Effects of verapamil and converting enzyme inhibition on bilateral renal function of two-kidney, one-clip hypertensive rats

Experiments were conducted in two-kidney, one-clip renal vascular hypertensive rats (GHR) to assess the responses of each kidney to acute treatment with the antihypertensive calcium channel blocking agent verapamil in the presence and in the absence of converting enzyme inhibitor (CEI). One group of GHR (0.2 mm inner diam. clip 3 weeks before study) were examined during a control period, and during a second period of infusion of verapamil (600 micrograms h-1 kg-1). A second group of GHR were examined during a control period, during CEI (teprotide, 3 mg h-1 kg-1) infusion and during a third period of verapamil (600 micrograms h-1 kg-1) infusion superimposed on CEI infusion. Although systemic blood pressure (BP) decreased from 175 +/- 4 to 149 +/- 5 mmHg (mean +/- SEM) in response to verapamil alone, renal blood flow for non-clipped kidneys increased from 5.9 +/- 0.4 to 6.5 +/- 0.3 ml/min, indicating a 30% reduction of renal vascular resistance (P values less than or equal to 0.01; n = 9). Glomerular filtration rate (GFR) for non-clipped kidneys (n = 24) increased from 0.91 +/- 0.09 to 1.47 +/- 0.14 ml/min and filtration fraction increased from 0.32 +/- 0.04 to 0.47 +/- 0.03 (P values less than or equal to 0.05). Urine flow rate and absolute and fractional sodium excretion for non-clipped kidneys increased. GFR for clipped kidneys decreased during verapamil. Treatment with CEI alone resulted in nearly identical responses of BP and function of the non-clipped kidney, except filtration fraction was unchanged. The addition of verapamil to ongoing converting enzyme blockade tended to augment the increased GFR of the non-clipped kidney. Plasma renin activity (PRA) increased from 30 +/- 3 to 59 +/- 7 ng of angiotensin (ANG) I h-1 ml-1 with verapamil alone, a significantly larger increment than the increase of PRA from 27 +/- 5 to 39 +/- 9 ng of ANG I h-1 ml-1 in GHR subjected to comparable blood pressure reduction by mechanical aortic constriction. Verapamil resulted in many similar effects on renal function to those observed during blockade of converting enzyme. The increased filtration fraction observed in response to verapamil may be the result of vasodilatation of the afferent arteriole or of an increase in the glomerular ultrafiltration coefficient.     

Effects of saponins from Herniaria glabra on blood pressure and renal function in spontaneously hypertensive rats

Experiments were performed on male and female spontaneously hypertensive rats weighing 310-340 g (10 animals per group). The oral administration of 200 mg/kg/day of saponins from Herniaria glabra for 30 days, resulted in a significant decrease in blood pressure in hypertensive rats. The systolic and diastolic blood pressure decreased significantly and respectively from 187.60 +/- 20.63/119.00 +/- 7.09 mmHg at day 0 (D0) to 141.60 +/- 7.51/90.40 +/- 7.68 mmHg at day 30 (D30), p < 0.001 (vs. 186.30 +/- 11.27/114.10 +/- 12.00 mm Hg at D0 to 154.50 +/- 6.38/132.3 +/- 7.68 mmHg at D30 in furosemide-treated group, p < 0.001). Control animals receiving placebo did not show any significant variation in the mean arterial pressure. The effect of saponins of Herniaria glabra on renal function was evaluated in spontaneously hypertensive rats using clearance techniques. Glomerular filtration rate was constant in the control rats and increased significantly in the hypertensive rats after saponins treatment (5.55 +/- 0.32 vs. 6.03 +/- 0.43 ml.min-1.kg-1 in the control (C) and saponins (S) groups, respectively, p < 0.05). Saponins administration provoked an increase in urinary flow (59.38 +/- 5.85 ml.kg-1.24 h-1 vs. 36.92 +/- 5.17 ml.kg-1.24 h-1, p < 0.001). Saponins also increased potassium excretion (6.89 +/- 0.81 mmol.kg-1.24 h-1 vs. 5.40 +/- 0.51 mmol.kg-1.24 h-1, p < 0.001) and sodium excretion (10.74 +/- 1.21 mmol.kg-1.24 h-1 vs. 7.25 +/- 0.54 mmol.kg-1.24 h-1, p < 0.001) as well as chloride excretion (13.59 +/- 1.04 mmol. kg-1.24 h-1 vs. 9.67 +/- 0.77 mmol.kg-1.24 h-1, p < 0.001). It is concluded that chronic oral administration of saponins from Herniaria glabra decreased the arterial blood pressure and affected salt and water transport in renal tubules.     

