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| 1 | Physiopathology of splanchnic vasodilation in portal hypertension显示文摘In liver cirrhosis, the circulatory hemodynamic alterations of portal hypertension signifi cantly contribute to many of the clinical manifestations of the disease. In the physiopathology of this vascular alteration, mesen- teric splanchnic vasodilation plays an essential role by initiating the hemodynamic process. Numerous studies performed in cirrhotic patients and animal models have shown that this splanchnic vasodilation is the result of an important increase in local and systemic vasodilators and the presence of a splanchnic vascular hyporesponsiveness to vasoconstrictors. Among the molecules and factors known to be potentially involved in this arterial vasodilation, nitric oxide seems to have a crucial role in the physiopathology of this vascular alteration. However, none of the wide variety of mediators can be described as solely responsible, since this phenomenon is multifactorial in origin. Moreover, angiogenesis and vascular remodeling processes alsoseem to play a role. Finally, the sympathetic nervous system is thought to be involved in the pathogenesis of the hyperdynamic circulation associated with portal hypertension, although the nature and extent of its role is not completely understood. In this review, we discuss the different mechanisms known to contribute to this complex phenomenon. | María Martell Mar Coll Nahia Ezkurdia Imma Raurell Joan Genescà | 2010 | World Journal of Hepatology2010，2，6： | 13 |
| 2 | Impaired Hypothalamic Regulation of Sympathetic Outflow in Primary Hypertension显示文摘The hypothalamic paraventricular nucleus(PVN) is a crucial region involved in maintaining homeostasis through the regulation of cardiovascular, neuroendocrine, and other functions. The PVN provides a dominant source of excitatory drive to the sympathetic outflow through innervation of the brainstem and spinal cord in hypertension. We discuss current findings on the role of the PVN in the regulation of sympathetic output in both normotensive and hypertensive conditions. The PVN seems to play a major role in generating the elevated sympathetic vasomotor activity that is characteristic of multiple forms of hypertension, including primary hypertension in humans. Recent studies in the spontaneously hypertensive rat model have revealed an imbalance of inhibitory and excitatory synaptic inputs to PVN presympathetic neurons as indicated by impaired inhibitory and enhanced excitatory synaptic inputs in hypertension.This imbalance of inhibitory and excitatory synaptic inputs in the PVN forms the basis for elevated sympathetic outflow in hypertension. In this review, we discuss the disruption of balance between glutamatergic and GABAergic inputs and the associated cellular and molecular alterations as mechanisms underlying the hyperactivity of PVN pre-sympathetic neurons in hypertension. | Jing-Jing Zhou Hui-Jie Ma Jian-Ying Shao Hui-Lin Pan De-Pei Li | 2019 | Neuroscience Bulletin2019，35，1： | 11 |
| 3 | Electroacupuncture at ST25 inhibits jejunal motility:Role ofsympathetic pathways and TRPV1显示文摘AIM: To investigate whether electroacupuncture(EA) at ST25 affects jejunal motility in vivo and if so, whether a sympathetic pathway is involved.METHODS: Jejunal motility was assessed using a manometric balloon placed in the jejunum approximately about 3-5 cm away from the suspensory ligament of the duodenum in anesthetized animals. The effects of EA at ST25 were measured in male Sprague-Dawley rats, some of which were treated with propranolol or clenbuterol(EA intensities: 1, 3, 5, 7, and 9 m A), and in male transient receptor potential vanilloid-1(TRPV1)(capsaicin receptor) knockout mice(EA intensities: 1, 2, and 4 m A).RESULTS: Anesthetized rats exhibited three types of fasting jejunal motor patterns(types A, B, and C), and only type C rats responded to EA stimulation. In type C rats, EA at ST25 significantly suppressed the motor activity of the jejunum in an intensity-dependent manner. The inhibitory effect of EA was weakened by propranolol(β adrenoceptor antagonist) and disappeared with clenbuterol(β adrenoceptor agonist) induced inhibition of motility, suggesting that the effect of EA on motility is mediated via a sympathetic pathway. Compared with wild-type mice, EA at ST25 was less effective in TRPV1 knockout mice, suggesting that this multi-modal sensor channel participates in the mechanism. CONCLUSION: EA at ST25 was found to inhibit jejunal motility in an intensity-dependent manner, via a mechanism in which sympathetic nerves and TRPV1 receptors play an important role. | Zhi Yu Na Zhang Chun-Xia Lu Ting-Ting Pang Kai-Yue Wang Jing-Feng Jiang Bing Zhu Bin Xu | 2016 | World Journal of Gastroenterology2016，22，5： | 9 |
