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The prevalence of obesity is rapidly increasing in the United States, particularly among women. Approximately 60−70% of hypertension in adults may be directly attributed to obesity. In addition, maternal obesity is a major risk factor for hypertensive disorders during pregnancy. The underlying mechanisms for the association between obesity and cardiovascular risk are multifactorial, but activation of the sympathetic nervous system is one significant contributing factor. This brief review summarizes the current knowledge on sex differences in sympathetic activity in obesity and its related hypertension, with a focus on studies in humans. Evidence suggests that abdominal visceral fat, rather than subcutaneous fat, is related to augmented sympathetic activity regardless of sex. Race/ethnicity may affect the relationship between obesity and sympathetic activity. Obesity‐related hypertension has an important neurogenic component, which is characterized by sympathetic overactivity. However, sex may influence the association between hypertension and sympathetic overactivity in obese people. Finally, both body weight and sympathetic overactivity seem to be involved in the development of gestational hypertensive disorders in women. Chronic hyperinsulinemia due to insulin resistance, high plasma levels of leptin, and/or obstructive sleep apnea may be responsible for sympathetic overactivity in obesity‐related hypertension. [ABSTRACT FROM AUTHOR]

Presents a study evaluating the response of vasomotor sympathetic nerve activity to lower body positive pressure (LBPP), muscle sympathetic nerve activity (MSNA). Methodology used to conduct the study; Atrial dimension by echocardiography; Mechanism of increase during LBPP; Findings of the study.

Muscle sympathetic nerve activity (MSNA) increases during isometric exercise via increased firing of low-threshold action potentials (AP), recruitment of larger, higher-threshold APs, and synaptic delay modifications. Recent work found that women with post-traumatic stress disorder (PTSD) demonstrate exaggerated early-onset MSNA responses to exercise; however, it is unclear how PTSD affects AP recruitment patterns during fatiguing exercise. We hypothesized that women with PTSD (n = 11, 43 [11] [SD] years) would exhibit exaggerated sympathetic neural recruitment compared to women without PTSD (controls; n = 13, 40 [8] years). MSNA and AP discharge patterns (via microneurography and a continuous wavelet transform) were measured during 1 min of baseline, isometric handgrip exercise (IHG) to fatigue, 2 min of post-exercise circulatory occlusion (PECO), and 3 min of recovery. Women with PTSD were unable to increase AP content per burst compared to controls throughout IHG and PECO (main effect of group: P = 0.026). Furthermore, relative to controls, women with PTSD recruited fewer AP clusters per burst during the first (controls: ∆1.3 [1.2] vs. PTSD: ∆−0.2 [0.8]; P = 0.016) and second minute (controls: ∆1.2 [1.1] vs. PTSD: ∆−0.1 [0.8]; P = 0.022) of PECO, and fewer subpopulations of larger, previously silent axons during the first (controls: ∆5 [4] vs. PTSD: ∆1 [2]; P = 0.020) and second minute (controls: ∆4 [2] vs. PTSD: ∆1 [2]; P = 0.021) of PECO. Conversely, PTSD did not modify the AP cluster size–latency relationship during baseline, the end of IHG, or PECO (all P = 0.658–0.745). Collectively, these data indicate that women with PTSD demonstrate inherent impairments in the fundamental neural coding patterns elicited by the sympathetic nervous system during IHG and exercise pressor reflex activation. [ABSTRACT FROM AUTHOR]

Group mean slopes and r2 are given in E and F. AP indicates action potential; PTSD, posttraumatic stress disorder; and TPR, total peripheral resistance. Keywords: action potentials; stress disorders, post-traumatic; sympathetic nervous system EN action potentials stress disorders, post-traumatic sympathetic nervous system 1483 1485 3 11/08/22 20221108 NES 221108 Posttraumatic stress disorder (PTSD) is highly prevalent in women and is associated with an increased risk of developing cardiovascular disease.[1] Sympathetic nervous system dysregulation (eg, exaggerated sympathetic outflow) is thought to contribute to this increased risk[2]; however, previous studies of sympathetic activity in individuals with PTSD were conducted in the supine position, despite humans spending majority of their day upright. Our hypothesis was that women with PTSD would display greater vasoconstrictor responses associated with exaggerated increases in sympathetic action potential (AP) recruitment patterns during orthostasis. [Extracted from the article]