Effects of endothelin-A receptor antagonism on bilateral renal function in renovascular hypertensive rats

Recent studies indicated an enhanced expression of Endothelin (ET) in the kidney contralateral to the vascular clip in two-kidney, one-clip (2K-1C) Goldblatt hypertension. We proposed that the enhanced intrarenal ET production might be responsible for altered haemodynamic and excretory capability of the unclipped kidney (UK) of 2K-1C renovascular hypertensive rats. Therefore, we examined the changes in arterial pressure and split renal function in the clipped (CK) and UK simultaneously, in response to chronic administration of the selective ETA receptor blocker (A-127722), given orally at a dose of 30 mg/kg/day for 3 weeks starting from the beginning of the 4th week of clipping. Systolic pressure averaged 177 +/- 7 mmHg in control rats (n=15) and 164 +/- 9 mmHg in treated rats (n=16) and the difference was not statistically different. Glomerular filtration rate (GFR), renal plasma flow (RPF) and renal vascular resistance (RVR) in the UK were not different between control and treated groups. Data were then analyzed by classifying rats as moderate hypertensives (MAP < 180 mmHg), and severe hypertensives (MAP > 180 mmHg). In the moderately hypertensive group, average MAP was 143 +/- 5 mmHg and 138 +/- 4 mmHg in control (n=9) and treated (n=10) groups, respectively. In the severely hypertensive group, average MAP was 192 +/- 5 mmHg and 188 +/- 5 mmHg in control (n=6) and treated (n=6) groups, respectively. GFR and RPF were significantly improved in the UK of only the severely hypertensives who received the antagonist. However, the ET(A) antagonist blunted the sodium loss in both CK and UK of severely hypertensive rats. We conclude that ET(A) receptors do not play a role in the progression of hypertension in 2K-1C renovascular hypertensive rats. Yet, ET(A) receptors play an important role in altering renal hemodynamics of the unclipped kidneys in severe degrees of renovascular hypertension.     

Effects of L-tryptophan on blood pressure in normotensive and hypertensive rats

The effects of L-tryptophan on blood pressure and brain serotonin have been investigated in normotensive and spontaneously hypertensive rats. Doses of L-tryptophan from 25 to 100 mg/kg increased the blood pressure of normotensive rats by 10 to 15 mm Hg. The lower doses of L-tryptophan also increased blood pressure in hypertensive rats but, in contrast, the highest dose (100 mg/kg) lowered blood pressure by 30 to 35 mm Hg. Blood pressure effects of L-tryptophan were evident within 30 min of treatment and reached maximal response by 60 min. L-Tryptophan-induced changes in serotonin neurochemistry were correlated on a temporal basis with changes in blood pressure. However, the dose-response relationship between blood pressure changes and increases in brain serotonin and 5-hydroxyindoleacetic acid content produced by L-tryptophan was not related. The effects of L-tryptophan on blood pressure in normotensive and spontaneously hypertensive rats cannot be explained entirely by its effects on brain serotonin.     

Effects of fosinopril or sustained-release verapamil on blood pressure and serum catecholamine concentrations in elderly hypertensive men

A randomized, double-blind, placebo-controlled clinical trial showed 14 of 18 (78%) of the elderly hypertensive men in this study had an uncomplicated and beneficial response to either fosinopril or verapamil. There was a well-tolerated reduction in systolic blood pressure (SBP) and diastolic blood pressure (DRP). There were no significant adverse drug events. Only the sitting SBP and the sitting DBP were significantly lowered by fosinopril and verapamil SR. Because reduction in both SBP and DBP in elderly hypertensives has been shown to be beneficial, these findings take on further importance when considering the choice of medication for antihypertensive therapy in the elderly. The increase in norepinephrine in the fosinopril-treated patients may explain why patients treated with long-term angiotensin-converting enzyme inhibitors alone or in combination with diuretics rarely complain of orthostatic symptoms.     

