorphonuclear leukocytes (PMNs) and Kupffer cells was studied in acutely ethanol-intoxicated, age-matched male and female rats. Acute ethanol intoxication in female rats is associated with a more effective phagocytic PMN response in the circulating blood, but with lower phagocytic activities by liver-recruited PMNs and Kupffer cells than in their male counterparts. Endotoxin [lipopolysaccharide (LPS)] treatment (consisting of a Wmin intravenous infusion of a nonlethal dose) of acutely ethanol-intoxicated male and female rats results in enhanced phagocytic responses in liver-sequestered PMNs and Kupffer cells, but not in circulating PMNs. However, the LPS challenge elicits a lesser phagocytic response in liver PMNs and Kupffer cells of female rats than in males. Significant gender differences exist in the extent of hepatic PMN infiltration in ethanol plus LPS-treated rats, which is paralleled by very similar difterences in CDll b/c adhesion molecule expression in circulating PMNs and cytokine-induced neutrophil chemoattractant generation by hepatocytes and Kupffer cells. Taken together, these data indicate a smaller phagocytic response to fight infection in the liver of acutely alcohol-intoxicated female rats, but also a mechanism to afford some protection against neu-trophil-associated tissue injury.     

Effects of Erythropoietin Administration on Blood Pressure and Urinary Albumin Excretion in Rats

The effects of recombinant human erythropoietin (rHuEPO) administration on blood pressure and urinary albumin excretion were studied in normotensive Wistar-Kyoto rats (WKY), in spontaneously hypertensive rats (SHR), and in SHR rats treated with an angiotensin converting enzyme inhibitor (SHR-ACEi). Rats were housed in metabolic cages and treated with rHuEPO (150 U/kg body weight [bw] three times a week) for 6 weeks. Control animals received the vehicle only (0.25 mL of physiological saline). An angiotensin converting enzyme inhibitor was administered in the drinking water for 6 weeks (spirapril 5 mg/kg bw). Systolic blood pressure (SBP), and 24 h urinary albumin excretion (UAE) were measured once a week. No significant differences in SBP were observed between rHuEPO and vehicle-treated normotensive animals at the end of the treatment (171.9 ± 4.9 v 172.1 ± 5.6 mm Hg, respectively). After 6 weeks, SBP was significantly higher in SHR and SHR-ACEi groups treated with rHuEPO than in control groups (239.8 ± 7.3 and 243.0 ± 7.3 mm Hg v 218.1 ± 6.0 and 187.9 ± 4.6 mm Hg, respectively); UAE was significantly higher in groups treated with rHuEPO than in control groups (WKY: 265.9 ± 19.5 v 127.0 ± 12.3 μg/100 g bw, SHR: 1668.4 ± 564.6 v 234.8 ± 22.9 μg/100 g bw, and SHR-ACEi: 1522.7 ± 448.3 v 143.0 ± 18.9 μg/100 g bw, respectively). We concluded that erythropoietin treatment causes an increase in arterial pressure in SHR only, and an increase in UAE in both normotensive and hypertensive rats. The albuminuric effect was not entirely dependent on increased blood pressure. The treatment with an angiotensin converting enzyme inhibitor did not modify either the proteinuric or the pressor effects.     

Cosegregation Analysis of Salt Appetite and Blood Pressure in Genetically Hypertensive and Normotensive Rats

Enhanced sodium appetite is a robust behavioral characteristic of spontaneously hypertensive rats (SHR) which neither causes nor depends upon elevated blood pressure. However, the possibility remains that salt appetite and blood pressure are related by some unidentified common factor. The present study investigated the possible genetic co-determination of blood pressure and salt appetite in this animal model of hypertension.

Blood pressure of SHR, Wistar/Kyoto (WKY), and their F1 and F2 populations was measured prior to salt appetite testing by the tail cuff method. Sodium intake in these groups was measured daily for 5 days as the ad lib consumption of a 1.5% NaCl solution by subjects maintained on sodium deficient chow and demineralized water. Dynamic and stable components of salt appetite were identified in the parent strains and analyzed in the hybrid offspring.