Background: Current-generation left ventricular assist devices provide circulatory support that is minimally or entirely nonpulsatile and are associated with marked increases in muscle sympathetic nerve activity (MSNA), likely through a baroreceptor-mediated pathway. We sought to determine whether the restoration of pulsatile flow through modulations in pump speed would reduce MSNA through the arterial baroreceptor reflex.Methods and Results: Ten men and 3 women (54 ± 14 years) with Heartmate II continuous-flow left ventricular assist devices underwent hemodynamic and sympathetic neural assessment. Beat-to-beat blood pressure, carotid ultrasonography at the level of the arterial baroreceptors, and MSNA via microneurography were continuously recorded to determine steady-state responses to step changes (200-400 revolutions per minute) in continuous-flow left ventricular assist device pump speed from a maximum of 10,480 ± 315 revolutions per minute to a minimum of 8500 ± 380 revolutions per minute. Reductions in pump speed led to increases in pulse pressure (high versus low speed: 17 ± 7 versus 26 ± 12 mm Hg; P<0.01), distension of the carotid artery, and carotid arterial wall tension (P<0.05 for all measures). In addition, MSNA was reduced (high versus low speed: 41 ± 15 versus 33 ± 16 bursts per minute; P<0.01) despite a reduction in mean arterial pressure and was inversely related to pulse pressure (P=0.037).Conclusions: Among subjects with continuous-flow left ventricular assist devices, the restoration of pulsatile flow through modulations in pump speed leads to increased distortion of the arterial baroreceptors with a subsequent decline in MSNA. Additional study is needed to determine whether reduction of MSNA in this setting leads to improved outcomes. [ABSTRACT FROM AUTHOR]

New Findings What is the central question of this study? The study was designed to investigate the age- and sex-related differences in muscle sympathetic nerve activity (MSNA) in relation to age- and sex-related differences in haemodynamics, blood volume and left ventricular size and function., What is the main finding and its importance? Age-related increases in MSNA were associated with decreases in blood volume in men only, and only in men was there a significant relation between MSNA and forearm vascular resistance. These results show that age and sex independently alter the neural control of blood pressure and may provide insights into the pathogenesis of hypertension., We compared the effect of age- and sex-related differences in haemodynamics, blood volume (BV) and left ventricular (LV) size and mass on resting muscle sympathetic nerve activity (MSNA) in healthy, normotensive adults. Twenty young men (19-47 years old) and 20 young women (21-46 years old) as well as 15 older men (62-80 years old) and 15 older women (60-82 years old) were studied. Cardiac output (acetylene rebreathing), total peripheral resistance, forearm vascular resistance (FVR; venous occlusion plethysmography) and MSNA were measured during supine rest. Blood volume was calculated (CO rebreathing), and LV mass, end-diastolic (LVEDV) and end-systolic volumes (LVESV) were measured using magnetic resonance imaging. Cardiac index ( P < 0.001 and P = 0.016), BV (both P < 0.001), LV mass ( P < 0.001 and P = 0.002), LVEDV ( P < 0.001 and P = 0.002) and LVESV (both P < 0.001) were lower in the older and female groups, respectively. Total peripheral resistance was significantly higher in the older ( P < 0.001) and female groups ( P = 0.014), but FVR was increased in the female groups ( P = 0.048) only (age, P = 0.089). The MSNA was greater in the older groups ( P < 0.001) only (sex, P = 0.228). Increased MSNA was shown to correlate with a decrease in BV ( P = 0.004) in men only when adjusted for age (women, P = 0.133). There was a positive relation between MSNA and FVR ( P = 0.020) in men but not women ( P = 0.422). There were no significant relations between MSNA and LV mass, LVEDV or LVESV. The findings suggest that the increase in resting MSNA with age may be related to the decline in BV in men only, but it is unknown whether sex differences in sympathetic adrenergic vasoconstriction occur independently of these changes. [ABSTRACT FROM AUTHOR]

