Abstract-Hypertension is a major cardiovascular risk factor in the metabolic syndrome (MS) in which the presence of insulin resistance, glucose intolerance, abnormal lipoprotein metabolism, and central obesity all confer an increased risk. Because essential hypertension (EHT), insulinemia, and visceral fat are associated with sympathetic hyperactivity, which is itself known to increase cardiovascular risk, the aim of this study was to see if MS is a state of sympathetic nerve hyperactivity and if the additional presence of EHT intensifies this hyperactivity. In 69 closely matched subjects, comprising hypertensive MS (MSϩEHT, 18), normotensive MS (MS-EHT, 17), hypertensives without MS (EHT, 16), and normotensive controls without MS (NC, 18), we measured resting muscle sympathetic nerve activity (MSNA) as assessed from multiunit discharges and from single units with defined vasoconstrictor properties (s-MSNA). The s-MSNA in MSϩEHT (76Ϯ3.1 impulses/100 beats) was greater (at least PϽ0.01) than in MS-EHT (62Ϯ3.2 impulses/100 beats) and in EHT (60Ϯ2.3 impulses/100 beats), and all these were significantly greater (at least PϽ0.01) than in NC (46Ϯ2.7 impulse/100 beats). The multi-unit MSNA followed a similar trend. These findings suggest that MS is a state of sympathetic nerve hyperactivity and that the additional presence of hypertension further intensifies this hyperactivity. The degree of sympathetic hyperactivity seen in this study could be argued at least partly to contribute to the higher cardiovascular risk and metabolic abnormalities seen in MSϩEHT patients. Key Words: sympathetic nervous system Ⅲ hypertension Ⅲ metabolism L ittle information exists on the level of sympathetic nerve activity in the metabolic syndrome (MS) and whether the presence of essential hypertension (EHT), which is itself a state of sympathetic nerve hyperactivity, 1-4 augments this activity. Sympathetic activation has already been associated with many of the individual components of the MS, such as visceral obesity, 5 insulinemia, 6 EHT, 1-4 and type 2 diabetes. 7 The majority of treated hypertensives have in addition at least one other MS component; 8 also, it is now widely recognized that MS constitutes a cluster of major cardiovascular risk factors, 9 represented mainly by insulin resistance and obesity in which hypertension as an individual component overlaps the least with the other components. 10 Hypertension is known to be one of the highest predictors of cardiovascular morbidity and mortality associated with the MS. 11,12 Furthermore, sympathetic activation in EHT is believed to contribute to cardiovascular risk. 13,14 We therefore tested the hypothesis that the level of sympathetic nerve activity would be increased in normotensive MS and that the additional presence of EHT would further amplify this sympathetic activation. Methods SubjectsA total of 72 white subjects were examined, comprising 18 subjects with hypertensive MS (MSϩEHT), 18 normotensive MS (MS-EHT), 18 hypertensives without MS (EHT), and 18 normotensive controls wi...

Background-Sympathetic activation has been implicated in the development of left ventricular hypertrophy (LVH).However, the relationship between sympathetic activation and LV mass (LVM) has not been clearly defined across a range of arterial pressure measurements. The present study was planned to determine that relationship, using cardiac magnetic resonance imaging to accurately quantify LVM, in hypertensive patients with and without LVH and in normal subjects.