The expected differences in blood pressure between SHR and WKY were observed, and the average blood pressure of the F1 and F2 groups fell roughly midway between SHR and WKY values. The SHR consumed substantially greater quantities of saline than WKY, but the F1 population consumed saline at a rate that was not different from WKY, rather than intermediate between SHR and WKY. There was no relationship in the F2 population between blood pressure and any measure of salt appetite. Thus, the high salt appetite and high blood pressure traits of SHR do not appear to share a common genetic basis. These results, considered with previously published work, suggest that approach and avoidance aspects of salt appetite may be separately inherited and also strongly suggest that neither is linked to hypertension.     

复方七芍降压片对自发性高血压大鼠血压及左室肥厚的影响

目的探讨复方七芍降压片降压及逆转左室肥厚(LVH)的作用机制.方法以10只14周龄WKY大鼠为阴性对照,32只14周龄自发性高血压大鼠(SHR)随机分为4组,分别采用尾动脉法测血压、测左室重量指数(LVMI)、放射免疫法测定血浆及局部心肌血管紧张素Ⅱ(AngⅡ).结果 复方七芍降压片能够降低SHR血压、LVMI、血浆及心肌AngⅡ.结论复方七芍降压片能有效地降低SHR血压及逆转左室肥厚.     

导入人内皮型一氧化氮合酶基因对高盐饮食大鼠的血压及肾脏功能的影响

目的 研究人内皮型一氧化氮合酶(eNOS)基因导入对高盐饮食诱导的高血压大鼠的降压作用和对肾功能的保护作用.方法 选取8周龄雄性SD大鼠18只随机分成3组,其中2组以高盐(8%氯化钠)饲料喂养,一组以正常饮食喂养;6周后高盐组形成高血压动物模型,再经尾静脉分别注射含人eNOScDNA的重组质粒(pcDNA3.1-eNOS)和对照质粒(pcDNA3.1),然后监测血压,收集尿液以测定尿微量白蛋白,处死动物后测定人eNOS基因在各主要器官的表达;并采用Western-Blot的方法检测了肾脏和主动脉组织的血管紧张素Ⅱ 1型受体(AT1R)蛋白表达情况.结果 静脉注射人eNOS基因的重组质粒后第7天高盐饮食大鼠的血压出现明显下降6.2 mm Hg,实验结束时,最大降压效应达到15.4 mm Hg,实验组动物血压降低的同时,尿微量白蛋白亦出现显著下降;而且发现人eNOS基因的导入下调了AT1R的表达.整个实验过程动物并未出现因为质粒载体注入和表达所引起的严重不良反应.结论 人eNOS基因的导入可能有助于降低血压,并预防高血压所导致的肾功能损害,为临床应用eNOS基因治疗并发肾功能损害的原发性高血压提供了可能.     

A New Model of Ethanol Self-Administration in Newborn Rats: Gender Effects on Ethanol Ingestion Through a Surrogate Nipple

BACKGROUND: Ethanol intake in the context of suckling may have distinct and potentially long-lasting consequences for further responsiveness to and acceptance of ethanol, compared to other, more indirect and less natural ways of ethanol exposure early in ontogeny. METHOD: Our findings presented in this paper show that a surrogate nipple technique can be used for the study of early ethanol intake in cesarean-derived rat pups tested before any suckling experience. RESULTS: Neonatal rats attached to and voluntary ingested ethanol through the surrogate nipple as early as 4 hr after birth. Moderate concentrations of ethanol (2% and 5%, v/v) promoted substantial initial suckling behavior, including sustained attachment to the nipple. Higher concentrations (10% and 15%) were not effective in sustaining suckling. Females responded less positively to 10% ethanol than did males. High concentrations of ethanol were less effective in eliciting suckling behavior, probably due to the aversiveness of ethanol odor. However, when ethanol was presented in solution with milk, newborn pups attached to the nipple and ingested even 15% ethanol. Contamination of milk with 15% ethanol was more aversive for females than for males. Newborn rat pups demonstrated similar patterns of nipple attachment and ingestive behavior for 5% ethanol and milk. Initial experience with milk in the context of suckling did not prevent further voluntary ethanol ingestion from the same nipple; furthermore, initial exposure to 5% ethanol did not impair subsequent responsiveness to milk. CONCLUSIONS: Gender differences in responsiveness or sensitivity to ethanol can be detected in rat pups as early as a few hours after birth. The results suggest a leftward shift in the dose-response curve for females compared with males, indicating that female neonates are more sensitive or more responsive than males to ethanol. The similarity of suckling behaviors produced by moderate concentrations of ethanol and milk suggests a certain unity in their reinforcing mechanisms in the context of the first suckling episode.     

