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Dingfeng Su - One of the best experts on this subject based on the ideXlab platform.
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effects of low dose Ketanserin on blood pressure variability baroreflex sensitivity and end organ damage in spontaneously hypertensive rats
Clinical Science, 2005Co-Authors: Fuming Shen, Huilin Li, Dingfeng SuAbstract:: The present study was designed to investigate the effects of low-dose Ketanserin on BPV (blood pressure variability), BRS (baroreflex sensitivity) and organ damage in SHR (spontaneously hypertensive rats). Ketanserin was mixed in rat chow at an estimated dose of 0.1 mg.kg(-1) of body weight.day(-1). SHR were treated for 4 months. BP (blood pressure) was then recorded continuously for 24 h in a conscious state. After determination of BRS, rats were killed for organ damage evaluation. It was found that long-term treatment with low-dose Ketanserin did not lower BP levels, but significantly decreased BPV, enhanced BRS and reduced organ damage in SHR. Multiple regression analysis showed that the decrease in left ventricular hypertrophy was most closely correlated (or associated) with the increase in BRS, whereas the decrease in aortic hypertrophy was most closely associated with the decrease in diastolic BPV and the amelioration in renal lesion, with the increase in BRS and the decrease in diastolic BPV. In conclusion, low-dose Ketanserin produces organ protection independently of its BP-lowering action in SHR, and this organ protection was importantly attributable to the enhancement of BRS and decrease in BPV.
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effects of long term treatment with Ketanserin on blood pressure variability and end organ damage in spontaneously hypertensive rats
Journal of Cardiovascular Pharmacology, 2003Co-Authors: Wenmin Du, Chaoyu Miao, Fuming Shen, Xiangqun Yang, Dingfeng SuAbstract:It has been proposed that instability of blood pressure may produce organ damage. Ketanserin is an anti-hypertensive drug with an ability to reduce blood pressure variability (BPV) in acute experiments in spontaneously hypertensive rats (SHRs). The present work was designed to observe the effects of long-term treatment with Ketanserin on BPV and end-organ damage in SHRs. Ketanserin was mixed in rat chow at an estimated dose of 10 mg/kg/d. After 5 months of drug administration, BP was continuously recorded in conscious, freely moving rats for 24 h. The heart, kidneys, and abdominal aorta were then isolated and examined by using histologic methods and computer image analysis. In another work, the effects of hydralazine (40 mg/kg/d, for 5 months) on BP, BPV, and organ damage were observed in SHRs. Ketanserin significantly decreased BP and BPV, ameliorated impaired arterial baroreflex function, and significantly prevented the target organs of SHRs from being damaged. This preventive effect was characterized by decrease in left ventricular hypertrophy, diminution of glomerulus damage, and amelioration in vascular lesion. Hydralazine decreased BP but did not lower BPV. No organ protection was found in hydralazine-treated rats. In conclusion, long-term treatment with Ketanserin reduced hypertensive organ damage. Lowering BP, decreasing BPV, and ameliorating arterial baroreflex function may contribute together to this effect.
Fuming Shen - One of the best experts on this subject based on the ideXlab platform.
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Ketanserin induced baroreflex enhancement in spontaneously hypertensive rats depends on central 5 ht2a receptors
Clinical and Experimental Pharmacology and Physiology, 2007Co-Authors: Fuming Shen, Jin Wang, Weizhong WangAbstract:SUMMARY 1 Ketanserin may influence baroreflex function by blocking 5-HT2A receptors and/or α1-adrenoceptors through central and/or peripheral mechanisms. 2 In the present study, we tested the hypothesis that the baroreflex sensitivity (BRS)-enhancing effects of Ketanserin are mediated by central 5-HT2A receptors in spontaneously hypertensive rats (SHR). 3 Using a conjugate of a monoclonal antibody to the serotonin reuptake transporter (SERT) and the toxin saporin (anti-SERT-SAP), which specifically eliminates the neurons that express SERT, the effects of Ketanserin (0.3 and 3.0 mg/kg, i.g.) on BRS, blood pressure (BP), heart period (HP) and blood pressure variability (BPV) were compared between conscious intact SHR and SHR pretreated with anti-SERT-SAP. 4 Immunochemistry showed that, 2 weeks after intracerebroventricular injection of the toxin, 5-HT expression was strikingly attenuated in the brain, whereas values of BRS, BPV and BP were similar to those in the sham group. In intact SHR, 0.3 mg/kg Ketanserin significantly improved BRS (191% control) and reduced BPV without affecting BP; at 3.0 mg/kg, Ketanserin significantly increased BRS (197% control) and decreased BPV and BP. In toxin-pretreated SHR, only the high dose of Ketanserin improved BRS (132% control), neither of the Ketanserin doses reduced BPV, but both significantly decreased BP. 5 We conclude that the BRS-enhancing effects of Ketanserin are mediated largely by central 5-HT2A receptors, whereas the antihypertensive effect of Ketanserin persists even after destruction of serotonergic neurons in the central nervous system.
