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1.
Am J Physiol Regul Integr Comp Physiol ; 317(3): R485-R490, 2019 Sep 01.
Artículo en Inglés | MEDLINE | ID: mdl-31314543

RESUMEN

Chronic kidney disease (CKD) is often complicated by difficult-to-control hypertension, in part due to chronic overactivation of the sympathetic nervous system (SNS). CKD patients also exhibit a greater increase in arterial blood pressure for a given increase in sympathetic nerve activation, suggesting an augmented vasoconstrictive response to SNS activation (i.e., neurovascular transduction). One potential mechanism of increased sympathetic neurovascular transduction is heightened sensitivity of the vascular α1-adrenergic receptors (α1ARs), the major effectors of vasoconstriction in response to norepinephrine release at the sympathetic nerve terminals. Therefore, we hypothesized that patients with CKD have increased vascular α1AR sensitivity. We studied 32 patients with CKD stages III and IV (age 59.9 ± 1.3 yr) and 19 age-matched controls (CON, age 63.2 ± 1.6 yr). Using a linear variable differential transformer (LVDT), we measured change in venoconstriction in response to exponentially increasing doses of the selective α1AR agonist phenylephrine (PE) administered sequentially into a dorsal hand vein. Individual semilogarithmic PE dose-response curves were constructed for each participant to determine the PE dose at which 50% of maximum venoconstriction occurred (ED50), reflecting α1AR sensitivity. In support of our hypothesis, CKD patients had a lower PE ED50 than CON (CKD = 2.23 ± 0.11 vs. CON = 2.63 ± 0.20, P = 0.023), demonstrating increased vascular α1AR sensitivity. Additionally, CKD patients had a greater venoconstrictive capacity to PE than CON (P = 0.015). Augmented α1AR sensitivity may contribute mechanistically to enhanced neurovascular transduction in CKD and may explain, in part, the greater blood pressure reactivity exhibited in these patients.

2.
Am J Physiol Heart Circ Physiol ; 317(2): H315-H322, 2019 Aug 01.
Artículo en Inglés | MEDLINE | ID: mdl-31149842

RESUMEN

Our laboratory has previously reported that total sleep deprivation (TSD) modifies muscle sympathetic neural activity (MSNA) differently in young men and women. Because postmenopausal women are among the highest risk for hypertension, this study compares MSNA responses with TSD in older men and women. We hypothesized that TSD would alter MSNA in older adults, with greater sympathoexcitation in postmenopausal women. Twenty-seven participants (14 men and 13 women) between the ages of 55 and 75 yr were tested twice, once after 24-h TSD and once after normal sleep (randomized, crossover design). Our primary outcome measure of MSNA (microneurography) was successful across both conditions in 20 participants (10 men and 10 women). Secondary outcome measures included seated blood pressure, heart rate, and fasting plasma testosterone, estradiol, and progesterone. Age (60 ± 1 vs. 61 ± 2 yr) and BMI (27 ± 1 vs. 26 ± 1 kg/m2) were not different between groups. TSD increased systolic blood pressure in both men (124 ± 5 to 130 ± 4 mmHg) and women (107 ± 5 to 116 ± 4 mmHg), but the increases were not different between groups (condition, P = 0.014; condition × sex, P > 0.05). In contrast, TSD elicited divergent MSNA responses in older men and women. Specifically, MSNA burst frequency increased in postmenopausal women (28 ± 3 to 34 ± 3 burst/min), but not older men (38 ± 3 to 35 ± 3 bursts/min; condition × sex, P = 0.032). In conclusion, TSD elicited sympathoexcitation in postmenopausal women but not age-matched men. These findings provide new mechanistic insight into reported links between sleep deprivation and hypertension.NEW & NOTEWORTHY Epidemiological studies report that sleep deprivation is more strongly associated with hypertension in women than in men. In the present study, 24-h total sleep deprivation (TSD) increased blood pressure in postmenopausal women and age-matched men. In contrast, only women demonstrated increases in muscle sympathetic nerve activity after TSD. The sympathoexcitation observed in postmenopausal women suggests a potential contributing mechanism for epidemiological observations and advances our understanding of the complex relations between sleep, sex, and hypertension.

