Ithas been demonstrated thatblood pressure variability (BPV) is increased in hypertension and related to or- gan damage.It will be important to lower BPV in the treatment of hypertension.The present study was designed...Ithas been demonstrated thatblood pressure variability (BPV) is increased in hypertension and related to or- gan damage.It will be important to lower BPV in the treatment of hypertension.The present study was designed to investi- gate the effect of ketanserin,a 5 - HT2 Areceptor antagonist with a weakα1 - adrenoceptor blocking effect,on BPV in conscious spontaneously hypertensive rats(SHR) .It was found that ketanserin decreased blood pressure(BP) and BPV in SHR when administered intravenously(3mg/ kg,i.v.) .Ketanserin decreased BPV,butnot the BP level,when adm inistered intracere- broventricularly (5 0μg/ rat,i.c.v.) . Prazosin,allα1 - adrenoceptor antagonist,lowered BP but did not affect BPV when giv- en either i.v. (0 .5 m g/ kg) or i.c.v. (30 μg/ rat) .Ritanserin(0 .6 2 5 mg/ kg,i.v.;4 0 μg/ rat,i.c.v.) ,a5 - HT2 A receptor antagonist,decreased BPV only when administered i.c.v.,and did not modify the BP level.Ketanserin enhanced arterial baroreflex function in SHR when given either i.v. or i.c.v.. The stabilizing effect of ketanserin on BP was persistent when administered intragastrically.This adm inistration route is similar to oral adm inistration clinically.It is concluded that ke- tanserin is an antihypertensive agent with an effect of reducing BPV. This effect is m ainly mediated by central 5 - HT2 Arecep- tors and is probably attributable to the restoration of arterial baroreflex function.展开更多
AIM： To study the stability of portal hypertension （PHT） caused by partial ligation of the portal vein ligation （PVL） in a rat model.METHODS： Thirty male adult Wistar rats were divided into two groups： 10 in Gr...AIM： To study the stability of portal hypertension （PHT） caused by partial ligation of the portal vein ligation （PVL） in a rat model.METHODS： Thirty male adult Wistar rats were divided into two groups： 10 in Group Ⅰ received a sham operation; and 20 in Group Ⅱreceived partial PVL. Portal vein pressure （PVP） was measured at four time periods： before ligation, 2 wk, 6 wk and 10 wk postsurgery. Portal venography, blood sampling and liver and spleen pathological examinations were conducted at 10 wk after surgery.RESULTS： The PVP was 9.15± 0.58 cmH2O before ligation, and increased to 17.32 ±0.63 cmH2O 2 wk after PVL. By repeat measurement of the PVP in each rat, it was shown to remain elevated for 10 wk. There were no significant differences in the pressure measurements at 2 wk, 6 wk and 10 wk. Varices were found mainly in the mesenteric vein 2 wk after PVL, which were more obvious later, while these manifestations were similar at week 6 and week 10. Portal venography demonstrated the varices and collaterals. There was no significant change in liver pathology. The volume of the spleen was enlarged 2-fold after ligation, and the sinus of the spleen was enlarged due to congestion. Significant sinus endothelial cell proliferation was observed, but no evidence of hypersplenia was found on hemogram and biochemical examination.CONCLUSION： These findings suggest that a satisfactory prehepatic PHT rat model can be obtained by partial ligation of the portal vein, and this PHT rat model was stable for at least 10 wk.展开更多
Objective To clarify whether the disturbances in metabolic kinetics of the essential aminoacid, phenylalanine (phe), are implicated in the genetic pathogenesis of essential hypertension (EH).Methods 1. L-(2, 3D3)-le...Objective To clarify whether the disturbances in metabolic kinetics of the essential aminoacid, phenylalanine (phe), are implicated in the genetic pathogenesis of essential hypertension (EH).Methods 1. L-(2, 3D3)-leucine, L-(2, 3D3)-isoleucine, L-15N-lysine, L-(2, 3D3)-valine and L-(2, 3D3)-phe were used for simultaneously studying comparative metabolic kinetics using stable isotope tracer methods with a GC-MS system. Study groups were the offspring with both parents suffering EH (n=10, FH+), 2 or more than 2 parents and grand-parents with EH and stroke (n=12, FS+) and those without genetic predisposition of EH and stroke (n=12, F) groups. 2. By comparing the radioactive counts of ［3H］-phe, and their weight transformation in blood after 1.5?Ci/kg i.v. administration at defined intervals and in tissues obtained after being sacrified among spontaneously hypertensive rats (SHR), 2 kidney-1 clip hypertensive rats (2K1C) and their normotensive controls (WKY). 3. The time transport and concentration transport of ［3H］-L-phe in cpm between the cultured vascular smooth muscle cell of 5th generation in SHR and WKY were compared.Results A single and unique disturbance of metabolic kinetics in phe were found in FH+, FS+ and SHR. The plasma pool or apparent volume of distribution was enlarged, and the turnover rate constants between plasma and cell tended to show a decrease. The pharmacokinetics of phe in 2K1C was not changed. Only phe content in heart and aorta, the vital organs for predicting BP, were higher in SHR than in WKY tissues studied. Both the time and concentration transport were higher in SHR, e.g., an increment in the net-uptake of L-phe by vascular tissue.Conclusion A unique aberrant of metabolic kinetics of phe might be implicated in the inherited pathogenesis of EH and stroke both from clinical and animal studies.展开更多
