Table of Content

15 October 1990, Volume 11 Issue 4

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多肽研究

Effects of Endothelin on Blood Vessels and Heart of Rats and Regional Cerebral Blood Flow in Rabbits

Sheng Shuli;Wu Jie;Wang Jian;Zhang Wanjiang;Chen Yanjiang;Wang Xiaohong;Ji Ying;Su Mincheng;Liu Jin;Zhou Li;Luo Lin

1990, 11(4):  239-246. 

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Endothelin(ET) is known as a most potent constrictor of blood vessel. The molecular structure of ET is similar to sarafotoxin S6b. In present study we examined the effects of ET on blood vessels and heart in rats in vitro and vivo and the effect of ET on regional cerebral blood flow (rCBF) in rabbits. Our results show that in vitro ET(10mol/L) strongly constricted all arteries we used including basal cerebral artery, coronary artery and femoral artery which were isolated from human. The effect of ET was more than 1000 times as strong as noradrenaline and serotonin and much stronger than CCK. The contractile effect of ET lasted more than 2 hours and the effect could be attenuated by CGRP and BNP. The administration of ET at a dose no less than 110pg through the internal carotid artery induced a decline of rCBF in rabbits, The effect was dose-dependent. The intravenous injection of ET(32μg/kg) elicited various ECG abnormalities from T wave change to ventricular arrest and a decline of blood pressure in rats. The cardiac-toxicity caused by ET could be prevented by the administration of CGRP (46μg) or Sodium Nitroprusside (1mg/kg). However, the cardiac-toxicity caused by isoadrenalin could not be prevented by CGRP, it indicated that the cardiac-toxisity of ET is a result of vasoconstriction of ET on coronary arteries. We also found that the intracerebroventricular injection of ET (5ng, 10μl) elevated plasma aldosterone in rats. In vitro, the perfusion experiment showed that ET inhibited vasopresin secretion from hypothalamus. We conclude that ET plays a most important role in regulation of blood pressure and blood flow.

Hindlimb Paralytic Effect of Endothelin following Spinal Subaraehnoid Injection in the Rat

Sheng Shuli;Wang Xiaohong;Cheng Yanjiang;Chao Li;Wu Jie;Su Mincheng

1990, 11(4):  247-250. 

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Our previous studies have demonstrated that CGRP could attenuate the effects of ET on blood vessels, regional cerebral blood flow and heart. This contribution of CGRP resulted from a most potent dilation of blood vessels. In this research, rats were administrated ET 10μl into the spinal subarachnoid space at lumbar-sacral region. Some rats were monitored BP, heart rate and the contents of plasma ANP and AVP were determined. The rat appeared variably paraplegic a few minutes after giving ET. When the ET dose was over 40ng, they had a high mortality. When no more than 30ng was administrated, the mortality of rat was 20%. Among survivors, 98% had reversible paraplegia, 25min after CGRP administration, a significantd egree of recovery of paraplegia recovered. Pathological examination 4h after onset of paraplegia showed serious ischemia of spinal cord. It indicates the hindlimb paraplytic effect of ET is probably due to potent constriction of blood vessels. We also observed a few increase of BP and heart rate in the rats I. T. injected ET, but no change after i. v. administration of the same dose of ET. It suggests that the pressor to I. T. ET did not resulted from I. T. ET to peripheral blood flow, it is possible to be induced by the neuronal reflex of I. T. injection of ET.

The Morphological Alteration of the Spinal Cord following Intrathecal Injection Endothelin in the Rat

Chao Li;Luo Ling;Wang Xiaohong;Chen Yanjiang;Sheng Shuli

1990, 11(4):  251-254. 

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Endothelin was injected into subarachnoid space of spinal cord in eighteen rats. The functional state of the animals hindlimbs was observed and recorded. After half an hour, two hours or four hours the rats were killed. Pathologicaly the spinal cord revealed ischemic and hypoxic changes. The changes at two hours and four hours were more severe than that of half an hour. The changes of thoracic and lumbar segment of the spinal cords were more severe than that of the cervices and sacra. We found that the founctional state of rat hindlimbs was not in proportion to the morphological changes of corresponding spinal cord.