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effects of low dose Ketanserin on blood pressure variability baroreflex sensitivity and end organ damage in spontaneously hypertensive rats
Clinical Science, 2005Co-Authors: Fuming Shen, Huilin Li, Dingfeng SuAbstract:: The present study was designed to investigate the effects of low-dose Ketanserin on BPV (blood pressure variability), BRS (baroreflex sensitivity) and organ damage in SHR (spontaneously hypertensive rats). Ketanserin was mixed in rat chow at an estimated dose of 0.1 mg.kg(-1) of body weight.day(-1). SHR were treated for 4 months. BP (blood pressure) was then recorded continuously for 24 h in a conscious state. After determination of BRS, rats were killed for organ damage evaluation. It was found that long-term treatment with low-dose Ketanserin did not lower BP levels, but significantly decreased BPV, enhanced BRS and reduced organ damage in SHR. Multiple regression analysis showed that the decrease in left ventricular hypertrophy was most closely correlated (or associated) with the increase in BRS, whereas the decrease in aortic hypertrophy was most closely associated with the decrease in diastolic BPV and the amelioration in renal lesion, with the increase in BRS and the decrease in diastolic BPV. In conclusion, low-dose Ketanserin produces organ protection independently of its BP-lowering action in SHR, and this organ protection was importantly attributable to the enhancement of BRS and decrease in BPV.
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effects of long term treatment with Ketanserin on blood pressure variability and end organ damage in spontaneously hypertensive rats
Journal of Cardiovascular Pharmacology, 2003Co-Authors: Wenmin Du, Chaoyu Miao, Fuming Shen, Xiangqun Yang, Dingfeng SuAbstract:It has been proposed that instability of blood pressure may produce organ damage. Ketanserin is an anti-hypertensive drug with an ability to reduce blood pressure variability (BPV) in acute experiments in spontaneously hypertensive rats (SHRs). The present work was designed to observe the effects of long-term treatment with Ketanserin on BPV and end-organ damage in SHRs. Ketanserin was mixed in rat chow at an estimated dose of 10 mg/kg/d. After 5 months of drug administration, BP was continuously recorded in conscious, freely moving rats for 24 h. The heart, kidneys, and abdominal aorta were then isolated and examined by using histologic methods and computer image analysis. In another work, the effects of hydralazine (40 mg/kg/d, for 5 months) on BP, BPV, and organ damage were observed in SHRs. Ketanserin significantly decreased BP and BPV, ameliorated impaired arterial baroreflex function, and significantly prevented the target organs of SHRs from being damaged. This preventive effect was characterized by decrease in left ventricular hypertrophy, diminution of glomerulus damage, and amelioration in vascular lesion. Hydralazine decreased BP but did not lower BPV. No organ protection was found in hydralazine-treated rats. In conclusion, long-term treatment with Ketanserin reduced hypertensive organ damage. Lowering BP, decreasing BPV, and ameliorating arterial baroreflex function may contribute together to this effect.
Chaoyu Miao - One of the best experts on this subject based on the ideXlab platform.
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effects of Ketanserin on endotoxic shock and baroreflex function in rodents
The Journal of Infectious Diseases, 2011Co-Authors: Chong Liu, Gufang Zhang, Shuwei Song, Guojun Cai, Wenhao Liu, Chaoyu MiaoAbstract:Background Ketanserin, a 5-hydroxytryptamine receptor antagonist, is clinically used as an antihypertensive agent and could enhance baroreflex function. The present work tested the hypothesis that restoration of baroreflex function is an effective treatment for lipopolysaccharide (LPS)-induced shock. Methods Kunming mice were injected with LPS (30 mg/kg; intraperitoneal) to induce endotoxic shock. Ketanserin (0.3, 1, 3, or 10 mg/kg; intraperitoneal) was administered immediately after LPS injection. Survival time was monitored, and serum cytokines were analyzed after the onset of LPS. Effects of Ketanserin were also examined in IL-10-deficient mice and mice with sinoaortic denervation. Finally, effects of Ketanserin on blood pressure, heart rate, and baroreflex sensitivity were examined in Wistar-Kyoto (WKY) rats with endotoxic shock. Results Ketanserin significantly increased survival time and decreased serum levels of tumor necrosis factor α and interleukin (IL) 1β in mice with endotoxic shock. At a dose of 10 mg/kg, Ketanserin also significantly increased serum IL-10 concentration. The antishock effect of Ketanserin was also apparent in IL-10-knockout mice. In mice with sinoaortic denervation, however, Ketanserin had little antishock effects. In WKY rats, Ketanserin significantly prevented the baroreflex impairment induced by LPS and prolonged the survival time. Conclusions Ketanserin could ameliorate endotoxic shock by restoring baroreflex function.
