Brain catecholamines and organ weight of mice genetically selected for high and low blood pressure.

Statistically significant differences were found between the high and low genetically selected blood pressure lines for systolic blood pressure, norepinephrine content of whole brain, absolute heart weight, heart to b. wt ratio, kidney weight, kidney to b. wt ratio, and adrenal to b. wt ratio.     

On the mineralocorticoid and hypertensogenic properties of 16beta-hydroxy-dehydroepiandrosterone.

Dosages of either 1 or 2 mg daily of 16beta-hydroxy-dehydroepiandrosterone, given to mononephrectomized, salt-loaded female rats, had no detectable effect upon saline consumption, blood pressure, kallikrein excretion or heart and kidney weight. Its alleged mineralocorticoid properties, as judged by these criteria, were not demonstrable.     

Methimazole treatment reduces cardiac hypertrophy and mortality without a concomitant reduction in blood pressure in established Goldblatt two-kidney one clip hypertension

The effects of methimazole, and antithyroid drug, on blood pressure and other parameters were evaluated in the established phase of Goldblatt two-kidney one clip (G2K-1C) hypertension. Methimazole was administered via drinking water for five weeks, starting five weeks after hypertension had been induced. After this period of treatment, similarly high blood pressures were observed in methimazole-treated and non-treated G2K-1C rats, despite the fact that a hypothyroid state had been achieved in methimazole-treated rats. Methimazole-treated G2K-1C rats showed reductions in heart rate, ventricular weight, ventricular/body weight ratio and mortality in comparison with rats not treated with methimazole. These results clearly demonstrate that hypothyroidism induced by methimazole: a) does not reverse G2K-1C hypertension, but b) improves the rate of survival and c) reduces relative cardiac hypertrophy, possibly by the reduction in cardiac work observed in Goldblatt hypothyroid rats.     

Methimazole treatment reduces cardiac hypertrophy and mortality without a concomitant reduction in blood pressure in established Goldblatt two-kidney one clip hypertension.

The effects of methimazole, an antithyroid drug, on blood pressure and other parameters were evaluated in the established phase of Goldblatt two-kidney one clip (G2K-1C) hypertension. Methimazole was administered via drinking water for five weeks, starting five weeks after hypertension had been induced. After this period of treatment, similarly high blood pressures were observed in methimazole-treated and non-treated G2K-1 C rats, despite the fact that a hypothyroid state had been achieved in methimazole-treated rats. Methimazole-treated G2K-1 C rats showed reductions in heart rate, ventricular weight, ventricular/body weight ratio and mortality in comparison with rats not treated with methimazole. These results clearly demonstrate that hypothyroidism induced by methimazole: a) does not reverse G2K-1 C hypertension, but b) improves the rate of survival and c) reduces relative cardiac hypertrophy, possibly by the reduction in cardiac work observed in Goldblatt hypothyroid rats.     

Calcitonin: effect on protein synthesis in different rat tissues

Protein synthesis was inhibited in the pancreas whereas it was enhanced in the kidney and intestine (jejunum-ileum) after a single injection of porcine calcitonin (20 MRC units/kg b.wt). The incorporation of [3H]leucine into total protein in the brain, heart, liver and stomach did not change after the hormone treatment.     

Monoaminoguanidine prevents sorbitol accumulation, nonenzymatic protein glycosylation and development of kidney lesions in diabetic rats

Monoaminoguanidine administration (25 mg/kg b.wt, i.p. for 14 weeks) to alloxan diabetic rats (blood glucose greater than or equal to 250 mg/dl) decreased the nonenzymatic protein glycosylation and sorbitol levels. It prevented development of Armanni-Ebstein tubular lesions, pathological changes in the glomerular capillary tufts and glomerular basement membrane thickening in the kidney.     

Effect of bilateral nephrectomy on the recovery of blood pressure after acute hemorrhage in rats: role of renin-angiotensin system

The effect of bilateral nephrectomy, and administration of an inhibitor of angiotensin converting enzyme, on the recovery of arterial blood pressure after hemorrhage (loss of 1% of b.wt), was studied in male Sprague-Dawley rats. Neither manoeuver significantly affected the recovery of blood pressure within the first 10 min after hemorrhage. Thereafter, the recovery of the blood pressure was markedly suppressed. The study suggests that the initial recovery of blood pressure is unrelated to the kidneys, but the later one requires their presence and depends on the activity of the renin-angiotensin system.     

