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Muscle Sympathetic Nerve Activity (muscle + sympathetic_nerve_activity)
Selected AbstractsForearm vasoconstrictor response in uncomplicated type 1 diabetes mellitusEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2006P. J. Van Gurp Abstract Background, According to the ,haemodynamic hypothesis', increased tissue perfusion predisposes to microangiopathy in diabetic patients. We hypothesized that the typical haemodynamic changes underlying the increased tissue perfusion can be explained by a decreased sympathetic nerve activity caused by chronic hyperglycaemia. In this study we investigated sympathetic activity in patients with uncomplicated type 1 diabetes mellitus (DM). Materials and methods, In 15 DM patients (DM duration 6·3 ± 3·8 year; HbA1c 7·9 ± 1·3%) and 16 age- and sex-matched healthy volunteers (Control), sympathetic nervous system activity was measured at rest (baseline) and during sympathoneural stimulation (lower body negative pressure (LBNP)) by means of interstitial and plasma noradrenaline (NA) sampling and power spectral analysis. Muscle sympathetic nerve activity (MSNA) was measured before (baseline) and during a cold pressure test. Forearm blood flow was measured during forearm vascular ,- and ,-adrenergic receptor blockade. Results, At baseline, forearm vascular resistance (FVR), plasma NA concentrations, MSNA and heart rate variability were similar in both groups. LBNP-induced vasoconstriction was significantly attenuated in the DM group compared with the Control group (,FVR: 12 ± 4 vs. 19 ± 3 arbitrary units, P < 0·05). The responses of plasma NA and heart rate variability did not differ. Conclusions,, Baseline FVR and sympathetic nerve activity are normal in patients with uncomplicated type 1 diabetes. However, the forearm vasoconstrictor response to sympathetic stimulation is attenuated, which cannot be attributed to an impaired sympathetic responsiveness. [source] Relationship between breathing and cardiovascular function at rest: sex-related differencesACTA PHYSIOLOGICA, Issue 2 2010B. G. Wallin Abstract Aim:, To compare relationships at rest between breathing rate, levels of muscle sympathetic nerve activity, total peripheral resistance and cardiac output among young men and women. Methods:, Recordings were made of respiratory movements, sympathetic nerve activity (peroneal microneurography), intra-arterial blood pressure, electrocardiogram, cardiac output (open-circuit acetylene uptake technique) in 19 healthy men (age 27 ± 2 years, mean ± SEM) and 17 healthy women (age 25 ± 1 years). Total peripheral resistance and stroke volume were calculated. Four minutes epochs of data were analysed. Results:, Breathing rates and sympathetic activity were similar in men and women but compared to men, women had significantly lower blood pressures, cardiac output and stroke volume. In men breathing rate correlated positively with sympathetic activity (r = 0.58, P < 0.05) but not in women (r = 0.12, P > 0.05). Furthermore, in men, respiratory rate correlated positively with total peripheral resistance (r = 0.65, P < 0.05) and inversely with cardiac output (r = ,0.84, P < 0.05) and heart rate (r = ,0.60, P < 0.05) but there were no such relationships in women (P > 0.05 for all). Conclusions:, The positive relationship between breathing and sympathetic activity in men, and the inverse coupling of breathing to cardiac output and heart rate suggest that influences of respiration may be important not only for dynamic but also for ,tonic' cardiovascular function. The lack of relationships among these variables in women shows that there are fundamental differences in basic blood pressure regulation between the sexes. [source] Pregnancy-induced sympathetic overactivity: a precursor of preeclampsia,EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 6 2004T. Fischer Abstract Background, Preeclampsia has been shown to constitute a state of sympathetic overactivity. However, it remains unclear if the sympathetic activity precedes preeclampsia or represents only a secondary phenomenon. To further investigate this issue, we performed a prospective study in pregnant women considered to be at increased risk for preeclampsia owing to preeclampsia during a preceding pregnancy. Materials and methods, Twenty-two women with a history of preeclampsia were longitudinally studied on three occasions: twice during pregnancy (M1: 22 ± 4, M2: 33 ± 