Aims/hypothesis: Previous studies have shown that alterations in vascular, metabolic, inflammatory and haemocoagulative functions characterise the metabolic syndrome. Whether this is also the case for sympathetic function is not clear. We therefore aimed to clarify this issue and to determine whether metabolic or reflex mechanisms might be responsible for the possible adrenergic dysfunction. Methods: In 43 healthy control subjects (age 48.2±1.0 years, mean±SEM) and in 48 untreated agematched subjects with metabolic syndrome (National Cholesterol Education Program's Adult Treatment Panel III Report criteria) we measured, along with anthropometric and metabolic variables, blood pressure (Finapres), heart rate (ECG) and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor manipulation (vasoactive drug infusion technique). Results: Compared with control subjects, subjects with metabolic syndrome had higher BMI, waist circumference, blood pressure, cholesterol, triglycerides, insulin and homeostasis model assessment (HOMA) index values but lower HDL cholesterol values. Sympathetic nerve traffic was significantly greater in subjects with metabolic syndrome than in control subjects (61.1± 2.6 vs 43.8±2.8 bursts/100 heartbeats, p<0.01), the presence of sympathetic activation also being detectable when the metabolic syndrome did not include hypertension as a component. Muscle sympathetic nerve traffic correlated directly and significantly with waist circumference (r= 0.46, p<0.001) and HOMA index (r=0.49, p<0.001) and was inversely related to baroreflex sensitivity (r=−0.44, p<0.001), which was impaired in the metabolic syndrome. Conclusions/interpretation: These data provide evidence that the metabolic syndrome is characterised by sympathetic activation and that this abnormality (1) is also detectable when blood pressure is normal and (2) depends on insulin resistance as well as on reflex alterations.
These data suggest that CO is characterized by a sympathetic activation greater for magnitude than that detectable in PO. This appears not to be related to gender or to baroreflex mechanisms but rather to metabolic factors, i.e. to the greater insulin resistance characterizing CO.
Abstract-Previous studies have shown that essential hypertension and obesity are both characterized by sympathetic activation coupled with a baroreflex impairment. The present study was aimed at determining the effects of the concomitant presence of the 2 above-mentioned conditions on sympathetic activity as well as on baroreflex cardiovascular control. In 14 normotensive lean subjects (aged 33.5Ϯ2.2 years, body mass index 22.8Ϯ0.7 kg/m 2[meanϮSEM]), 16 normotensive obese subjects (body mass index 37.2Ϯ1.3 kg/m 2 ), 13 lean hypertensive subjects (body mass index 24.0Ϯ0.8 kg/m 2 ), and 16 obese hypertensive subjects (body mass index 37.5Ϯ1.3 kg/m 2 ), all age-matched, we measured beat-to-beat arterial blood pressure (by Finapres device), heart rate (HR, by ECG), and postganglionic muscle sympathetic nerve activity (MSNA, by microneurography) at rest and during baroreceptor stimulation and deactivation induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Blood pressure values were higher in lean hypertensive and obese hypertensive subjects than in normotensive lean and obese subjects. MSNA was significantly (PϽ0.01) greater in obese normotensive subjects (49.1Ϯ3.0 bursts per 100 heart beats) and in lean hypertensive subjects (44.5Ϯ3.3 bursts per 100 heart beats) than in lean normotensive control subjects (32.2Ϯ2.5 bursts per 100 heart beats); a further increase was detectable in individuals with the concomitant presence of obesity and hypertension (62.1Ϯ3.4 bursts per 100 heart beats). Furthermore, whereas in lean hypertensive subjects, only baroreflex control of HR was impaired, in obese normotensive subjects, both HR and MSNA baroreflex changes were attenuated, with a further attenuation being observed in obese hypertensive patients. Thus, the association between obesity and hypertension triggers a sympathetic activation and an impairment in baroreflex cardiovascular control that are greater in magnitude than those found in either of the above-mentioned abnormal conditions alone. (Hypertension. 2000;36:538-542.) Key Words: nervous system, sympathetic Ⅲ nervous system, autonomic Ⅲ baroreceptors Ⅲ hypertension, essential Ⅲ obesity S tudies on the sympathoadrenal function in animal and human obesity have provided somewhat heterogeneous results. [1][2][3][4][5] However, several recent data have shown that sympathetic activity, as directly assessed by regional norepinephrine (NE) spillover or by microneurographic recording of muscle sympathetic nerve activity (MSNA), is increased in normotensive overweight subjects. 6 -9 A similar increase has been shown to occur in lean individuals with essential hypertension. 10 -14 However, whether this increase and the one characterizing obesity are additive in an obese hypertensive individual is not clear. In one study, the renal spillover of NE was shown to be greater in obese hypertensive than in obese normotensive subjects. 15 However, this was not the case in the cardiac and systemic circulation and in obese and lean hypertensive indivi...
Abstract-Direct and indirect indices of neuroadrenergic function have shown that end-stage renal disease is characterized by a marked sympathetic overdrive. It is unknown, however, whether this phenomenon represents a peculiar feature of end-stage renal disease or whether it is also detectable in the early clinical phases of the disease. The study has been performed in 73 hypertensive patients, of which there were 42 (age: 60.7Ϯ1.8 years, meanϮSEM) with a stable moderate chronic renal failure (mean estimated glomerular filtration rate: 40.7 mL/min per 1.73 m 2 , MDRD formula) and 31 age-matched controls with a preserved renal function. Measurements included anthropometric variables, sphygmomanometric and beat-to-beat blood pressure, heart rate (ECG), venous plasma norepinephrine (highperformance liquid chromatography), and efferent postganglionic muscle sympathetic nerve activity (microneurography, peroneal nerve). For similar anthropometric and hemodynamic values, renal failure patients displayed muscle sympathetic nerve activity values significantly and markedly greater than controls (60.0Ϯ2.1 versus 45.7Ϯ2.0 bursts per 100 heartbeats; PϽ0.001). Muscle sympathetic nerve activity showed a progressive and significant increase from the first to the fourth quartile of the estimated glomerular filtration rate values (first: 41.0Ϯ2.7; second: 51.9Ϯ1.7; third: 59.8Ϯ3.0; fourth: 61.9Ϯ3.3 bursts per 100 heartbeats), the statistical significance (PϽ0.05) between groups being maintained after adjustment for confounders. In the population as a whole, muscle sympathetic nerve activity was significantly and inversely correlated with the estimated glomerular filtration rate (rϭϪ0.59; PϽ0.0001). Thus, adrenergic activation is a phenomenon not confined to advanced renal failure but already detectable in the initial phases of the disease. The sympathetic overdrive parallels the severity of the renal failure, state and, thus, it might participate, in conjunction with other factors, at the disease progression. (Hypertension. 2011;57:846-851.) Key Words: chronic renal failure Ⅲ microneurography Ⅲ sympathetic nervous system A dvanced renal failure is accompanied by a marked activation of sympathetic cardiovascular influences, as documented by the increase in the circulating plasma levels of norepinephrine, the elevated number of sympathetic neural bursts recorded in the peroneal nerve via the microneurographic technique, and the augmented oscillations in the high-frequency band of the heart rate power spectra. [1][2][3][4][5][6][7][8][9][10][11][12][13] Whether the sympathetic activation also characterizes the earlier clinical phases of the renal failure state is not clear, however. This is because in the few studies performed so far in patients with mild renal disease, the population sample was small, and the plasma levels of norepinephrine showed inconsistent changes. 11,12 Furthermore, in the 2 previously published studies that assessed sympathetic nerve traffic via microneurography, approximately half of the patients evaluated ...
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