Calcitonin: Effect on protein synthesis in different rat tissues

Summary Protein synthesis was inhibited in the pancreas whereas it was enhanced in the kidney and intestine (jejunumileum) after a single injection of porcine calcitonin (20 MRC units/kg b.wt). The incorporation of [³H]leucine into total protein in the brain, heart, liver and stomach did not change after the hormone treatment.Acknowledgment. This work has been achieved at the Institute of Medical Biochemistry, University of Aarhus, Aarhus, Denmark.     

On the mineralocorticoid and hypertensogenic properties of 16β-Hydroxy-Dehydroepiandrosterone

Summary Dosages of either 1 or 2 mg daily of 16-hydroxy-dehydroepiandrosterone, given to mononephretomized, salt-loaded female rats, had no detectable effect upon saline consumption, blood pressure, kallikrein excretion or heart and kidney weight. Its alleged mineralocorticoid properties, as judged by these criteria, were not demonstrable.This study was supported by a grant No. HL 15319 from the United States Public Health Service.     

WNK signalling pathways in blood pressure regulation

Hypertension (high blood pressure) is a major public health problem affecting more than a billion people worldwide with complications, including stroke, heart failure and kidney failure. The regulation of blood pressure is multifactorial reflecting genetic susceptibility, in utero environment and external factors such as obesity and salt intake. In keeping with Arthur Guyton’s hypothesis, the kidney plays a key role in blood pressure control and data from clinical studies; physiology and genetics have shown that hypertension is driven a failure of the kidney to excrete excess salt at normal levels of blood pressure. There is a number of rare Mendelian blood pressure syndromes, which have shed light on the molecular mechanisms involved in dysregulated ion transport in the distal kidney. One in particular is Familial hyperkalemic hypertension (FHHt), an autosomal dominant monogenic form of hypertension characterised by high blood pressure, hyperkalemia, hyperchloremic metabolic acidosis, and hypercalciuria. The clinical signs of FHHt are treated by low doses of thiazide diuretic, and it mirrors Gitelman syndrome which features the inverse phenotype of hypotension, hypokalemic metabolic alkalosis, and hypocalciuria. Gitelman syndrome is caused by loss of function mutations in the thiazide-sensitive Na/Cl cotransporter (NCC); however, FHHt patients do not have mutations in the SCL12A3 locus encoding NCC. Instead, mutations have been identified in genes that have revealed a key signalling pathway that regulates NCC and several other key transporters and ion channels in the kidney that are critical for BP regulation. This is the WNK kinase signalling pathway that is the subject of this review.     

Effect of bilateral nephrectomy on the recovery of blood pressure after acute hemorrhage in rats: Role of renin-angiotensin system

Summary The effect of bilateral nephrectomy, and administration of an inhibitor of angiotensin converting enzyme, on the recovery of arterial blood pressure after hemorrhage (loss of 1% of b.wt), was studied in male Sprague-Dawley rats. Neither manuver significantly affected the recovery of blood pressure within the first 10 min after hemorrhage. Thereafter, the recovery of the blood pressure was markedly suppressed. The study suggests that the initial recovery of blood pressure is unrelated to the kidneys, but the later one requires their presence and depends on the activity of the renin-angiotensin system.     

Monoaminoguanidine prevents sorbitol accumulation,nonenzymatic protein glycosylation and development of kidney lesions in diabetic rats

Summary Monoaminoguanidine administration (25 mg/kg b.wt, i.p. for 14 weeks) to alloxan diabetic rats (blood glucose 250 mg/dl) decreased the nonenzymatic protein glycosylation and sorbitol levels. It prevented development of Armanni-Ebstein tubular lesions, pathological changes in the glomerular capillary tufts and glomerular basement membrane thickening in the kidney.CDRI Communication no. 4694.     

Glomerular filtration rate and kidney blood flow in alloxan and streptozotocin diabetic rats.

Glomerular filtration rate (GFR), cardiac output, regional blood flow and kidney weight were measured in alloxan and streptozotocin diabetic rats at different times after the administration of diabetogen. A high GFR was found together with increased kidney weight and reduced blood flow.     

Bombesin promotes pancreatic growth in suckling rats

The pancreatic growth promoting effect of long term administration of bombesin was investigated in suckling rats. The authors showed that bombesin given in 10 micrograms/kg b.wt doses s.c. every 8 h for 10 days from the day of parturition stimulated pancreatic growth: it increased pancreatic weight, protein and DNA content, trypsin and amylase activity and trypsin/DNA ratio. Conclusion: Bombesin is an effective stimulator of pancreatic growth in suckling rats.     