Stress and High Sodium Effects on Blood Pressure and Brain Catecholamines in Spontaneously Hypertensive Rats

The following experiments were designed to determine if territorial stress, dietary sodium (Na), or the combination of stress and Na effect the rate of development of hypertension in the spontaneously hypertensive rat (SHR 4-18 wks) and if central catecholamines (C) were altered by these treatments. BP was significantly elevated from 2-8 weeks of stress treatment as compared to SHR controls. Norepinephrine (NE) levels in the nucleus tractus solitarius and amygdala (A), and dopamine (D) levels in the hippocampus and A showed significant elevations in the stressed group. High Na (3%) treatment combined with stress treatment produced an even further BP increase and elevated D levels in the amygdala, and elevated NE levels in the area postrema as compared to control SHR's. Selected brain C variables were able to correctly classify animals into high and low BP groups with 90-100% accuracy. Our data support the concept that there are important stress and Na effects upon brain neurochemistry which influence the development of hypertension in the SHR.     

经皮肾动脉成形术对肾动脉狭窄患者血压和肾功能的影响

目的探讨经皮肾动脉成形术对肾动脉狭窄患者血压和肾功能的影响。方法选择经皮肾动脉成形术治疗的23例肾动脉狭窄患者作为研究对象,对其临床资料进行回顾性分析,观察术后血压和肾功能的变化并分析疗效。结果 23例患者均成功植入肾动脉支架,术后残留狭窄均小于30%,手术成功率为100%,术中术后均未发生严重并发症。术后均随访12个月,高血压治愈3例,改善17例,总改善率为86.9%;肾功能改善6例,稳定13例,总获益率为82.6%。收缩压由180.3±35.6 mmHg降为131.2±25.4 mmHg,舒张压由106.2±21.5 mmHg降为80.6±14.2 mmHg,血肌酐由286.4±113.7μmol/L降为166.5±84.8μmol/L,手术前后比较差异有统计学意义(P<0.05)。结论经皮肾动脉成形术和肾动脉支架植入治疗肾动脉狭窄的手术成功率高,有助于控制血压和稳定肾功能,远期疗效需进一步随访观察。     

Different Mechanisms Maintaining High Blood Pressure in Chronic One-Kidney,One-Clip,and Two-Kidney,One-Clip Hypertensive Rats

To evaluate the difference of the blood pressure regulating mechanisms of chronic(12–14 weeks) one-kidney, one-clip(1K-1C) and chronic two-kidney, one-clip(2K-1C) hypertensive rats, we administered captopril, captopril plus indomethacin, and indomethacin to the rats. Pretreatment values of plasma renin concentration, plasma aldosterone concentration and urinary kallikrein excretion were significantly higher in 2K-1C than in 1K-1C hypertensive rats. Captopril-induced blood pressure reduction was greater in 2K-1C than in 1K-1C hypertensive rats. When captopril was administered to the rats treated with indomethacin, captopril-induced blood pressure reduction was attenuated only in 2K-1C hypertensive rats. Indomethacin produced renal impairment and further raised the blood pressure in 1K-1C hypertensive rats, but did not in 2K-1C hypertensive rats. These results suggest that the renin-angiotensin system functions to maintain high blood pressure more predominantly in chronic 2K-1C than in 1K-1C hypertensive rats. The renal kallikrein-kinin system is suppressed in chronic 1K-1C hypertensive rats but not in 2K-1C hypertensive rats. The renal prostaglandin system is more important for regulating the renal circulation in chronic 1K-1C than in 2K-1C hypertensive rats.     