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restoration of baroreflex function by Ketanserin is not blood pressure dependent in conscious freely moving rats
Journal of Hypertension, 2004Co-Authors: He Shu, Chaoyu Miao, Minwei WangAbstract:OBJECTIVE: Since the end of the 1980s, the pathological importance of baroreflex function has attracted the attention of many investigators. In our previous studies, it was found that Ketanserin lowered blood pressure (BP), decreased BP variability and enhanced baroreflex sensitivity (BRS). The present work was designed to test the hypothesis that the restoration of BRS by Ketanserin is not dependent on BP level in conscious rats. DESIGN AND METHODS: Spontaneously hypertensive rats (SHR) aged 8-12 months were used. Blood pressure was recorded for 60 min and BRS was determined separately before and after intragastric administration of Ketanserin, with four doses. In a second experiment, 10-week-old Sprague-Dawley rats were used for preparing a myocardial infarction (MI) model by ligating the coronary artery. MI rats were treated with Ketanserin for 5 weeks, with two doses. At the end of the treatment, BP and BRS of the MI rats were studied in conscious state. In addition, the effects of Ketanserin on BRS in Sprague-Dawley rats with normal BRS and the effects of prazosin and ritanserin on BRS in SHR were also observed. RESULTS: It was found that Ketanserin significantly decreased BP and improved BRS in the conscious SHR. The decrease in BP was dose-dependent but the improvement of BRS was not. At the smallest dose (0.3 mg/kg), Ketanserin did not lower BP but enhanced BRS. In MI rats, the treatment with Ketanserin did not significantly decrease BP, but it improved BRS at both doses administered (0.6 and 10 mg/kg). Ketanserin [3 and 10 mg/kg, intragastric (i.g.)] did not affect BRS in SD rats with normal BRS. Prazosin and ritanserin did not enhance BRS in SHR when administered intravenously. Ritanserin markedly and prazosin slightly enhanced BRS in SHR following intracerebroventricular administration. CONCLUSION: The restoration of baroreflex function by Ketanserin is not BP dependent and this effect is mediated by central 5-HT2A receptor.
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Ketanserin stabilizes blood pressure in conscious spontaneously hypertensive rats
Clinical and Experimental Pharmacology and Physiology, 2003Co-Authors: Chaoyu Miao, Hehui Xie, Zhengxu ChuAbstract:Summary 1. It has been demonstrated that blood pressure variability (BPV) is increased in hypertension and related to organ damage. It will be important to lower BPV in the treatment of hypertension. The present study was designed to investigate the effect of Ketanserin, a 5-HT2A receptor antagonist with a weak α1-adrenoceptor blocking effect, on BPV in conscious spontaneously hypertensive rats (SHR). 2. It was found that Ketanserin decreased blood pressure (BP) and BPV in SHR when administered intravenously (3 mg/kg, i.v.). Ketanserin decreased BPV, but not the BP level, when administered intracerebroventricularly (50 µg/rat, i.c.v.). 3. Prazosin, an α1-adrenoceptor antagonist, lowered BP but did not affect BPV when given either i.v. (0.5 mg/kg) or i.c.v. (30 ug/rat). Ritanserin (0.625 mg/kg, i.v.; 40 'ug/rat, i.c.v.), a 5-HT2A receptor antagonist, decreased BPV only when administered i.c.v. and did not modify the BP level. 4. Ketanserin enhanced arterial baroreflex function in SHR when given either i.v. or i.c.v. 5. The stabilizing effect of Ketanserin on BP was persistent when administered intragastrically. This administration route is similar to oral administration clinically. 6. It is concluded that Ketanserin is an antihypertensive agent with an effect of reducing BPV. This effect is mainly mediated by central 5-HT2A receptors and is probably attributable to the restoration of arterial baroreflex function.