膳食钙对高血压大鼠血压的影响

目的：观察膳食钙对一氧化氮缺乏性高血压大鼠血压、血清一氧化氮浓度及一氧化氮合酶活性的影响。方法：实验于2005-10—22／20016—01—13在解放军第四军医大学动物实验室及形态学实验室进行。取雄性SD大鼠24只，随机区组等分成4组（n=6）：①对照组：基础饲料喂养，40mg／（kg&;#183;d）去离子水灌胃，饲养期间饮去离子水。②高钙组：第3周开始给予5．0％的高钙膳食，40mg/（kg&;#183;d）去离子水灌胃，饲养期间饮去离子水。③L-NAME＋高钙组：第3周始将40mg／（kg&;#183;d）左旋硝基精氨酸甲酯（L-NAME）溶于去离子水中每天灌胃，第7周停止给予L—NAME，开始给予5．0％的高钙膳食，饲养期间饮去离子水。④L—NAME组：第3周始将40me,／（kg&;#183;d）L—NAME溶于去离子水中灌胃，基础饲料喂养，饮去离子水。每周应用RBP—1型大鼠血压仪测量血压，10周后处死所有大鼠，硝酸还原酶法检测血清中一氧化氮的浓度和一氧化氮合酶活性。结果：24只大鼠全部进入结果分析。①血压：从实验第4周开始L-NAME＋高钙组和L-NAME组明显高于对照组和高钙组（P〈0．01）。从第7周到第10周实验结束时，L-NAME组血压明显高于其他3组（P〈0．01）。②血清一氧化氮浓度：对照组低于高钙组和L-NAME＋高钙组[（8．81&;#177;6．63），（14．80&;#177;5．32），（15．26&;#177;3．55）μmol／L，P〈0．05]，但高于L-NAME组[（2．89&;#177;1．71）μmol／LP〈0．05]；高钙组和L-NAME＋高钙组比较差异无显著性（P〉0．05）；L-NAME＋高钙组则高于L-NAME组（P〈0．05）。③血清一氧化氮合酶活性：对照组低于高钙组和L-NAME＋高钙组[（334．57&;#177;74．35），（436．09&;#177;69．35），（448．76&;#177;45．68）μkat／L，P〈0．05]，但高于L-NAME组[（255．88&;#177;35．17）μkat/L,P〈0．05]；高钙组和L-NAME＋高钙组比较差异不显著（P〉0．05）；L-NAME＋高钙组则高于L-NAME组（P〈0．05）。结论：①高钙膳食可以降低一氧化氮缺乏型高血压大鼠的血压，升高其血清一氧化氮浓度和一氧化氮合酶活性。②高钙膳食可以增加正常血压大鼠体内一氧化氮水平和一氧化氮合酶活性。     

膳食钙对高血压大鼠血压的影响

目的:观察膳食钙对一氧化氮缺乏性高血压大鼠血压、血清一氧化氮浓度及一氧化氮合酶活性的影响。方法:实验于2005-10-22/2006-01-13在解放军第四军医大学动物实验室及形态学实验室进行。取雄性SD大鼠24只,随机区组等分成4组(n=6):①对照组:基础饲料喂养,40mg/(kg·d)去离子水灌胃,饲养期间饮去离子水。②高钙组:第3周开始给予5.0%的高钙膳食,40mg/(kg·d)去离子水灌胃,饲养期间饮去离子水。③L-NAME 高钙组:第3周始将40mg/(kg·d)左旋硝基精氨酸甲酯(L-NAME)溶于去离子水中每天灌胃,第7周停止给予L-NAME,开始给予5.0%的高钙膳食,饲养期间饮去离子水。④L-NAME组:第3周始将40mg/(kg·d)L-NAME溶于去离子水中灌胃,基础饲料喂养,饮去离子水。每周应用RBP-1型大鼠血压仪测量血压,10周后处死所有大鼠,硝酸还原酶法检测血清中一氧化氮的浓度和一氧化氮合酶活性。结果:24只大鼠全部进入结果分析。①血压:从实验第4周开始L-NAME 高钙组和L-NAME组明显高于对照组和高钙组(P<0.01),从第7周到第10周实验结束时,L-NAME组血压明显高于其他3组(P<0.01)。②血清一氧化氮浓度:对照组低于高钙组和L-NAME 高钙组[(8.81±6.63),(14.80±5.32),(15.26±3.55)μmol/L,P<0.05],但高于L-NAME组[(2.89±1.71)μmol/L,P<0.05];高钙组和L-NAME 高钙组比较差异无显著性(P>0.05);L-NAME 高钙组则高于L-NAME组(P<0.05)。③血清一氧化氮合酶活性:对照组低于高钙组和L-NAME 高钙组[(334.57±74.35),(436.09±69.35),(448.76±45.68)μkat/L,P<0.05],但高于L-NAME组[(255.88±35.17)μkat/L,P<0.05];高钙组和L-NAME 高钙组比较差异不显著(P>0.05);L-NAME 高钙组则高于L-NAME组(P<0.05)。结论:①高钙膳食可以降低一氧化氮缺乏型高血压大鼠的血压,升高其血清一氧化氮浓度和一氧化氮合酶活性。②高钙膳食可以增加正常血压大鼠体内一氧化氮水平和一氧化氮合酶活性。     

