Hypertension is a multifactorial condition which makes the development of treatment approaches difficult. The vast majority of patients are treated with lifestyle measures either alone or in combination with antihyper...Hypertension is a multifactorial condition which makes the development of treatment approaches difficult. The vast majority of patients are treated with lifestyle measures either alone or in combination with antihypertensive drugs, and this approach is largely successful in controlling blood pressure. However, for a subgroup of patients, control of blood pressure remains resistant to this approach and therefore the development of new strategies is im- perative. The sympathetic nervous system has been known to be implicated in hypertension for many decades, and evidence from studies in the past has revealed the benefit of reducing sympathetic nerve activity in the control of blood pressure albeit with severe side effects. Recent technological advances have allowed for specific targeting of the renal sympathetic nerves by catheter ablation. The Symplicity HTN-1 and HTN-2 trials have provided strong evidence for renal denervation giving rise to considerable blood pressure reductions in treatment-resistant hyper- tensives and, due to the high incidence of hypertension worldwide, this carries the promise of further reducing the global burden of hypertension and its attendant complications. Here we review the evidence for renal denervation in the management of hypertension.展开更多
Objective The aim of the present study was to examine levels of inflammatory cell infiltration and matrix metalloproteinase (MMP)-1 expression in atherosclerotic plaques of diabetic rabbits. Methods Diabetes was induc...Objective The aim of the present study was to examine levels of inflammatory cell infiltration and matrix metalloproteinase (MMP)-1 expression in atherosclerotic plaques of diabetic rabbits. Methods Diabetes was induced in rabbits by alloxan injection, and atherosclerotic plaque formation was stimulated both in diabetic and non-diabetic (sham-injected) rabbits by balloon injury of the abdominal aorta together with high lipid feeding. The morphology of atherosclerosis thus generated was studied by angiography and intravascular ultrasound (IVUS). Transverse sections of diseased aorta were examined by immunohistochemistry to analyze numbers of macrophages and smooth muscle cells as well as expression of MMP-1.展开更多
Objective The aim of the present study was to explore potential mechanism underlying reduced basal circulating endothelial progenitor cells (EPCs) in diabetes, and to determine how diabetes impairs ischemia-induced mo...Objective The aim of the present study was to explore potential mechanism underlying reduced basal circulating endothelial progenitor cells (EPCs) in diabetes, and to determine how diabetes impairs ischemia-induced mobilization of bone marrow-derived EPCs. Methods Circulating c-Kit+/Sca-1+/flk-1+ EPCs and CD31bright/Annexin V+ endothelial microparticles (EMPs) were analyzed by flow cytometry in control and streptozotocin-induced diabetic C57BL/6 mice. Results Compared with nondiabetic controls, diabetic mice had lower level of circulating EPCs, higher level of plasma EMPs, and increased ratio of EMPs to EPCs. Circulating EMPs count and EPCs level were negatively associated with each other. In a hindlimb ischemia model, diabetes suppressed bone marrow-derived EPCs mobilization, accompanied by insufficient upregulaiton of vascular endothelial growth factor (VEGF) and over-activation of matrix metalloproteinases (MMPs) system. As a consequence, diabetic mice showed deficient increase of capillary density and hampered restoration of transcutaneous oxygen pressure (tcpO2) in the ischemic tissue.Concluslon These results suggest that lower circulating EPCs level detected in diabetes may be partly attributed to consumptive loss of EPCs due to increased endothelial damage. Impairment in ischemia-induced EPCs mobilization presents a novel mechanism for defective post-ischemia neovascularization in diabetes.展开更多
文摘Hypertension is a multifactorial condition which makes the development of treatment approaches difficult. The vast majority of patients are treated with lifestyle measures either alone or in combination with antihypertensive drugs, and this approach is largely successful in controlling blood pressure. However, for a subgroup of patients, control of blood pressure remains resistant to this approach and therefore the development of new strategies is im- perative. The sympathetic nervous system has been known to be implicated in hypertension for many decades, and evidence from studies in the past has revealed the benefit of reducing sympathetic nerve activity in the control of blood pressure albeit with severe side effects. Recent technological advances have allowed for specific targeting of the renal sympathetic nerves by catheter ablation. The Symplicity HTN-1 and HTN-2 trials have provided strong evidence for renal denervation giving rise to considerable blood pressure reductions in treatment-resistant hyper- tensives and, due to the high incidence of hypertension worldwide, this carries the promise of further reducing the global burden of hypertension and its attendant complications. Here we review the evidence for renal denervation in the management of hypertension.
文摘Objective The aim of the present study was to examine levels of inflammatory cell infiltration and matrix metalloproteinase (MMP)-1 expression in atherosclerotic plaques of diabetic rabbits. Methods Diabetes was induced in rabbits by alloxan injection, and atherosclerotic plaque formation was stimulated both in diabetic and non-diabetic (sham-injected) rabbits by balloon injury of the abdominal aorta together with high lipid feeding. The morphology of atherosclerosis thus generated was studied by angiography and intravascular ultrasound (IVUS). Transverse sections of diseased aorta were examined by immunohistochemistry to analyze numbers of macrophages and smooth muscle cells as well as expression of MMP-1.
文摘Objective The aim of the present study was to explore potential mechanism underlying reduced basal circulating endothelial progenitor cells (EPCs) in diabetes, and to determine how diabetes impairs ischemia-induced mobilization of bone marrow-derived EPCs. Methods Circulating c-Kit+/Sca-1+/flk-1+ EPCs and CD31bright/Annexin V+ endothelial microparticles (EMPs) were analyzed by flow cytometry in control and streptozotocin-induced diabetic C57BL/6 mice. Results Compared with nondiabetic controls, diabetic mice had lower level of circulating EPCs, higher level of plasma EMPs, and increased ratio of EMPs to EPCs. Circulating EMPs count and EPCs level were negatively associated with each other. In a hindlimb ischemia model, diabetes suppressed bone marrow-derived EPCs mobilization, accompanied by insufficient upregulaiton of vascular endothelial growth factor (VEGF) and over-activation of matrix metalloproteinases (MMPs) system. As a consequence, diabetic mice showed deficient increase of capillary density and hampered restoration of transcutaneous oxygen pressure (tcpO2) in the ischemic tissue.Concluslon These results suggest that lower circulating EPCs level detected in diabetes may be partly attributed to consumptive loss of EPCs due to increased endothelial damage. Impairment in ischemia-induced EPCs mobilization presents a novel mechanism for defective post-ischemia neovascularization in diabetes.