| 4 | Renal sympathetic nervous system and the effects of denervation on renal arteries显示文摘Resistant hypertension is associated with chronic activation of the sympathetic nervous system resulting in various comorbidities. The prevalence of resistant hypertension is often under estimated due to various reasons. Activation of sympathetic nervous system at the renal-as well as systemic-level contributes to the increased level of catecholamines and resulting increase in the blood pressure. This increased activity was demonstrated by increased muscle sympathetic nerve activity and renal and total body noradrenaline spillover. Apart from the hypertension, it is hypothesized to be associated with insulin resistance, congestive heart failure and obstructive sleep apnea. Renal denervation is a novel procedure where the sympathetic afferent and efferent activity is reduced by various techniques and has been used successfully to treat drug-resistant hypertension improvement of various metabolic derangements.Renal denervation has the unique advantage of offering the denervation at the renal level, thus mitigating the systemic side effects. Renal denervation can be done by various techniques including radiofrequency ablation, ultrasound guided ablation and chemical ablation. Various trials evaluated the role of renal denervation in the management of resistant hypertension and have found promising results. More studies are underway to evaluate the role of renal denervation in patients presenting with resistant hypertension in different scenarios. Appropriate patient selection might be the key in determining the effectiveness of the procedure. | Arun Kannan Raul Ivan Medina Nagapradeep Nagajothi Saravanan Balamuthusamy | 2014 | World Journal of Cardiology2014，6，8： | 8 |
| 5 | Renal sympathetic denervation in therapy resistant hypertension-pathophysiological aspects and predictors for treatment success显示文摘Many forms of human hypertension are associated with an increased systemic sympathetic activity. Especially the renal sympathetic nervous system has been found to play a prominent role in this context. Therefore, catheterinterventional renal sympathetic denervation(RDN) has been established as a treatment for patients suffering from therapy resistant hypertension in the past decade. The initial enthusiasm for this treatment was markedly dampened by the results of the Symplicity-HTN-3 trial, although the transferability of the results into clinical practice to date appears to be questionable. In contrast to the extensive use of RDN in treating hypertensive patients within or without clinical trial settings over the past years, its effects on the complex pathophysiological mechanisms underlying therapy resistant hypertension are only partly understood and are part of ongoing research. Effects of RDN have been described on many levels in human trials: From altered systemic sympathetic activity across cardiac and metabolic alterations down to changes in renal function. Most of these changes could sustainably change long-term morbidity and mortality of the treated patients, even if blood pressure remains unchanged. Furthermore, a number of promising predictors for a successful treatment with RDN have been identified recently and further trials are ongoing. This will certainly help to improve the preselection of potential candidates for RDN and thereby optimize treatment outcomes. This review summarizes important pathophysiologic effects of renal denervation and illustrates the currently known predictors for therapy success. | Karl Fengler Karl Philipp Rommel Thomas Okon Gerhard Schuler Philipp Lurz | 2016 | World Journal of Cardiology2016，8，8： | 5 |
| 6 | Investigating neurogenic bowel in experimental spinal cord injury: where to begin?显示文摘The devastating losses following traumatic spinal cord injury(SCI) encompass the motor, sensory and autonomic nervous systems. Neurogenic bowel is a slow transit colonic dysfunction marked by constipation, rectal evacuation difficulties, decreased anorectal sensation, fecal incontinence or some combination thereof. Furthermore, neurogenic bowel is one of the most prevalent comorbidities of SCI and is recognized by afflicted individuals and caregivers as a lifelong physical and psychological challenge that profoundly affects quality of life. The restoration of post-injury control of movement has received considerable scientific scrutiny yet the daily necessity of voiding the bowel and bladder remains critically under-investigated. Subsequently, physicians and caregivers are rarely presented with consistent, evidence-based strategies to successfully address the consequences of dysregulated voiding reflexes. Neurogenic bowel is commonly believed to result from the interruption of the supraspinal control of the spinal autonomic circuits regulating the colon. In this mini-review, we discuss the clinical challenges presented by neurogenic bowel and emerging pre-clinical evidence that is revealing that SCI also initiates functional remodeling of the colonic wall concurrent with a decrease in local enteric neurons. Since the enteric input to the colonic smooth muscle is the final common pathway for functional contractions of the colon, changes to the neuromuscular interface must first be understood in order to maximize the efficacy of therapeutic interventions targeting colonic dysfunction following SCI. | Amanda R.White Gregory M.Holmes | 2019 | Neural Regeneration Research2019，14，2： | 4 |