肝细胞生长因子对自发性高血压大鼠血压的影响

背景：肝细胞生长因子是一种多功能生长因子，它能促进多种细胞生长与移行及各种组织器官的发生。在心血管系统，它具有抗凋亡、抗纤维化、促进内皮细胞损伤后修复作用，推测其可能具有降压效应。 目的：观察外源性肝细胞生长因子对自发性高血压大鼠血压、血管内皮系统和肾素-血管紧张素系统的影响并探讨其调节血压的可能机制。设计、时间及地点：随机对照动物实验，于2007—03／07在安徽医科大学第一附属医院心内科完成。材料：外源性肝细胞生长因子粉剂购于美国Peprotech公司，成年白发性高血压大鼠组和WKY大鼠，均14周龄，体质量200～250g。自发性高血压大鼠随机分为实验组和单纯自发性高血压大鼠组，WKY大鼠为正常对照组，每组12只。方法：实验组每间隔24h从尾静脉依次给予肝细胞生长因子5，10，15，20，25u玳g，自发性高血压大鼠组和正常对照组同时给予等量生理盐水。每次注射安抚大鼠5min后测血压与心率，最后一次注射后观察血压降至最低值时（约注射后30min），麻醉后处死，各取右心室血2mL。 主要观察指标：①观察肝细胞生长因子对自发性高血压大鼠组收缩压及心率的影响。②分别用比色法测血清一氧化氮水平、放射免疫法测血浆内皮素、血管紧张素Ⅱ水平。 结果：实验组注射肝细胞生长因子5μg/g血压下降不明显，注射10ug／kg约5min后血压开始下降，30min降至最低，1h后血压开始逐渐回升，5h后血压基本回到原先水平。注射20ug／kg达最大降压幅度，收缩压下降达40～50mmHg，再增加剂量最大降压幅度及持续时间不变。整过程心率无明显变化。两个对照组血压无明显变化。实验组较自发性高血压大鼠组内皮素、血管紧张素Ⅱ含量下降，一氧化氮含量上升（P〈0．05）。 结论：从静脉给予外源性肝细胞生长因子能快速降低自发性高血压大鼠组的血压，在一定剂量范围内，呈剂量-效应与时间-效应关系。肝细胞生长因子系统、血管内皮系统、肾素-血管紧张素系统可能共同参与血压的调节。     

Effect of clentiazem on arterial pressure and renal function in normotensive and hypertensive rats.