Effect of Brain Natriuretic Peptide on Secretion of Atrial Natriuretic Peptide in Rats

Zhang Wanjiang;Liu Jin;Chen Yanjiang;Ji Ying;Sheng Shuli

1990, 11(4):  255-258. 

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Brain natriuretic peptide (BNP) is a 26 amino acid peptide which not only shows a high sequence homology to atrial natriuretic peptide (ANP), but also has very similar pharmacological effects to that of ANP. It have also been found that BNP interacts with ANP receptor. We consider that the secretions of BNP and ANP must interrelate and interact with each other. Based on that fact, we conducted the present study. Our results show that the infusion of BNP (40ug/kg) for 60 minutes leads to an increase of both ANP level in plasma and ANP content in atria, In vitro BNP (10mol/L) perfusion cannot stimulate the atrium to secrete ANP. We consider that the increase of both ANP level in plasma and ANP content in atriums is a result of an increase of synthesis and secretion of ANP in atria, but it is not a direct effect of BNP on atria. We infer that because of the binding of BNP to ANP receptor, there is a decrease in quantity of ANP receptors and it leads to a compensatory increase of ANP. We also found that NPY plasma concentration increased foolowing the infusion of BNP. We consider that it is a result of conpensation to weaken the vasodilatory effect of BNP on arteries.

The Effect of CGRP on Human Cerebral Artery and Cerebral Blood Flow

Sheng Shuli;Zhang Wanjiang;Wu Jie;Sun Bo;Liu Yanjin;Gao Fengqin;Ji Ying;Wu Jianzhong;Wang Tianyou;Zhan Qimin;Yang Rushan;Xu Dong

1990, 11(4):  259-265. 

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CGRP is present in nerve fibres in central and peripheral arteries, where it is a potent vasodilator. The purpose of our research is to examine the effect of CGRP on human cerebral arteries and cerebral blood flow (CBF). Our results show that 1) CGRP can significnatly blunt the vasoconstriction caused by ebdothelin, neuropeptide Y (NPY), serotonin, noradrenaline, and CCK; 2) 50μg CGRP injected iv for 10 minutes into three patients who had cerebral embolisms increased CBF 32%～80% as measured by single photon emission computed tomography (SPECT), the levels of NPY, renin and angiotensin II in the patients' blood did not change after administration of CGRP; 3) an increase in CBF was seen in rabbits following injections of CGRP (4μg) into the internal carotid artery; 4) the intracerebroventricular (i. c. v. ) administration of endothelin (5ng) caused a decrease in CBF in rats, but it was reversed by CGRP (5ng, i. c. v. ); and 5) endothelin (5ng, i. c. v.) also induced an elevation of plasma alsosterone, but it was not antagonized by CGRP (5ng, i. c. v.). We conclude that CGRP can counteract the constriction of human arteries by various agents and increase CBF significantly. We deduce that the effect of CGRP is mediated by the increased calcium influx through dihydropyridine-sensitive calcium channels.

Effect of Calcitonin Gene Related Peptide on the Arrhythmia Caused by Adenosine Diphosphate and Deacetyl-Lanatoside C in Rats

Zhang Jianfeng;LiuJin;Sheng Shuli;Zhang Wanjiang

1990, 11(4):  266-269. 

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We investigated the effect of CGRP on the arrhythmia induced by two drugs in rats, The result of our experiment has proved that CGRP could reduce the degrees of A-V block, resist the attack of sinus stanstill and ventricular fibrillation produced by ADP, and improve restoration of sinus rhythm. CGRP could obviously eliminate sinus stanstill and ventricular fibrillation resulted from deacetyl-lanatoside C. These evidences demonstrate that CGRP is a peptide with a strong antiarrhythmic effect.