| 7 | Heart failure in subjects with chronic kidney disease:Best management practices显示文摘Renal dysfunction is common in patients with heart failure(HF) and can complicate HF therapy.Treating patients with HF and kidney disease is difficult and requires careful assessment,monitoring and balancing of risk between potential benefits of treatment and adverse impact on renal function.In this review,we address the pathophysiological contexts and management options in this adversarial relation between the heart and the kidney,which exists in a substantial proportion of HF patients.Angiotensin converting enzyme inhibitors and β-blockers are associated with similar reductions in mortality in patients with and without renal insufficiency but usually are less often prescribed in patients with renal insufficiency.Careful monitoring of side effects and renal function should be done in all patients with renal insufficiency and prompt measures should be adopted to prevent further complications. | Farhan Aslam Attiya Haque Javeria Haque Jacob Joseph | 2010 | World Journal of Cardiology2010，2，5： | 1 |
| 8 | Transcatheter therapies for resistant hypertension: Clinical review显示文摘Resistant hypertension(RHTN) is a commonly encountered clinical problem and its management remains a challenging task for healthcare providers. The prevalence of true RHTN has been difficult to assess due to pseudoresistance and secondary hypertension. Atherosclerotic renal artery stenosis(RAS) has been associated as a secondary cause of RHTN. Initial studies had shown that angioplasty and stenting for RAS were a promising therapeutic option when added to optimal medical management. However, recent randomized controlled trials in larger populations have failed to show any such benefit. Sympathetic autonomic nervous system dysfunction is commonly noted in individuals with resistant hypertension. Surgical sympathectomy was the treatment of choice for malignant hypertension and it significantly improved mortality. However, postsurgical complications and the advent of antihypertensive drugs made this approach less desirable and it was eventually abandoned. Increasing prevalence of RHTN in recent decades has led to the emergence of minimally invasive interventions such as transcatheter renal denervation for better control of blood pressure. It is a minimally invasive procedure which uses radiofrequency energy for selective ablation of renal sympathetic nerves located in the adventitia of the renal artery. It is a quick procedure and has a short recovery time. Early studies in small population showed significant reduction in blood pressure. The most recent Symplicity HTN-3 study, which is the largest randomized control trial and the only one to use a sham procedure in controls, failed to show significant BP reduction at 6 mo. | Adil Lokhandwala Abhijeet Dhoble | 2014 | World Journal of Cardiology2014，6，8： | 1 |
| 9 | Hypertension in children with obesity显示文摘The prevalence of obesity related hypertension has dramatically increased in children with the parallel increase in pediatric obesity.This pediatric health problem may adversely affect cardiovascular health in adult life.The pathogenesis of hypertension in obese children is not widely understood.We therefore undertake this review to raise public awareness.Early childhood parameters like birth weight and postnatal weight gain may play important roles in risk for obesity and obesity related hypertension later in childhood and adult life.Further information is required to confirm this origin of hypertension so that appropriate measures are taken in the peri-natal period.The role of sympathetic nervous system has now been well established as one of the principle mechanisms involved in obesity related hypertension.The Renin-Angiotensin system,insulin resistance due to obesity and as a part of metabolic syndrome along with imbalance in adipokines such as leptin and adiponectin,cause activation of the sympathetic system,vasoconstriction,endothelial dysfunction and sodium reabsorption among other perturbations.Multi-step interventions targeting these various mech-anisms are required to break the cycle of obesity and metabolic syndrome.Vitamin D deficiency,sleep apnea due to airway obstruction and hyperuricemia may also play a significant role and should not be ignored in its early stages.Obesity is a risk factor for other comorbid conditions like chronic kidney disease and fatty liver which further accentuate the risk of hypertension.Increased awareness is required to prevent,diagnose and treat obesity related hypertension among the pediatric population. | Sujana S Gunta Robert H Mak | 2014 | World Journal of Hypertension2014，4，2： | 0 |