The present study evaluated the effects of a new benzothiazepine calcium channel antagonist, clentiazem, on arterial pressure and renal function in spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto (WKY) and Munich-Wistar rats (MWR). Administration of clentiazem in doses from 1 to 20 micrograms/kg/min produced dose-dependent increases in sodium and water excretion in MWR, reaching maximum values of 292 and 376% of control, respectively, at the 20-micrograms/kg/min dose. Clentiazem (10 micrograms/kg/min) lowered arterial pressure by 16% and doubled glomerular filtration rate (GFR) in MWR. The rise in GFR was associated with an increase in glomerular capillary pressure of 16 mm Hg, produced by a combination of preglomerular vasodilation and efferent arteriolar vasoconstriction. In SHR, administration of clentiazem (10 micrograms/kg/min) lowered arterial pressure by 30 mm Hg and increased urine flow and sodium excretion by 137 and 200%, respectively. In WKY rats, the same dose of clentiazem decreased arterial pressure by only 10 mm Hg, whereas urine flow and sodium excretion increased 62 and 38%, respectively. A high dose of clentiazem (1 mg/kg bolus plus 1 mg/kg/hr infusion i.v.) lowered arterial pressure by 63 mm Hg in SHR. Renal vascular resistance fell by 39% and there was a 5-fold increase in sodium excretion. In WKY rats, the same dose of clentiazem reduced arterial pressure by 20 mm Hg, but it had no significant effect on sodium excretion. These results indicate that clentiazem increases sodium excretion and GFR in normotensive rats in part by preferentially dilating the renal preglomerular vasculature. This compound is also an antihypertensive agent that lowers arterial pressure and promotes sodium excretion in SHR.     

Effects of antihypertensive drugs on renal function and atrial natriuretic polypeptide in spontaneously hypertensive rats with renal ablation

To determine whether pharmacological control of blood pressure could affect the renal function and levels of atrial natriuretic polypeptide (ANP) in spontaneously hypertensive rats (SHR) with renal ablation, and to ascertain the benefits of antihypertensive drugs, we studied effects of oral administration of captopril (50 mg/kg/day), an inhibitor of angiotensin converting enzyme, benidipine (3 mg/kg/day) and nilvadipine (10 mg/kg/day), newly developed blockers of calcium channel, and indapamide (10 mg/kg/day) for 14 days on systolic blood pressure, serum creatinine, blood urea nitrogen, and plasma ANP concentration in SHR subjected to surgical removal of the left kidney and infarction of two-thirds of the right kidney (5/6 nephrectomy) a week before. Three weeks after the surgery, systolic blood pressure (mmHg) in the untreated group was 253 +/- 9 (n = 10), in the captopril group 156 +/- 9 (n = 7, p less than 0.05), in the benidipine group 197 +/- 9 (n = 7, p less than 0.05), in the nilvadipine group 146 +/- 9 (n = 7, p less than 0.05) and in the indapamide group 206 +/- 5 (n = 7, p less than 0.05). Serum creatinine (mg/100 ml) was lower in the captopril group (0.58 +/- 0.02, n = 7, p less than 0.05) and in the benidipine group (0.50 +/- 0.03, n = 7, p less than 0.05) but not in the nilvadipine group and in the indapamide group 3 weeks after 5/6 nephrectomy compared to the untreated group. Blood urea nitrogen was also lower in the captopril group and in the benidipine group but not in the nilvadipine group and in the indapamide group. Plasma ANP concentration was significantly reduced by the treatment with captopril and benidipine but not with nilvadipine and indapamide. These results suggest that the reduction of blood pressure by the inhibition of angiotensin converting enzyme with captopril has the potential to ameliorate renal function of the SHR with remnant kidney, a model of chronic renal failure with hypertension, associated with the decreased concentration of plasma ANP. However, it remains to be determined whether the reduction of blood pressure by calcium channel blockers may be involved in the delayed progression of renal failure in this model since there were disparate effects on renal function and plasma ANP concentration with these two calcium channel blockers.     

Circadian renal rhythms influenced by implanted encapsulated hANP-producing cells in Goldblatt hypertensive rats

Renal excretion in experimental hypertensive rats implanted with encapsulated human atrial natriuretic peptide (hANP)-producing cells is circadian periodic. Chinese hamster ovary (CHO) cells transfected with the plasmid hANP-cDNA were encapsulated in biocompatible polycaprolactone capsules for intraperitoneal implantation into two-kidney, one-clip (2K1C) hypertensive rats. During a 12:12 light-dark cycle, as compared to control CHO cells, the implantation of encapsulated hANP-producing CHO cells was associated with an increase in the net excretion of water, sodium and potassium, and with a reversal of the advanced circadian phases related to renovascular hypertension in 2K1C rats. The increase in blood pressure postimplantation was delayed, and increases in renal blood flow, glomerular filtration rate, sodium output, urinary excretion and urinary cyclic GMP concentrations were also found. Implantation of encapsulated hANP-producing cells affects circadian rhythms in kidney excretion functions of 2K1C rats, and may be useful for the treatment of cardiovascular disease.     