5 weeks) and once postpartum (M3: 26 ± 6 weeks postpartum). We measured muscle sympathetic nerve activity (MSNA), forearm blood flow, and blood pressure at rest and during reactive hyperaemia after forearm occlusion. Results, At M1 and M2, none of the subjects was hypertensive, however, muscle sympathetic nerve activity levels were significantly augmented, compared with their postpartum values (M1: 21 ± 9, M2: 29 ± 14, M3: 9 ± 5 bursts min,1; P < 0·05). Forearm vascular resistance did not significantly change from M1 through M3 (M1: 16 ± 9, M2: 15 ± 7, M3: 16 ± 7 U; P = NS). Gestational muscle sympathetic nerve activity values did not differ significantly among the subjects with subsequent preeclampsia compared with those who remained normotensive [with preeclampsia (n = 6): M1: 21 ± 5, M2: 27 ± 6, M3: 7 ± 4 bursts min,1; without preeclampsia (n = 16): M1: 21 ± 11, M2: 30 ± 16, M3: 9 ± 6 bursts min,1; P = NS]. Conclusion, Invariably, all women at risk for preeclampisa showed a pregnancy-induced increase in MSNA (pregnancy-induced sympathetic overactivity, PISO), which normalized after delivery. Most importantly, PISO is not necessarily associated with peripheral vasoconstriction and hypertension. Furthermore, only a subset of patients developed preeclampsia later on. Therefore, we hypothesize that PISO constitutes a precursor of preeclampsia which is physiologically compensated for by vasodilating mechanisms, leading to preeclampsia only when they fail. [source] Daytime sympathetic hyperactivity in OSAS is related to excessive daytime sleepinessJOURNAL OF SLEEP RESEARCH, Issue 3 2007VINCENZO DONADIO Summary The aim of this study was to investigate the relationships among sympathetic hyperactivity, excessive daytime sleepiness (EDS) and hypertension in obstructive sleep apnoea syndrome (OSAS). Ten newly diagnosed OSAS patients with untreated EDS and daytime hypertension underwent polysomnography (PSG) and daytime measurements of plasma noradrenaline (NA), ambulatory blood pressure (BP), muscle sympathetic nerve activity (MSNA) by microneurography and objective assessment of EDS before and during 6 months of compliance-monitored continuous positive airway pressure (CPAP) treatment. One month after the start of CPAP, BP, MSNA and NA were significantly lowered, remaining lower than baseline also after 3 and 6 months of treatment. CPAP use caused a significant improvement of sleep structures, and reduced EDS. A statistical correlation analysis demonstrated that EDS was not correlated with sleep measures obtained from baseline PSG (% sleep stages, apnoea and arousal index, mean oxygen saturation value), whereas daytime sleepiness was significantly correlated with MSNA. Furthermore, MSNA and BP showed no correlation. Our data obtained from selected patients suggest that the mechanisms inducing EDS in OSAS are related to the degree of daytime sympathetic hyperactivity. Additionally, resting MSNA was unrelated to BP suggesting that factors other than adrenergic neural tone make a major contribution to OSAS-related hypertension. The results obtained in this pilot study need, however, to be confirmed in a larger study involving more patients. [source] Influence of endogenous angiotensin II on control of sympathetic nerve activity in human dehydrationTHE JOURNAL OF PHYSIOLOGY, Issue 22 2009J. A. Rabbitts Arterial blood pressure can often fall too low during dehydration, leading to an increased incidence of orthostatic hypotension and syncope. Systemic sympathoexcitation and increases in volume regulatory hormones such as angiotensin II (AngII) may help to maintain arterial pressure in the face of decreased plasma volume. Our goals in the present study were to quantify muscle sympathetic nerve activity (MSNA) during dehydration (DEH), and to test the hypothesis that endogenous increases in AngII in DEH have a mechanistic role in DEH-associated sympathoexcitation. We studied 17 subjects on two separate study days: DEH induced by 24 h fluid restriction and a euhydrated (EUH) control day. MSNA was measured by microneurography at the peroneal nerve, and arterial blood pressure, electrocardiogram, and central venous pressure were also recorded continuously. Sequential nitroprusside and phenylephrine (modified Oxford test) were used to evaluate baroreflex control of MSNA. Losartan (angiotensin type 1 receptor (AT1) antagonist) was then administered and measurements were repeated. MSNA was elevated during DEH (42 ± 5 vs. EUH: 32 ± 4 bursts per 100 heartbeats, P= 0.02). Blockade of AT1 receptors partially reversed this change in MSNA during DEH while having no effect in the control EUH condition. The sensitivity of baroreflex control of MSNA was unchanged during DEH compared to EUH. We conclude that endogenous increases in AngII during DEH contribute to DEH-associated sympathoexcitation. [source] Effects of deep and superficial experimentally induced acute pain on muscle sympathetic nerve activity in human subjectsTHE JOURNAL OF PHYSIOLOGY, Issue 1 2009A. R. Burton Human studies conducted more than half a century ago have suggested that superficial pain induces excitatory effects on the sympathetic nervous system, resulting in increases in blood pressure (BP) and heart rate (HR), whereas deep pain is believed to cause vasodepression. To date, no studies have addressed whether deep or superficial pain produces such differential effects on muscle sympathetic nerve activity (MSNA). Using microneurography we recorded spontaneous MSNA from the common peroneal nerve in 13 awake subjects. Continuous blood pressure was recorded by radial arterial tonometry. Deep pain was induced by intramuscular injection of 0.5 ml hypertonic saline (5%) into the tibialis anterior muscle, superficial pain by subcutaneous injection of 0.2 ml hypertonic saline into the overlying skin. Muscle pain, with a mean rating of 4.9 ± 0.8 (s.e.m.) on a 0,10 visual analog scale (VAS) and lasting on average 358 ± 32 s, caused significant increases in MSNA (43.9 ± 10.0%), BP (5.4 ± 1.1%) and HR (7.0 ± 2.0%) , not the expected decreases. Skin pain, rated at 4.9 ± 0.6 and lasting 464 ± 54 s, also caused significant increases in MSNA (38.2 ± 12.8%), BP (5.1 ± 2.1%) and HR (5.6 ± 2.0%). The high-frequency (HF) to low-frequency (LF) ratio of heart rate variability (HRV) increased from 1.54 ± 0.25 to 2.90 ± 0.45 for muscle pain and 2.80 ± 0.52 for skin pain. Despite the different qualities of deep (dull and diffuse) and superficial (burning and well-localized) pain, we conclude that pain originating in muscle and skin does not exert a differential effect on muscle sympathetic nerve activity, both causing an increase in MSNA and an increase in the LF : HF ratio of HRV. Whether this holds true for longer lasting experimental pain remains to be seen. [source] Vasomotor sympathetic neural control is maintained during sustained upright posture in humansTHE JOURNAL OF PHYSIOLOGY, Issue 2 2006Qi Fu Vasomotor sympathetic activity plays an important role in arterial pressure maintenance via the baroreflex during acute orthostasis in humans. If orthostasis is prolonged, blood pressure may be supported additionally by humoral factors with a possible reduction in sympathetic baroreflex sensitivity. We tested the hypothesis that baroreflex control of muscle sympathetic nerve activity (MSNA) decreases during prolonged upright posture. MSNA and haemodynamics were measured supine and during 45 min 60 deg upright tilt in 13 healthy individuals. Sympathetic baroreflex sensitivity was quantified using the slope of the linear correlation between MSNA and diastolic pressure during spontaneous breathing. It was further assessed as the relationship between MSNA and stroke volume, with stroke volume derived from cardiac output (C2H2 rebreathing) and heart rate. Total peripheral resistance was calculated from mean arterial pressure and cardiac output. We found that MSNA increased from supine to upright (17 ± 8 (s.d.) versus 38 ± 12 bursts min,1; P < 0.01), and continued to increase to a smaller degree during sustained tilt (39 ± 11, 41 ± 12, 43 ± 13 and 46 ± 15 bursts min,1 after 10, 20, 30 and 45 min of tilt; between treatments P < 0.01). Sympathetic baroreflex sensitivity increased from supine to upright (,292 ± 180 versus,718 ± 362 units beat,1 mmHg,1; P < 0.01), but remained unchanged as tilting continued (,611 ± 342 and ,521 ± 221 units beat,1 mmHg,1 after 20 and 45 min of tilt; P= 0.49). For each subject, changes in MSNA were associated with changes in stroke volume (r= 0.88 ± 0.13, P < 0.05), while total peripheral resistance was related to MSNA during 45 min upright tilt (r= 0.82 ± 0.15, P < 0.05). These results suggest that the vasoconstriction initiated by sympathetic adrenergic nerves is maintained by ongoing sympathetic activation during sustained (i.e. 45 min) orthostasis without obvious changes in vasomotor sympathetic neural control. [source] | |||||||||||||