3.
Am J Physiol Regul Integr Comp Physiol ; 317(2): R312-R318, 2019 Aug 01.
Artículo en Inglés | MEDLINE | ID: mdl-31141417

RESUMEN

Chronic kidney disease (CKD) patients experience augmented blood pressure (BP) reactivity during exercise that is associated with an increased risk of cardiovascular mortality. Exaggerated exercise pressor responses in CKD are in part mediated by augmented sympathetic nerve activation due to heightened muscle mechanoreflex. One mechanism that may lead to sensitization of the muscle mechanoreflex in CKD is metabolic acidosis. We hypothesized that CKD patients with low serum [bicarbonate] would exhibit exaggerated increases in arterial BP, greater reductions in muscle interstitial pH, and fatigue earlier during exercise compared with CKD patients with normal serum bicarbonate concentration ([bicarbonate]). Eighteen CKD participants with normal serum [bicarbonate] (≥24 mmol/l, normal-bicarb) and 9 CKD participants with mild metabolic acidosis ([bicarbonate] range 20-22 mmol/l, low-bicarb) performed rhythmic handgrip (RHG) exercise to volitional fatigue at 40% of maximal voluntary contraction. BP, heart rate, and muscle interstitial pH using near infrared spectroscopy were measured continuously. While mean arterial pressure (MAP) increased with exercise in both groups (P ≤ 0.002), CKD with low-bicarb had an exaggerated MAP response compared with CKD with normal-bicarb (+5.9 ± 1.3 mmHg/30 s vs. +2.6 ± 0.5 mmHg/30 s, P = 0.01). The low-bicarb group reached exhaustion earlier than the normal-bicarb group (179 ± 21 vs. 279 ± 19 s, P = 0.003). There were no differences in the change in muscle interstitial pH during exercise between groups (P = 0.31). CKD patients with metabolic acidosis have augmented exercise-induced increases in BP and poorer exercise tolerance. There was no difference in change in muscle interstitial pH between groups, however, suggesting that augmented exercise BP responses in metabolic acidosis are not due to impaired muscle-buffering capacity.

4.
Am J Med Sci ; 358(1): 11-18, 2019 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-31084910

RESUMEN

BACKGROUND: End stage renal disease (ESRD) is characterized by autonomic dysfunction. During orthostatic stress, sympathetic (SNS) activity increases and parasympathetic (PNS) activity decreases to maintain arterial blood pressure (BP). We hypothesized that ESRD patients have impaired ability to adjust cardiac SNS and PNS activity during orthostasis, which could contribute to increased blood pressure variability, orthostatic intolerance and falls. METHODS: We measured beat-to-beat BP and Electrocardiography at baseline and during increasing lower body negative pressure (LBNP) in 20 ESRD patients and 18 matched controls (CON). Heart rate variability was quantified as total power (TP) and standard deviation of the N-N interval, reflecting both SNS and PNS; high frequency (HF), root mean square of successive differences of neighboring N-N intervals (RMSSD), and percent of consecutive N-N intervals differing >50 milliseconds (pNN50), reflecting cardiac PNS activity; and low frequency (LF) and LF/HF, reflecting sympoathovagal balance. BP variability was quantified as the standard deviation in systolic (SDSAP) and diastolic (SDDAP) BP. RESULTS: Baseline HF, RMSSD, and pNN50 were significantly lower in ESRD (P < 0.05). While CON had a significant decrease in HF (P = 0.015), RMSSD (P = 0.003), and pNN50 (P = 0.005) during LBNP, there was no change in heart rate variability in ESRD. There was no significant difference in BP response, but ESRD had a significantly blunted heart rate response during graded LBNP compared to controls (P < 0.001). There was no significant difference in SDSAP or SDDAP during LBNP between groups (P > 0.05). CONCLUSIONS: These data suggest that ESRD patients have impaired autonomic adjustments to orthostatic stress.