运动对高血压大鼠血压和内皮素的影响

目的押观察原发性高血压大鼠运动后血压、体质量以及血清内皮素的变化。方法押实验于2003-07/09在扬州大学实验动物中心完成。采用18只高血压大鼠作为实验动物,按实验需要将动物分为运动组穴10只雪和安静组穴8只雪。运动组经过10周的60min/d的训练熏5d/周,与安静组一起测量其血压、体质量;取静脉血,用放射免疫法测定内皮素。结果押实验进行至第5周运动组死亡1只大鼠。①血压:运动前两组大鼠血压无显著差异熏经过4,10周运动后运动组大鼠与安静组相比血压明显降低眼(174.1±1.4),(185.0±1.4)mmHg;(166.6±1.1),(193.9±1.8)mmHg,P<0.01演。②体质量:两组动物在生长过程中体质量均逐渐增高,但运动组增长的趋势低于安静组,经10周运动后运动组的体质量明显低于安静组眼(344.60±2.57),(362.00±5.26)g,P<0.05演。③内皮素:经过10周的游泳训练后,运动组内皮素明显低于安静组眼穴44.75±4.45雪,穴68.36±5.93雪ng/L,P<0.01演。结论押运动对高血压大鼠的体质量增长有抑制作用,且高血压大鼠经过游泳训练后其血内皮素水平下降,而血压也随之下降,提示运动对高血压大鼠的降压部分是通过影响内皮素的产生和释放来实现的。     

低强度游泳运动对自发性高血压大鼠C反应蛋白的影响

目的研究低强度游泳运动对自发性高血压大鼠(SHR)C反应蛋白(CRP)的影响。方法24只8周龄SHR大鼠随机分为对照组及运动组,运动组进行游泳运动1 h/d,5 d/w,共10 w。每周测量大鼠尾动脉压,实验结束时检测CRP水平。结果10 w低强度游泳运动明显降低SHR大鼠血压及CRP水平。结论低强度游泳运动有助于降低高血压患者的血压并减少心血管系统并发症。     

运动训练联合基因治疗对自发性高血压大鼠心功能的影响

目的：研究运动训练联合β1肾上腺素能受体反义基因治疗对自发性高血压大鼠（SHR）血压、心功能、心脏β1受体mRNA、蛋白的影响，探讨运动训练联合β1受体反义基因治疗改善心功能的机制。方法：阳离子脂质体混合物与β1反义寡核苷酸（β1-AS-ODN）经鼠尾静脉注射，Tail—cuff法检测血压，颈动脉插管测定血流动力学指标，半定量RT—PCR测定β1 mRNA水平，Western印迹测定心脏β1受体的蛋白水平。结果：与SHR组比较，运动联合基因治疗可以使血压下降维持4周，血压最大下降40mmHg，LVSP、LVEDP显著降低（P〈0．01，P〈0．01），左室最大收缩和舒张速率显著升高（P〈0．01，P〈0．01），β1受体mRNA明显降低（P〈0．05），β1受体蛋白表达水平显著降低（P〈0．01）。结论：运动训练联合β1受体反义基因治疗可以明显地降低血压，改善心功能；其机制是运动训练增强基因治疗对β1受体mRNA和蛋白的抑制作用，在转录和转录后抑制过度激活的β1受体的表达。     

Thyroid function and blood pressure in two new strains of spontaneously hypertensive and normotensive rats

1. The influence of thryoid function on the development of hypertension was studied in strains of spontaneously hypertensive (SH) and normotensive rats. 2. Surgical thyroidectomy decreased systolic blood pressure more markedly in SH rats than in normotensive rats. The effects of oral administration of 5 and 100 micrograms of thyroxine 24 h-1 100 g-1 were studied in the thyroidectomized animals. In the two strains the blood pressure returned to control levels only after administration of the larger dose. 3. The evolution of body weight, total plasma tri-iodothyronine (T3) and tetraiodothyronine (T4) concentrations were followed as a function of age in SH rats and normotensive rats from 5 to 21 weeks. At each age, SH rats showed significantly larger body weight and decreased T4 concentrations. Plasma T3 in SH rats was lower than in normotensive rats until 15 weeks of age, after which the difference was not significant. At 11 weeks, plasms free T3 and T4 concentrations were slightly lower in SH rats than in normotensive rats. 4. The more marked hypotensive effects of surgical thyroidectomy in SH rats cannot be related to increased thyroid function.     