Abstract-Although the ␤ 1 -adrenergic blocking agent atenolol is an established antihypertensive therapy, its effect on peripheral sympathetic vasoconstrictor drive has remained controversial. In patients with hypertension, atenolol therapy has been reported to either increase or have no effect on peripheral vascular resistance, despite other reports showing no change or a decrease in peripheral sympathetic drive. This study was designed, in patients with untreated essential hypertension (EHT), to quantify changes in simultaneously measured peroneal muscle sympathetic nerve activity (MSNA) and calf vascular resistance (CVR) accompanying atenolol therapy. MSNA was quantified as the mean frequency of single units (s-MSNA) and as multiunit bursts (MSNA bursts) using the technique of microneurography, and CVR was measured using a standard plethysmographic technique. Firstly, by comparing two age-and body weightmatched groups, each of 14 patients with hypertension, we found that the group on atenolol therapy (treated-HT) had similar MSNA values counted over the same number of cardiac beats and similar CVR levels (at least PϾ0.40) to the group without therapy (untreated-HT). Secondly, we examined 10 EHT patients before and after 8Ϯ0.4 weeks of oral atenolol therapy (HT-A) in comparison to seven control patients with hypertension and no treatment (HT-C) who were examined over a similar period of time. We found that the measures of MSNA and CVR did not significantly change in both groups. We conclude that the arterial pressure lowering effect of atenolol was not related to significant changes in central vasoconstrictor sympathetic drive to the periphery. Key Words: antihypertensive therapy Ⅲ sympathetic nervous system Ⅲ hypertension, essential Ⅲ vascular resistance A lthough ␤-adrenergic blocking agents are widely used to lower arterial pressure in essential hypertension (EHT), the mechanisms underlying this effect are not entirely clear. [1][2][3][4] In the case of cardioselective ␤ 1 -adrenoceptor antagonists, there has been controversy as to whether or not their arterial pressure lowering effect involves changes to peripheral sympathetic vasoconstrictor drive and hence vascular resistance. For instance, in patients with EHT, atenolol therapy that produced a reduction in arterial pressure and heart rate has been found either to have no effect on forearm and calf vascular resistance or to increase it. 5-9 Similar results have been reported using metoprolol, another ␤ 1 -adrenoceptor antagonist. 6,10 -12 Furthermore, in patients with hypertension treated with ␤ 1 -adrenoceptor antagonists, reports of an effect on peripheral sympathetic drive mediating the arterial pressure reduction have also been inconsistent. For example, atenolol therapy has been reported to have no effect on biomedical indicators of sympathetic activity such as plasma norepinephrine levels or total body norepinephrine spillover rates. 9,13,14 Even direct measurements of muscle sympathetic nerve activity (MSNA) by peroneal microneurography have bee...

IntroductionDynamic reconfiguration of FPGAs has recently become viable with the introduction of devices that allow high speed partial reconfiguration, e.g., the Xilinx XC6200 series [14]. Dynamic reconfiguration is usually performed by a software system that decides when to reprogram part of the FPGA and with what. The simplest kind of run-time software simply selects a precompiled circuit and transmits the programming data directly to the FPGA. At the University of Glasgow's Department of Computing Science, the Reconfigurable Architecture Group (RAGE) has a number of projects examining applications of dynamic reconfiguration. These applications have highlighted the need for a more complex run-time system. Rather than developing different run-time systems for each application, as is common, we have extracted a set of common requirements from several applications. This has formed the basis of the design of a proposed, core, run-time system, able to support all of these applications. There are many parallels that can be drawn between this design and conventional operating system design-as the techniques used to manage conventional resources, such as memory and the CPU, are also applicable to the management of FPGAs.The next section of this paper describes three applications of dynamic reconfiguration and their requirements, and draws from these a set of core requirements. We follow this with an overview of the proposed system, and more detailed discussions of the rôles of the identified system components. We close with a discussion of how our system might support other applications in the field.

Sympathetic activation has been associated with the development and complications of hypertension. While the prevalence of hypertension and its cardiovascular risks in women are found to be less than in men and tend to become similar to men after the menopause, there have been no data on the level of sympathetic activation in postmenopausal women relative to men. Therefore, we planned to find out whether muscle sympathetic nerve hyperactivity of essential hypertension (EHT) in postmenopausal women is different from that in matched men. We quantified muscle sympathetic nerve activity (MSNA) as mean frequency of single units (s-MSNA) and multiunit bursts (b-MSNA) in 21 postmenopausal women with EHT (W-EHT) relative to 21 matched men with EHT (M-EHT), in comparison to two control groups of 21 normal women (W-NC) and 21 men (M-NC), respectively. The EHT groups had greater MSNA indices than NC groups. W-EHT had lower (Po0.05) s-MSNA (63 ± 22.7 impulses per 100 cardiac beats) than M-EHT (78 ± 11.2 impulses per 100 cardiac beats). W-NC had lower (Po0.05) s-MSNA (53 ± 12.4 impulses per 100 cardiac beats) than M-NC (65±16.3 impulses per 100 cardiac beats). Similar results were obtained for b-MSNA. Postmenopausal women with EHT had lower level of central sympathetic hyperactivity than men. Similarly, normal postmenopausal women had lower MSNA than men. These findings suggest that postmenopausal women continue to have a lower sympathetic nerve activity than men even after the development of EHT, and that this could have implications for genderspecific management of hypertension.