Key points Cardiovascular risk remains high in elderly patients with hypertension even with adequate blood pressure control; one possible mechanism may be sympathetic activation via the baroreflex in response to blood pressure reduction., We found that chronic diuresis increased vasomotor sympathetic activity in both the supine and the upright positions, while chronic renin inhibition did not affect sympathetic activity in the supine position but attenuated its response to head-up tilt in elderly hypertensive patients., The change of sympathetic activity by anti-hypertensive drug treatment was correlated with the change of aldosterone level in all patients., Upright sympathetic baroreflex sensitivity remained unchanged after diuresis or renin inhibition., These results suggest that chronic renin inhibition lowers blood pressure in elderly hypertensive patients without sympathetic activation, in contrast to diuresis which increases sympathetic activity through the augmented renin-angiotensin-aldosterone system., Abstract Cardiovascular risk remains high in patients with hypertension even with adequate blood pressure (BP) control. One possible mechanism may be sympathetic activation via the baroreflex. We tested the hypothesis that chronic inhibition of renin reduces BP without sympathetic activation, but diuresis augments sympathetic activity in elderly hypertensives. Fourteen patients with stage-I hypertension (66 ± 5 (SD) years) were treated with a direct renin inhibitor, aliskiren ( n= 7), or a diuretic, hydrochlorothiazide ( n= 7), for 6 months. Muscle sympathetic nerve activity (MSNA), BP, direct renin and aldosterone were measured during supine and a graded head-up tilt (HUT; 5 min 30° and 20 min 60°), before and after treatment. Sympathetic baroreflex sensitivity (BRS) was assessed. Both groups had similar BP reductions after treatment (all P < 0.01), while MSNA responses were different between hydrochlorothiazide and aliskiren ( P= 0.006 pre/post × drug). Both supine and upright MSNA became greater after hydrochlorothiazide treatment (supine, 72 ± 18 post vs. 64 ± 15 bursts (100 beats)−1 pre; 60° HUT, 83 ± 10 vs. 78 ± 13 bursts (100 beats)−1; P= 0.002). After aliskiren treatment, supine MSNA remained unchanged (69 ± 13 vs. 64 ± 8 bursts (100 beats)−1), but upright MSNA was lower (74 ± 15 vs. 85 ± 10 bursts (100 beats)−1; P= 0.012 for pre/post × posture). Direct renin was greater after both treatments (both P < 0.05), while upright aldosterone was greater after hydrochlorothiazide only ( P= 0.002). The change in upright MSNA by the treatment was correlated with the change of aldosterone ( r= 0.74, P= 0.002). Upright sympathetic BRS remained unchanged after either treatment. Thus, chronic renin inhibition may reduce upright MSNA through suppressed renin activity, while diuresis may evoke sympathetic activation via the upregulated renin-angiotensin-aldosterone system, without changing intrinsic sympathetic baroreflex function in elderly hypertensive patients. [ABSTRACT FROM AUTHOR]

Key points Sympathetic activity has been reported to increase in normotensive pregnant women, and to be even greater in women with gestational hypertension and preeclampsia at term., Whether sympathetic overactivity develops early during pregnancy, remaining high throughout gestation, or whether it only occurs at term providing the substrate for hypertensive disorders is unknown., We found that vasomotor sympathetic activity was markedly greater, diastolic pressure trended lower, total peripheral resistance decreased, sympathetic vascular transduction was blunted, and renin and aldosterone both were higher during early pregnancy (i.e. ≤8 weeks of gestation) than pre-pregnancy., It is suggested that sympathetic activation is a common characteristic of early pregnancy in normotensive women., These results help us better understand blood pressure control mechanisms during normal pregnancy in humans., Abstract Sympathetic activity has been reported to increase in normotensive pregnant women, and to be even greater in women with gestational hypertension and preeclampsia at term. Whether sympathetic overactivity develops early during pregnancy, remaining high throughout gestation, or whether it only occurs at term providing the substrate for hypertensive disorders is unknown. We tested the hypothesis that sympathetic activation occurs early during pregnancy in humans. Eleven healthy women (29 ± 3 (SD) years) without prior hypertensive pregnancies were tested during the mid-luteal phase (PRE) and early pregnancy (EARLY; 6.2 ± 1.2 weeks of gestation). Muscle sympathetic nerve activity (MSNA) and haemodynamics were measured supine, at 30 deg and 60 deg upright tilt for 5 min each. Blood samples were drawn for catecholamines, direct renin, and aldosterone. MSNA was significantly greater during EARLY than PRE (supine: 25 ± 8 vs. 14 ± 8 bursts min−1, 60 deg tilt: 49 ± 14 vs. 40 ± 10 bursts min−1; main effect, P < 0.05). Resting diastolic pressure trended lower ( P= 0.09), heart rate was similar, total peripheral resistance decreased (2172 ± 364 vs. 2543 ± 352 dyne s cm−5; P < 0.05), sympathetic vascular transduction was blunted (0.10 ± 0.05 vs. 0.36 ± 0.47 units a.u.−1 min−1; P < 0.01), and both renin (supine: 27.9 ± 6.2 vs. 14.2 ± 8.7 pg ml−1, P < 0.01) and aldosterone (supine: 16.7 ± 14.1 vs. 7.7 ± 6.8 ng ml−1, P= 0.05) were higher during EARLY than PRE. These results suggest that sympathetic activation is a common characteristic of early pregnancy in humans despite reduced diastolic pressure and total peripheral resistance. These observations challenge conventional thinking about blood pressure regulation during pregnancy, showing marked sympathetic activation occurring within the first few weeks of conception, and may provide the substrate for pregnancy induced cardiovascular complications. [ABSTRACT FROM AUTHOR]