Intrarenal hemodynamics and blood pressure in hypertensive patients with renal artery anomalies

AIM: To determine characteristics of a clinical course, 24-h profile of arterial pressure (AP), of renal hemodynamics, involvement of target organs in patients with arterial hypertension (AH) of the third degree and anomalies of renal arteries. MATERIAL AND METHODS: 24-h monitoring of AP, echocardiography, measurement of microalbuminuria, renal hemodynamic were made in 15 patients (9 female, 6 male) having resistant AH of the third degree and different anomalies of renal arteries (mean age 45.3 +/- 1.9 years). The control group consisted of patients with essential AH stage III (mean age 45.3 +/- 1.8 years). The groups were comparable by sex, age, duration of AH. RESULTS: The patients of the study group had a significantly lower pulsatility index in the renal artery and interlobular level and resistance index at the segmental and interlobular level of the RA on the side of the anomaly. There was a significantly higher minimal diastolic blood flow velocity in the segmental level of RA on the side of the anomaly. Renal scintigraphy revealed a decreased index of radiopharmaceutical accumulation. A positive correlation was found between the pulsatility index, resistance at a segment RA level and variability, an increase of morning diastolic blood pressure. The groups had significant differences neither by 24-h AP indices nor by severity of target organ lesion. CONCLUSION: Patients with RA anomalies have specific renal hemodynamics determining renal hypoperfusion on the side of the anomaly which may be involved in development of resistance to hypotensive therapy.     

高血压合并慢性肾脏病患者的动态血压分析

目的 探讨原发性高血压合并慢性肾功能不全后动态血压的变化特点.方法 对28例单纯原发性高血压患者(A组)和25例合并慢性肾脏功能不全的高血压患者(B组)进行动态血压监测.结果 ①血压比较:24 h舒张压B组高于A组[(80.9±13.4)mm Hg比(70.3±15.6)mm Hg,P＜0.05)];B组夜间的收缩压与舒张压均高于A组[(160.2±17.8)mm Hg比(140.3±25.9)mm Hg和(82.6±16.1)姗Hg比(68.8±20.2)mm Hg,P＜0.01].②血压变异性比较:B组24 h收缩压变异性和舒张压变异性均高于A组[(13.5±3.9)mm Hg比(11.3±2.1)mm Hg和(9.2±1.2)mm Hg比(8.3±1.8)mm Hg,P＜0.05],B组夜间的收缩压与舒张压变异性均高于A组[(14.9±3.3)mm Hg比(9.3±2.1)mm Hg和(9.7±2.4)mm Hg比(8.0±2.2)mm Hg,P＜0.01)].③血压趋势比较:A组血压趋势以非勺型为多,占64.3%(18/28),反勺型占10.7%(3/28);而B组反勺型占48.0%(12/25),非勺型占40.0%(10/25).结论 肾性因素参与的高血压患者血压趋势紊乱,夜间血压及变异性明显增加,均可成为肾功能继续恶化和心脑血管事件发生的重要因素.     

运动训练及依那普利对自发性高血压慢性肾功能衰竭大鼠模型肾功能的影响

目的:应用高血压肾功能衰竭大鼠模型,探讨运动训练与肾素血管紧张素转换酶抑制剂依那普利联合应用对肾功能的影响。方法:8周龄雄性自发性高血压大鼠24只,行右肾2/3切除,左肾全摘除,建立5/6肾切除自发性高血压慢性肾功能衰竭模型。于10周龄时,随机分为非运动组、中等强度运动训练组和运动训练加依那普利组。其中运动训练组所有动物进行跑台训练,速度20m/min,60min/d,5d/w。依那普利2mg/(kg·d)腹腔内持续给药。结果:4周运动训练明显抑制尿蛋白分泌,减小肾小球硬化指数。而运动训练加依那普利使血压明显下降和进一步减小肾小球硬化指数。结论:中等强度运动训练对慢性高血压肾功能衰竭模型有延缓肾衰进展、保护肾功能的作用。运动训练与依那普利联合应用能进一步增强这种肾脏保护作用。