Effects of Salt Rich Diet in the Obese Zucker Rats: Studies on Renal Function During Isotonic Volume Expansion

Obese Zucker rats (OZR) are hyperinsulenemic, hyperglycemic and dyslipidemic and develop salt dependent hypertension. Since salt sensitivity is considered to be due to impaired handling of renal sodium excretion, these studies were conducted in the obese and lean Zucker rats (LZR) anesthetized with Inactin to evaluate renal function under basal conditions and during acute isotonic fluid volume expansion (VE). Mean Arterial blood pressure (MBP), heart rate (HR), renal blood flow(RBF) and glomerular filtration rate (GFR) were not significantly different between the lean Zucker rats fed normal diet or that fed salt rich diet(8% NaCl). However, basal UV and UNaV were significantly greater in the LZR fed high salt. During VE essentially identical increases occurred in GFR, UV and UNaV in both the lean groups. In the OZR fed salt rich diet also, there were no significant changes in the heart rate, RBF and GFR. However, arterial blood pressure of the OZR fed salt rich diet was significantly greater than that of the OZR on the normal diet as well as that of both the lean groups. Also, as in the LZR, basal UV and UNaV were significantly greater in the salt fed obese rats. During volume expansion there were no impairments in the ability of the obese groups fed normal or salt rich diet to eliminate sodium and water during volume load. In fact, the net sodium and water excretions during and 60 min after VE in both the obese groups were significantly greater than that of corresponding lean groups. Furthermore, these values in the OZR fed salt rich diet were significantly greater than that of the obese rats on normal salt diet perhaps due to the contribution of ‘pressure natriuretic mechanisms’. These data demonstrate that although OZR are salt sensitive, the renal mechanisms that would collectively respond to acute isotonic VE were fully functional. An unexpected and a novel finding in these studies is that the salt rich diet, in addition to increasing arterial blood pressure also significantly lowered plasma of insulin levels and enhanced glucose and cholesterol levels in the obese Zucker rats.     

原发性高血压盐敏感者肾脏损害特征及氨氯地平的保护作用

目的：探讨原发性高血压盐敏感者肾脏损害特征及氨氯地平治疗对其尿微白蛋白及β２ 微球蛋白排泄的影响。　　方法：６０ 例临床确诊的原发性高血压患者确定盐敏感性后,监测２４ 小时血压、肾血流动力学、２４小时尿微白蛋白及β２ 微球蛋白排泄等改变,并随机分为氨氯地平组（ｎ＝ ３０）及依那普利组（ｎ＝ ３０）对比治疗观察。　　结果：原发性高血压盐敏感者与盐不敏感者相比,２４ 小时尿微白蛋白及β２ 微球蛋白排泄量均增多,肾血流量减低,滤过分数增高（Ｐ均＜ ０．０１）,氨氯地平治疗１２周后,随着血压降低,尿微白蛋白及β２ 微球蛋白排泄量明显减少。　　结论：原发性高血压盐敏感者肾损害程度大于盐不敏感者;氨氯地平对盐敏感者在有效控制血压的同时能显著减少尿微白蛋白及β２ 微球蛋白排泄量。     

Dietary Sodium Intake and Urinary Dopamine and Sodium Excretion During the Course of Blood Pressure Development in Dahl Salt-Sensitive and Salt-Resistant Rats

ABSTRACT

Recent studies have suggested that dopamine (DA) formed within the kidney may play an important role in promoting sodium excretion, and that renal production and excretion of DA is determined by dietary sodium intake. Inasmuch as increased sodium consumption produces hypertension in Dahl salt-sensitive (DS) rats but not in Dahl salt-resistant (DR) rats, the present study was designed to examine the relationship between sodium consumption and urinary excretion of DA in these rats. DS and DR rats were placed on either high sodium chloride (8%) or low sodium chloride (0. 4%) diets at 4 weeks of age and their systolic blood pressure (SBP), urine volume, urinary sodium and catecholamine excretion were measured once every week for the next 4 weeks. High sodium chloride diet increased SBP in DS rats at 6 weeks of age and SBP continued to rise until they were 8 weeks old. The SBP of DR rats did not reach hypertensive levels when they were given high sodium chloride diet. The SBP of DS rats on low sodium chloride diet was significantly higher than DR rats on the same diet. The urinary DA excretion increased with age in all four groups of rats and was similar when they were 8 weeks old. However, both DS and DR rats on high sodium chloride diet excreted greater amounts of sodium and had increased urine volume compared to the DS and DR rats on low sodium chloride diet. There were no significant differences in urinary NE or E excretion in these four groups of rats. Kidney levels of DA and NE were significantly lower in DS compared to DR rats on high sodium chloride diet. These results show that although there are no differences in urinary DA excretion between rats on low and high sodium intake, both DS and DR rats on high sodium chloride diet are able to exhibit a natriuretic response. The DS rats eliminate sodium at the expense of an elevated SBP whereas DR rats stay normotensive. Therefore, it appears that alterations in mechanisms controlling renal vascular resistance rather than sodium excretion are responsible for the development of hypertension in DS rats.     