The Role of Measurement of Plasma Level of Atrial Natriuretic Peptide in the Appraisal of Heart Failure and Essential Hypertetnion of Different Stages

Liu Jin;Liu Xuanzhong;Zhang Jianfeng;Sheng Shuli;Chert Yanjiang;Su Mincheng;Zhang Wanjiang

1990, 11(4):  272-275. 

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The plasma ANP level of patient with heart failure and essential hypertention Was measured by the radioimmunoassay. The results showed that there was relationship between the plasma ANP level and heart failure (r= 0.71, Ｐ <0.01). The concentration of ANP increased while cardiac failure occured; The increase of plasma ANP level of patients suffered from hypertention with low different stages of hypertention Was found (r=0.74, P <0.01).

Improvement of Synthetic Method of Thyrotropin Releasing Hormone

Zhangjia Jin;Zhang Shaodong;She Shuli

1990, 11(4):  276-278. 

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TRH was synthesized by a new method introduced by G. Hotanaka in 1974. According to this principle of this method, we have made each step concrete and obtained a good result. This method is easy to undertake and not necessary to make chromatography for purification.

Biolgical Activity of a New AngiotensinⅠConverting Enzyme Inhibitor and a N-terminal Fragment of Substance P

Guo Chunyuan;Liu Chuandi;Sheng Shuli;Liu Aimin;Chen Yanjiang;Hu xiaoyu

1990, 11(4):  279-282. 

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A new angiotensin I converting enzyme inhibitor(AI, Pro-Thr-His-Ile-Lys Trp-Gly-Asp) and a N-terminal fragment of substance P (SP3-4, Gly-Phy) were synthesized by solid phase method. Their capacity to inhibit angiotensin I converting enzyme (ACE) seperated from human blood, brain and lung was tested by biochemical assay. Results showed that 1. All of the synthetic peptides were_assayed and their purity was>95% as established by HPLC analysis. 2. The AI inhibited the ACE from human blood(IC50 19±4.6μmol/L) brain (IC50 26±6.3μmol/L) and lung (2 cases, IC5011.9～14.1μmol/L) but the SP3-4 failed to inhibited the ACE from human being.

The Morphological Change of “Pituitary Dwarf” Induced by Monosodium Glutamate on Rats

Yang Peisun;Lin kai;Sheng Shuli;Gao Lin

1990, 11(4):  283-288. 

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Wister newborn male rats were divided into two groups, one group was administrated MSG(4g/kg)by s.c. every two days from the second day to the tenth after birth. Another group was gaven N.S. as control. At the hundredth day, the rats were decapitated. We found that the rats' body weight and length in experimental grounp reduced significantly as compared with those in control group. There was no difference between two groups on brain weight and intelligence, although the reduction of weight of viscera was obvious in experimental group. The nucleus arcuatus were apparently smaller and the number of neurone were obviously less than those in the control. The weights of piutitary glands in experimental group were as 55.8 per cent as those in control group. The result of immunohistochemistry revealed the presence of GH-secreting cell in the pituitary glands of rats treated with MSG, but the number and area of these cells measured by image analyser were smaller. According to these results, we consider that the damage of nucleus arcuatus induced by MSG obviously decreases the secretion of growth hormon releasing factor, therefore, the secretion of GH is insufficant in pituitary gland and the differentiation of GH-secreting cells can not be promoted. The conc- lusion is that the dwarfism model induced by MSG in rats is very similar to pituitary dwarf of human being,

Effect and Mechanism of Growth Hormone-Releasing Factor to Growth Hormone Release

Guo Chunyuan;Liu Chuandi;Sheng Shuli;Gao Lin;Chen Yanjiang;Liu Yanjin;Hu Xiaoyu

1990, 11(4):  289-294. 

