ORCID Profile
0000-0002-4534-9586
Current Organisation
University of Bristol
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Publisher: American Physiological Society
Date: 05-2017
DOI: 10.1152/AJPHEART.00703.2016
Abstract: Over the past several decades, studies of the sympathetic nervous system in humans, sheep, rabbits, rats, and mice have substantially increased mechanistic understanding of cardiovascular function and dysfunction. Recently, interest in sympathetic neural mechanisms contributing to blood pressure control has grown, in part because of the development of devices or surgical procedures that treat hypertension by manipulating sympathetic outflow. Studies in animal models have provided important insights into physiological and pathophysiological mechanisms that are not accessible in human studies. Across species and among laboratories, various approaches have been developed to record, quantify, analyze, and interpret sympathetic nerve activity (SNA). In general, SNA demonstrates “bursting” behavior, where groups of action potentials are synchronized and linked to the cardiac cycle via the arterial baroreflex. In humans, it is common to quantify SNA as bursts per minute or bursts per 100 heart beats. This type of quantification can be done in other species but is only commonly reported in sheep, which have heart rates similar to humans. In rabbits, rats, and mice, SNA is often recorded relative to a maximal level elicited in the laboratory to control for differences in electrode position among animals or on different study days. SNA in humans can also be presented as total activity, where normalization to the largest burst is a common approach. The goal of the present paper is to put together a summary of “best practices” in several of the most common experimental models and to discuss opportunities and challenges relative to the optimal measurement of SNA across species. Listen to this article's corresponding podcast at /guidelines-for-measuring-sympathetic-nerve-activity/
Publisher: Springer Science and Business Media LLC
Date: 19-09-2014
DOI: 10.1007/S11906-014-0493-1
Abstract: Hypertension is a leading risk factor for the development of several cardiovascular diseases. As the global prevalence of hypertension increases, so too has the recognition of resistant hypertension. Whilst figures vary, the proportion of hypertensive patients that are resistant to multiple drug therapies have been reported to be as high as 16.4 %. Resistant hypertension is typically associated with elevated sympathetic activity and abnormal homeostatic reflex control and is termed neurogenic hypertension because of its presumed central autonomic nervous system origin. This resistance to conventional pharmacological treatment has stimulated a plethora of medical devices to be investigated for use in hypertension, with varying degrees of success. In this review, we discuss a new therapy for drug-resistant hypertension, deep brain stimulation. The utility of deep brain stimulation in resistant hypertension was first discovered in patients with concurrent neuropathic pain, where it lowered blood pressure and improved baroreflex sensitivity. The most promising central target for stimulation is the ventrolateral periaqueductal gray, which has been well characterised in animal studies as a control centre for autonomic outflow. In this review, we will discuss the promise and potential mechanisms of deep brain stimulation in the treatment of severe, resistant hypertension.
Publisher: Wiley
Date: 08-11-2010
DOI: 10.1111/J.1748-1716.2010.02160.X
Abstract: Alterations in the carotid baroreflex (CBR) control of arterial pressure may explain the reduction in arterial pressure and left ventricular (LV) function after prolonged exercise. We examined the CBR control of heart rate (HR) and mean arterial pressure (MAP), in addition to changes in LV function, pre- to post-exercise. Seven males (age, mean ± SEM 29 ± 4 years) completed 4 h of ergometer rowing at a workload of 10-15% below the lactate threshold. The CBR control of HR and MAP was assessed via the rapid neck-suction ressure protocol. LV systolic function was measured by echocardiography, where ejection fraction (EF), the ratio of systolic blood pressure to end systolic volume (SBP/ESV) and stroke volume (SV) were estimated. Following exercise MAP was reduced (12 ± 3%) and HR was elevated (35 ± 5% P < 0.05). Furthermore, CBR control of MAP was relocated to the left on the stimulus-response curve (P < 0.05) demonstrating that the CBR operated around a lower arterial pressure. Concomitantly, LV systolic function was reduced, indicated by a decrease in EF (22 ± 2%), SBP/ESV (32 ± 14%) and SV (25 ± 5%, P < 0.05). The reduced EF and SBP/ESV were associated with the decreased MAP operating point (r² = 0.71 and r² = 0.47, respectively, P < 0.05). The CBR is reset after prolonged exercise to a lower prevailing arterial pressure. This resetting of the CBR may contribute to the reduction arterial pressure and LV function after exercise.
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Emma Hart.