Effect of Renal Perfusion Pressure on Excretion of Calcium,Magnesium, and Phosphate in the Rat

Abnormalities in renal handling of calcium, magnesium, or phosphate have been implicated in the development and/or maintenance of human hypertension. We have shown recently that renal excretion of these ions is correlated to blood pressure in Dahl salt-sensitive as well as salt-resistant rats. The present study was designed to determine whether renal perfusion pressure per se could affect excretion of these ions. Urinary excretion of calcium, magnesium, and phosphate was studied in anaesthetized Sprague-Dawley rats under basal conditions and during an intravenous infusion of angiotensin I1 (ANG 11). vasopressin (AVP) or phenylephrine (PE). A cuff, placed around t h e aorta between the two renal arteries, allowed maintenance of normal perfusion pressure in the left kidney, while that in the right kidney was allowed to rise. Infusion of pressor agents raised mean arterial blood pressure to comparable levels (means±SE): ANG II (n=7), before = 102±4, during = 133±3 mmHg, AVP (n=8), before = 110±7, during = 136±5 mmHg, PE (n=6), before - 111±6, during = 141±6 mmHg. Although there was no difference in excretion of calcium, magnesium and phosphate between the two kidneys under basal conditions, infusion of ANG I1 or PE induced hypercalciuria, hypermagnesiuria and hyperphosphaturia in the right kidney which was exposed to t h e increased arterial pressure. Such effects did not appear in the pressure- controlled left kidney. Infusion of AVP was associated with reduced excretion of calcium and magnesium, and increased excretion of phosphate, in the normotensive kidney. The response to the similarly increased renal perfusion pressure in this group was also reduced for calcium and magnesium, and enhanced for phosphate. The results indicate (1) renal excretion of calcium, magnesium and phosphate is renal perfusion pressure-dependent; the higher the renal perfusion pressure, the greater the excretion of these ions. (2) Independently of perfusion pressure, AVP can inhibit phosphate reabsorption and stimulate divalent cation reabsorption.     

Effect of Chronic Infusion of Atrial Natriuretic Factor On Plasma and Urinary Aldosterone,Plasma Renin Activity,Blood Pressure and Sodium Excretion in 2-k, 1-c Hypertensive Rats

Conscious two-kidney, one-clip (2-K, 1-C) hypertensive rats and their normotensive sham-operated controls were infused during 13 days with synthetic ANF (Arg 101 Tyr-126) at 35 pmol/hr/rat by means of osmotic minipumps connected to the jugular vein. The initial blood pressure of 186 ± 6 mmHg maximally decreased to 118 ± 7 mmHg at day 5 and slowly rose after wards without reaching basal values. concomitant drop in pressure natriuresis and diuresis was observed. No changes were observed in ANF-infused sham-operated rats. Urinary aldosterone excretion declined in ANF-treated rats from a basal value of 63.38 ± 21.04 μg/24 hr to 13.36 ± 3.78 μg/24 hr the last infusion day. No change in urinary aldosterone was observed in either non-infused 2-K, 1-C or ANF-infused sham-operated rats.