| 10 | Intracerebroventricular administration of interferon-α enhanced splenic nerve in rats显示文摘Objective: To study the effect of intracerebroventricular administration of interferon (IFN-α) on the splenic sympathetic nerve activity. Methods: IFN-α (3×104 U/rat ) was microinjected into the third cerebroven-tricle of urethane and α-chloralose anesthetized rats. Electrical activity of the splenic nerve. body temperature and blood pressure were determined simultaneously. Results: Intracerebroventricular administration of IFN-α caused amarked and long term (>120 min) increase in the splenic nerve activity, which could be reversed by naloxonetreatment. No changes in blood pressure and body temperature. which could alter the sympathetic nerve actlvity by reflex. were observed during IFN-α and naloxone treatment. Naloxone intravenous injection alone had no effecton the splenic nerve activity. Conclusion: IFN-α in the brain can activate the splenic sympathetic nerve, and thisaction is, in some way, mediated by the opioid receptor. | 李德敏 林树新 | 1997 | Journal of Medical Colleges of PLA(China)1997，12，4： | 0 |
| 11 | Catheter-based renal denervation: treating hypertension or beyond?显示文摘The renal nerves regulatehomeostasis, cardiac outputkidney function, volumeand BP.2 Renal sympatheticactivation results in volume retention, sodium reabsorption,reduction of blood flow, and rennin-angiotensin-aldosteronesystem activation.2 The kidneys however, also have anextensive network of afferent unmyelinated fibers thattransmit important sensory information to the centralnervous system.2'3 Afferent fibers from the kidneys havebeen shown to travel along with the sympathetic nerves atthe level of the kidneys and then enter the dorsal roots andproject to neurons at both spinal and supraspinal levels.Most of the brainstem regions involved in cardiovascularcontrol including the hypothalamus receive inputsfrom the renal afferents, which carry information to thecentral nervous system from renal chemo- and mechano-receptors.2'3 Direct electrical stimulation of the renal afferentnerves in animals can produce both sympathoinhibitoryand sympathoexcitatory reflexes, illustrating the diversefunctional nature of various populations of renal receptors. | | 2014 | Chinese Medical Journal2014，，6： | 0 |
| 12 | Is Takotsubo syndrome in patients receiving chemotherapy drug-specific?显示文摘In commenting on a case report of a 55-year-old man who suffered Takotsubo syndrome(TTS), in the setting of receiving chemotherapy with cytarabine and daunorubicin for acute myeloid leukemia, the author expresses his views that TTS in the setting of chemotherapy for malignancies may not be chemotherapeutic drug-specific(like in the chemotherapeutic drug induced-cardiomyopathy), but may be due to the emotional and physical stresses resulting from the realization of having diagnosed with a malignancy, and the diagnostic testing, and therapeutic management which follows. | John E Madias | 2015 | World Journal of Clinical Cases2015，3，2： | 0 |
| 13 | The Schlager mouse as a model of altered retinal phenotype显示文摘Hypertension is a risk factor for a large number of vision-threatening eye disorders.In this study,we investigated for the first time the retinal neural structure of the hypertensive BPH/2J mouse(Schlager mouse)and compared it to its control counterpart,the normotensive BPN/3J strain.The BPH/2J mouse is a selectively inbred mouse strain that develops chronic hypertension due to elevated sympathetic nervous system activity.When compared to the BPN/3J strain,the hypertensive BPH/2J mice showed a complete loss of outer layers of the neural retina at 21 weeks of age,which was indicative of a severe vision-threatening disease potentially caused by hypertension.To elucidate whether the retinal neural phenotype in the BPH/2J strain was attributed to increased BP,we investigated the neural retina of both BPN/3J and BPH/2J mice at 4 weeks of age.Our preliminary results showed for the first time that the BPH/2J strain develops severe retinal neural damage at a young age.Our findings suggest that the retinal phenotype in the BPH/2J mouse is possibly due to elevated blood pressure and may be contributed by an early onset spontaneous mutation which is yet to be identified or a congenital defect occurring in this strain.Further characterization of the BPH/2J mouse strain is likely to i)elucidate gene defects underlying retinal disease;ii)understand mechanisms leading to neural retinal disease and iii)permit testing of molecules for translational research to interfere with the progression of retinal disease.The animal experiments were performed with the approval of the Royal Perth Hospital Animal Ethics Committee(R535/17-18)on June 1,2017. | Lakshini Y.Herat Aaron L.Magno Márcio G.Kiuchi Kristy L.Jackson Revathy Carnagarin Geoffrey A.Head Markus P.Schlaich Vance B.Matthews | 2020 | Neural Regeneration Research2020，15，3： | 0 |
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