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effects of long term treatment with Ketanserin on blood pressure variability and end organ damage in spontaneously hypertensive rats
Journal of Cardiovascular Pharmacology, 2003Co-Authors: Wenmin Du, Chaoyu Miao, Fuming Shen, Xiangqun Yang, Dingfeng SuAbstract:It has been proposed that instability of blood pressure may produce organ damage. Ketanserin is an anti-hypertensive drug with an ability to reduce blood pressure variability (BPV) in acute experiments in spontaneously hypertensive rats (SHRs). The present work was designed to observe the effects of long-term treatment with Ketanserin on BPV and end-organ damage in SHRs. Ketanserin was mixed in rat chow at an estimated dose of 10 mg/kg/d. After 5 months of drug administration, BP was continuously recorded in conscious, freely moving rats for 24 h. The heart, kidneys, and abdominal aorta were then isolated and examined by using histologic methods and computer image analysis. In another work, the effects of hydralazine (40 mg/kg/d, for 5 months) on BP, BPV, and organ damage were observed in SHRs. Ketanserin significantly decreased BP and BPV, ameliorated impaired arterial baroreflex function, and significantly prevented the target organs of SHRs from being damaged. This preventive effect was characterized by decrease in left ventricular hypertrophy, diminution of glomerulus damage, and amelioration in vascular lesion. Hydralazine decreased BP but did not lower BPV. No organ protection was found in hydralazine-treated rats. In conclusion, long-term treatment with Ketanserin reduced hypertensive organ damage. Lowering BP, decreasing BPV, and ameliorating arterial baroreflex function may contribute together to this effect.
H Liberman - One of the best experts on this subject based on the ideXlab platform.
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evaluation of Ketanserin in the prevention of restenosis after percutaneous transluminal coronary angioplasty a multicenter randomized double blind placebo controlled trial
Circulation, 1993Co-Authors: P W Serruys, S G Ball, W Klein, Jan Tijssen, Wolfgang Rutsch, G Heyndrickx, Hakan Emanuelsson, O Decoster, Erwin Schroeder, H LibermanAbstract:BACKGROUND Ketanserin is a serotonin S2-receptor antagonist that inhibits the platelet activation and vasoconstriction induced by serotonin and also inhibits the mitogenic effect of serotonin on vascular smooth muscle cells. METHODS AND RESULTS We conducted a randomized, double blind, placebo-controlled trial to assess the effect of Ketanserin in restenosis prevention after percutaneous transluminal coronary angioplasty (PTCA). Patients received either Ketanserin (loading dose, 40 mg 1 hour before PTCA; maintenance dose, 40 mg bid for 6 months) or matched placebo. In addition, all patients received aspirin for 6 months. Coronary angiograms before PTCA, after PTCA, and at 6 months were quantitatively analyzed. Six hundred fifty-eight patients were entered into the intention-to-treat analysis. The primary clinical end point of the study was the occurrence between PTCA and 6 months of any one of the following: cardiac death, myocardial infarction, the need for repeat angioplasty, or bypass surgery. It also included the need for revascularization actuated by findings at 6-month follow-up angiography. The primary clinical end point was reached by 92 (28%) patients in the Ketanserin group and 104 (32%) in the placebo group (RR, 0.89; 95% CI, 0.70, 1.13; P = .38). Quantitative angiography after PTCA and at follow-up was available in 592 patients (Ketanserin, 287; control, 305). The mean difference in minimal lumen diameter between post-PTCA and follow-up angiogram (primary angiographic end point) was 0.27 +/- 0.49 mm in the Ketanserin group and 0.24 +/- 0.52 mm in the control group (difference, 0.03 mm; 95% CI, -0.05, 0.11; P = .50). CONCLUSIONS Ketanserin at the dose administered in this trial failed to reduce the loss in minimal lumen diameter during follow-up after PTCA and did not significantly improve the clinical outcome.
Gustaaf A. Dekker - One of the best experts on this subject based on the ideXlab platform.
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Ketanserin versus dihydralazine in the management of severe early-onset preeclampsia: Maternal outcome
American Journal of Obstetrics and Gynecology, 1999Co-Authors: Antionette C. Bolte, Jim Van Eyck, Herman P. Van Geijn, H H Kanhai, H W Bruinse, Gustaaf A. DekkerAbstract:Abstract Objective: An open, randomized, prospective, multicenter trial was conducted to compare the efficacy and safety of intravenous Ketanserin, a selective serotonin 2 receptor blocker, with that of intravenous dihydralazine in the management of severe early-onset ( Study Design: Patients with a diastolic blood pressure >110 mm Hg were randomly assigned to receive either Ketanserin (n = 22) or dihydralazine (n = 22) as initial therapy. Plasma volume expansion preceded antihypertensive treatment, which was administered according to a fixed schedule. Results: The reductions in blood pressure with the 2 drugs were similar; however, adequate blood pressure control was reached significantly earlier with Ketanserin (84 ± 63 vs 171 ± 142 minutes, P = .017). Occurrence of maternal complications was significantly lower among patients who received Ketanserin than among patients who received dihydralazine (n = 6 vs n=18, P = .0007). A significant difference in favor of Ketanserin was noted in daily fluid balance. Conclusion: Antihypertensive efficacies of Ketanserin and dihydralazine were comparable, but significantly fewer maternal complications were noted among the patients receiving Ketanserin. Ketanserin is an attractive alternative in the management of severe early-onset preeclampsia. (Am J Obstet Gynecol 1999;180:371-7.)