Plasma aldosterone was significantly higher only in non-treated 2-K, 1-C rats. Renal aldosterone clearance was significantly lower in ANF-infused 2-K, 1-C rats than in the other experimental groups. Plasma renin activity (PRA) was lower in treated (3.92 ± 2.26 AI ng/ml/hr) than in non-treated (9.08 ± 2.32 AI ng/ml/hr) hypertensive rats, and not different from ANF-infused or non-infused sham-operated rats. No differences in body weight between infused and non-infused rats, or hematocrit between any group were observed. Atrial immunoreactive ANF was not different in any group. These results demonstrate that chronic administration of ANF not only reduces blood pressure and PRA in 2-K, 1-C hypertensive rats but also plasma and urinary aldosterone. Whether the latter is a direct inhibitory effect or secondary to the normalization of PRA is not known. The hypotensive response may be due to a direct effect on vascular smooth muscle but a role of renin cannot be excluded. Because blood pressure returned toward basal values during the last days of the observation period, the possibility of a tachyphylactic effect of ANF on vascular smooth muscle cannot be excluded     

长期饮酒对浙江景宁畲族人群血压、血脂及肾功能的影响

目的探讨长期过量饮酒对血压、血脂及肾功能的影响。方法在浙江省景宁畲族自治县随机选择6个自然村,运用水银柱血压计听诊法连续测量坐位右臂血压3次,取平均值用做统计分析。运用问卷收集饮酒、吸烟、高血压用药史。采集静脉血,全自动生化仪检测血脂及肾功能。结果1168例畲族受检者中包括648名(0·55)女性,372例(0·32)高血压患者,526例(0·45)有饮酒习惯,325例(0·28)每周饮酒超过300g。和不饮酒者相比,饮酒者的收缩压(130·6比126·0mm Hg)、舒张压(81·0比78·7mmHg)、脉压(49·6比47·2mm Hg)、高密度脂蛋白胆固醇(1·48比1·33mmol/L)、血尿酸(342比331μmol/L)明显升高(P<0·01)。在畲族男性中,收缩压及舒张压随饮酒量的增加呈线性增加(P<0·01);饮酒是高血压的一个独立的危险因素(OR,1·61;95%可信区间,1·05~2·47;P=0·03)。结论长期过量饮酒可升高血压,增加高密度脂蛋白胆固醇及血尿酸水平。     

The Effect of Salt Loading on the Urinary Excretion of Dopamine and Sodium Transport Inhibitor in the Rat

1. The temporal relationship between the excretion of dopamine and sodium transport inhibitor (STI) during salt loading was examined in the rat.

2. Urine samples were collected before and during salt loading (given as 18 g/1 NaC1 solution to replace drinking water) for the measurement of sodium, creatinine, dopamine and STI in 6 female rats. Dopamine was measured by HPLC and STI was extracted and measured by its ability to inhibit purified Na⁺, K⁺-ATPase enzyme.

3. Urinary sodium and STI (expressed in relation to creatinine) on day 1 of salt loading were 4.6 and 4.2 times respectively of the control values.     

维生素C对糖尿病大鼠血脂和主动脉硫酸肝素蛋白聚糖蛋白表达的影响

目的观察维生素C对糖尿病大鼠血脂和主动脉硫酸肝素蛋白聚糖表达的影响。方法利用链脲佐菌素腹腔注射法诱导建立1型糖尿病大鼠模型,将实验用SD大鼠随机分正常对照组、糖尿病组、维生素C治疗组。治疗16周,观察治疗期间及实验后大鼠的一般状况、血糖、甘油三酯、总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、糖化血红蛋白、糖化低密度脂蛋白,分离主动脉,HE染色及免疫组织化学检测主动脉内膜硫酸肝素蛋白聚糖表达。结果①造模4组大鼠均出现血脂异常及主动脉病理形态改变。②维生素C对血糖无影响,但能改善基本状况,维生素C能降低糖尿病大鼠的甘油三酯(P<0.05)、总胆固醇(P<0.05)、低密度脂蛋白胆固醇(P<0.05)、糖化血红蛋白(P<0.05)、糖化低密度脂蛋白(P<0.05),升高高密度脂蛋白胆固醇(P<0.05);维生素C增强主动脉硫酸肝素蛋白聚糖(P<0.05)表达。结论维生素C无降糖作用,但具有确切的主动脉保护作用。