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Growth hormone releasing factor(GRF), growth hormone releasing peptide (GHRP) and GRF-antagonist (GRF-AN, D-Arg2-GRF₄₄) were synthesized by solid phase method and their biological activities were detected in our institute. The result is reported as follows. 1.Both GHRP and GRF can stimulate human pituitory growth hormone (GH) secretion in vitro and in vivo.2.Both GHRP and GRF can stimulate bovine pituitory GH secretion in vitro,3.GHRP can accelerate immature rats growth 4 GRF-AN has a strong seletive inhibition on human and animal pituitory GH secretion stimulated by GRF and has no inhibition on GH secretion stimulated by GHRP. Our investigation indicates that both GRF and GHRP can stimulate pituitary GH secretion, but there is a essential distinction in mechanism between them.

Immunostimulatory Effect of Artificial Systhetic TP5

Liu Junda;Li Changlong;Shi HongWei;Gao Lin;Liu Yanjing;Sheng Shuli

1990, 11(4):  295-298,325. 

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This study reported on the systhesis of thymopoietin pentapeptide (TP5) and its biochemical properties. We have investigated the immunostimulatory effect of this artificial systhetic TP5. The results showed that TP5 has markedly promotive influence on weight and histological characteristic of spleen of mice, The transformation, rate of E-rosete formation and plaque forming cell (PFC) of spleen lymphocyte in experimental animal group that were injected TP5 are significantly higher than that of control group. Author discussed mechanism of effect and prospect of clinical trial of TP5 in future.

多肽研究

Synthesis of KA8 Peptide and its Inhibitory Effect on Pentagastric-Stimulated Gastric Acid Secretion in Rats

Zhang Jiajin;Zhang Shaodong;Zhang Hui;Guan Lingling;Sheng Shuli;Liang Peixia

1990, 11(4):  299-301. 

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KA8 peptide is a c-terminal octapeptide 30～37 of oxyntomodulin 1～37. Oxyntomodulin 1～29 is a glucagon, which can increasa the concentration of blood glucose, but oxyntomodulin has a obvious inhibition of gastrie acid secretion. In order to understand the KA8 biologieal activity, we have synthesized KA8 and injected to rats before administration of pentagastrin. The experiment showed that pentagastrin stimulated definitively gastric acid secretion. However, KA8 could eliminated the pentagastrin induced gastric acid secretion. Our result reveals that KA8 plaies probably a important role in the regulation of gastric acid secretion.

KA8 Inhibite Gastric Acid Secretion Induced by Cold-restraint Stress and Intracisteral TRH in Rat

Zhang Shaodong;Guan Lingling;Liang Peixia;Wang Xiaohong;Zhang Jiajing;Yang Zhaoxiu Zhang Hui;Chen Yanjiang;Sheng Shuli

1990, 11(4):  302-304. 

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KA8 is a C-terminal octapeptide (30-37) of oxyntomodulin and glicentin. KA8 could inhibite gastric secrection. But it is not clear if KA8 is able to inhibite gastric secrection induced by cold-restraint and TRH administration in intracerebroventricle. We designed two experiments. All the rats were fasted for 24 h before experiment. The rats with light ether anaesthesia were undertook the operation of pylorus and cardia ligation. After the rats remained consciousness, the rats were divided into two groups. One Was injected by iv KA8 (60μg/kg), another was gaven NS as control, then the rats were sxposed 4 C enviroment for 2 hours. In the second experiment, the rats were implanted with tube in cerebro-ventricle before one week. The rats were administrated TRH (60μg/kg) through the tube and divided into two groups. One was injected by iv KA8, another Was received NS as a control. Each rat was placed in separated cage for 4 hours. All rats were decapitated and plasmas were stored in -20℃ for gastrin determination. The resoults shown that KA8 could significantly inhibited gastric secretion not only for rats exposed to cold, but also for TRH icy administration. But KA8 was not able to infulence the plasma concentration of pentogastrin. It suggest that KA8 inhibit gastric secretion but the biologica activity of KA8 is not associated with pentogastrin.