Glomerular filtration rate and kidney blood flow in alloxan and streptozotocin diabetic rats

Summary Glomerular filtration rate (GFR), cardiac output, regional blood flow and kidney weight were measured in alloxan and streptozotocin diabetic rats at different times after the administration of diabetogen. A high GFR was found together with increased kidney weight and reduced blood flow.     

Potentiating effect of aldosterone on the diuretic action of atrial extract

The typical stimulatory effect of a rat heart atrial extract on urinary water, sodium, potassium and kallikrein excretion is significantly increased by a previous administration of aldosterone (0.5 microgram/100 g b. wt) in the rat.     

解聚复肾宁对糖尿病肾病大鼠TNF—OL、MCP-1的影响

目的观察解聚复肾宁（Jiejufushenning,JJFSN）对糖尿病（Diabetes mellitus,DM）大鼠肾组织肿瘤坏死因子-α（Tumorneerosisfactor-alpha,TNF-α）、单核细胞趋化蛋白-1（Monocyte chemoattractant protein-1,MCP-1）和血清TNF-α的影响,探讨其肾保护作用机制。方法腹腔注射链脲佐菌素（Streptozotocin,STZ）建立SD大鼠DM模型,将成模DM大鼠随机分为3组：DM模型组（B组）、JJFSN组（C组）、厄贝沙坦（Irbesartan）组（D组）,另设正常对照组（A组）。采用相应干预措施处理12周。常规方法测定12周末各组大鼠空腹血糖（FBG）、血尿素氮（BUN）、血肌酐（Scr）、肾重／体重（KW／BW）、24h尿蛋白（24huFro）;放免法测血清TNF-α含量：免疫组织化学方法测肾组织TNF—Ot、MCP-1的表达;PAS染色评估细胞外基质;电镜观察肾组织超微结构改变。结果与A组相比．B组大鼠FBG、BUN、Scr、KW／BW、24huPro及血清TNF-α升高（P〈0．05）,肾组织TNF—Ot、MCP-1表达明显增高（P〈0．05）;肾组织超微结构明显异常;C组和D组上述指标显著改善（P〈0．05）,肾组织超微结构异常改善。结论竹FSN能延缓DM大鼠肾损害进程,其机制可能与抑制TNF-α、MCP-1上调有关。     

一种基于集总参数的心血管系统仿真模型及心音产生机理

基于流体力学与电气网络的相关基础理论,建立一种基于集总参数的心血管系统仿真模型.该心血管系统仿真模型分为三个子模型:体循环子模型、肺循环子模型及心脏子模型.重点分析了体循环子模型和心脏子模型,给出收缩压、舒张压、射血分数等血流参数和仿真波形图,并对心音产生机理进行了分析.然后在此基础上进行扩展,增加了肺循环、血管、耦合壁等,使其形成一个闭合的循环回路,构成了心血管系统仿真模型.利用状态变量分析法建立该模型的数学表达式,并进行模拟仿真,得出心室心房血容量、心房心室压力、动脉血流量等仿真结果,该结果符合健康心脏的生理状况,并且利用该模型仿真了高血压病态和心衰病态状况,仿真结果与临床表现基本一致,表明本文提出的心血管系统仿真模型具有实际的可行性.     

Effect of insulin in vivo on the synthesis of free fatty acids (FFA) in chicken heart and skeletal muscle

Summary The effect of insulin on the synthesis of free fatty acids from glucose in the skeletal and heart muscles of chicken is examined. 10 min after glucose-(U-¹⁴C) administration, labeled free fatty acids (FFA) appeared in both skeletal and heart muscles. 0.75 IU of insulin kg^–1 b. wt significantly increased the labeled FFA at the 30, 60 and 120 min intervals, with a maximum at 60 min.     

Bombesin promotes pancreatic growth in suckling rats

Summary The pancreatic growth promoting effect of long term administration of bombesin was investigated in suckling rats. The authors showed that bombesin given in 10 g/kg b.wt doses s.c. every 8 h for 10 days from the day of parturition stimulated pancreatic growth: it increased pancreatic weight, protein and DNA content, trypsin and amylase activity and trypsin/DNA ratio. Conclusion: Bombesin is an effective stimulator of pancreatic growth in suckling rats.