文摘Ithas been demonstrated thatblood pressure variability (BPV) is increased in hypertension and related to or- gan damage.It will be important to lower BPV in the treatment of hypertension.The present study was designed to investi- gate the effect of ketanserin,a 5 - HT2 Areceptor antagonist with a weakα1 - adrenoceptor blocking effect,on BPV in conscious spontaneously hypertensive rats(SHR) .It was found that ketanserin decreased blood pressure(BP) and BPV in SHR when administered intravenously(3mg/ kg,i.v.) .Ketanserin decreased BPV,butnot the BP level,when adm inistered intracere- broventricularly (5 0μg/ rat,i.c.v.) . Prazosin,allα1 - adrenoceptor antagonist,lowered BP but did not affect BPV when giv- en either i.v. (0 .5 m g/ kg) or i.c.v. (30 μg/ rat) .Ritanserin(0 .6 2 5 mg/ kg,i.v.;4 0 μg/ rat,i.c.v.) ,a5 - HT2 A receptor antagonist,decreased BPV only when administered i.c.v.,and did not modify the BP level.Ketanserin enhanced arterial baroreflex function in SHR when given either i.v. or i.c.v.. The stabilizing effect of ketanserin on BP was persistent when administered intragastrically.This adm inistration route is similar to oral adm inistration clinically.It is concluded that ke- tanserin is an antihypertensive agent with an effect of reducing BPV. This effect is m ainly mediated by central 5 - HT2 Arecep- tors and is probably attributable to the restoration of arterial baroreflex function.
基金Supported by National 10th 5-year Science Research Plan of China,No.2001BA705B10-15
文摘AIM： To study the stability of portal hypertension （PHT） caused by partial ligation of the portal vein ligation （PVL） in a rat model.METHODS： Thirty male adult Wistar rats were divided into two groups： 10 in Group Ⅰ received a sham operation; and 20 in Group Ⅱreceived partial PVL. Portal vein pressure （PVP） was measured at four time periods： before ligation, 2 wk, 6 wk and 10 wk postsurgery. Portal venography, blood sampling and liver and spleen pathological examinations were conducted at 10 wk after surgery.RESULTS： The PVP was 9.15± 0.58 cmH2O before ligation, and increased to 17.32 ±0.63 cmH2O 2 wk after PVL. By repeat measurement of the PVP in each rat, it was shown to remain elevated for 10 wk. There were no significant differences in the pressure measurements at 2 wk, 6 wk and 10 wk. Varices were found mainly in the mesenteric vein 2 wk after PVL, which were more obvious later, while these manifestations were similar at week 6 and week 10. Portal venography demonstrated the varices and collaterals. There was no significant change in liver pathology. The volume of the spleen was enlarged 2-fold after ligation, and the sinus of the spleen was enlarged due to congestion. Significant sinus endothelial cell proliferation was observed, but no evidence of hypersplenia was found on hemogram and biochemical examination.CONCLUSION： These findings suggest that a satisfactory prehepatic PHT rat model can be obtained by partial ligation of the portal vein, and this PHT rat model was stable for at least 10 wk.
基金ThisstudywassupportedbythegrantoftheNationalNaturalSciencesFoundationofChina (No 391735 0 No 39470 62 6)
文摘Objective To clarify whether the disturbances in metabolic kinetics of the essential aminoacid, phenylalanine (phe), are implicated in the genetic pathogenesis of essential hypertension (EH).Methods 1. L-(2, 3D3)-leucine, L-(2, 3D3)-isoleucine, L-15N-lysine, L-(2, 3D3)-valine and L-(2, 3D3)-phe were used for simultaneously studying comparative metabolic kinetics using stable isotope tracer methods with a GC-MS system. Study groups were the offspring with both parents suffering EH (n=10, FH+), 2 or more than 2 parents and grand-parents with EH and stroke (n=12, FS+) and those without genetic predisposition of EH and stroke (n=12, F) groups. 2. By comparing the radioactive counts of ［3H］-phe, and their weight transformation in blood after 1.5?Ci/kg i.v. administration at defined intervals and in tissues obtained after being sacrified among spontaneously hypertensive rats (SHR), 2 kidney-1 clip hypertensive rats (2K1C) and their normotensive controls (WKY). 3. The time transport and concentration transport of ［3H］-L-phe in cpm between the cultured vascular smooth muscle cell of 5th generation in SHR and WKY were compared.Results A single and unique disturbance of metabolic kinetics in phe were found in FH+, FS+ and SHR. The plasma pool or apparent volume of distribution was enlarged, and the turnover rate constants between plasma and cell tended to show a decrease. The pharmacokinetics of phe in 2K1C was not changed. Only phe content in heart and aorta, the vital organs for predicting BP, were higher in SHR than in WKY tissues studied. Both the time and concentration transport were higher in SHR, e.g., an increment in the net-uptake of L-phe by vascular tissue.Conclusion A unique aberrant of metabolic kinetics of phe might be implicated in the inherited pathogenesis of EH and stroke both from clinical and animal studies.