5.
Physiol Rep ; 7(7): e14057, 2019 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-30968587

RESUMEN

Elevated Resting Blood Pressure (ERBP) in the prehypertensive range is associated with increased risk of hypertension and cardiovascular disease, the mechanisms of which remain unclear. Prior studies have suggested that ERBP may be associated with overactivation and dysregulation of the sympathetic nervous system (SNS). We hypothesized that compared to normotensives (≤120/80 mmHg), ERBP (120/80-139/89 mmHg) has higher SNS activity, impaired arterial baroreflex sensitivity (BRS), and increased vascular inflammation. Twenty-nine participants were studied: 16 otherwise healthy individuals with ERBP (blood pressure (BP) 130 ± 2/85 ± 2 mmHg) and 13 matched normotensive controls (mean BP 114 ± 2/73 ± 2 mmHg). We measured muscle sympathetic nerve activity (MSNA), beat-to-beat BP, and continuous electrocardiogram at rest and during arterial BRS testing via the modified Oxford technique. Blood was analyzed for the following biomarkers of vascular inflammation: lipoprotein-associated phospholipase A2 (Lp-PLA2), E-selectin, and intercellular adhesion molecule 1 (ICAM-1). Resting MSNA burst frequency (22 ± 2 vs. 16 ± 2 bursts/min, P = 0.036) and burst incidence (36 ± 3 vs. 25 ± 3 bursts/100 heart beats, P = 0.025) were higher in ERBP compared to controls. Cardiovagal BRS was blunted in ERBP compared to controls (13 ± 2 vs. 20 ± 3 msec/mmHg, P = 0.032), while there was no difference in sympathetic BRS between groups. Lp-PLA2 (169 ± 8 vs. 142 ± 9 nmol/min/mL, P = 0.020) and E-selectin (6.89 ± 0.6 vs. 4.45 ± 0.51 ng/mL, P = 0.004) were higher in ERBP versus controls. E-selectin (r = 0.501, P = 0.011) and ICAM-1 (r = 0.481, P = 0.015) were positively correlated with MSNA, while E-selectin was negatively correlated with cardiovagal BRS (r = -0.427, P = 0.030). These findings demonstrate that individuals with ERBP have SNS overactivity and impaired arterial BRS that are linked to biomarkers of vascular inflammation.

6.
Am J Physiol Regul Integr Comp Physiol ; 316(5): R504-R511, 2019 May 01.
Artículo en Inglés | MEDLINE | ID: mdl-30726117

RESUMEN

Patients with end-stage renal disease (ESRD) have decreased exercise capacity and exercise intolerance that contribute to cardiovascular risk. One potential mechanism underlying exercise intolerance in ESRD is impaired ability to oppose sympathetically mediated vasoconstriction within exercising skeletal muscle (i.e., functional sympatholysis, FS). We hypothesized that ESRD patients have impaired FS compared with healthy (CON) and hypertensive (HTN) controls and that impaired FS is related to circulating levels of the uremic toxin asymmetric dimethyl arginine (ADMA), an endogenous nitric oxide synthase inhibitor. Near-infrared spectroscopy-derived oxygen tissue saturation index (TSI) of the forearm muscle was measured continuously in 33 participants (9 CON, 14 HTN, 10 ESRD) at rest and during low-dose (-20 mmHg) lower body negative pressure (LBNP), moderate rhythmic handgrip exercise, and LBNP with concomitant handgrip exercise (LBNP+handgrip). Resting muscle TSI was lower in ESRD than in CON and HTN groups (CON = 67.8 ± 1.9%, HTN = 67.2 ± 1.1%, ESRD = 62.7 ± 1.5%, P = 0.03). Whereas CON and HTN groups had an attenuation in sympathetically mediated reduction in TSI during LBNP + handgrip compared with LBNP alone (P ≤ 0.05), this response was not present in ESRD (P = 0.71), suggesting impaired FS. There was no difference in plasma [ADMA] between groups (CON = 0.47 ± 0.05 µmol/l, HTN = 0.42 ± 0.06 µmol/l, ESRD = 0.63 ± 0.14 µmol/l, P = 0.106) and no correlation between plasma [ADMA] and resting muscle TSI (P = 0.84) or FS (P = 0.75). Collectively, these findings suggest that ESRD patients have lower muscle perfusion at rest and impaired FS but that these derangements are not related to circulating [ADMA].

7.
Kidney Int Rep ; 3(6): 1394-1402, 2018 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-30450466

RESUMEN

Introduction: End-stage renal disease (ESRD) patients with a paradoxical increase in blood pressure (BP) during hemodialysis (HD), termed intradialytic hypertension (ID-HTN), are at significantly increased risk for mortality and adverse cardiovascular events. ID-HTN affects up to 15% of all HD patients, and the pathophysiologic mechanisms remain unknown. We hypothesized that ESRD patients prone to ID-HTN have heightened volume-sensitive cardiopulmonary baroreflex sensitivity (BRS) that leads to exaggerated increases in sympathetic nervous system (SNS) activation during HD. Methods: We studied ESRD patients on maintenance HD with ID-HTN (n = 10) and without ID-HTN (controls, n = 12) on an interdialytic day, 24 to 30 hours after their last HD session. We measured continuous muscle sympathetic nerve activity (MSNA), beat-to-beat arterial BP, and electrocardiography (ECG) at baseline, and during graded lower body negative pressure (LBNP). Low-dose LBNP isolates cardiopulmonary BRS, whereas higher doses allow assessment of physiologic responses to orthostatic stress. Results: The ID-HTN patients had significantly higher pre- and post-HD BP, and greater interdialytic fluid weight gain compared to controls. There was a significantly greater increase in MSNA burst incidence (P = 0.044) during graded LBNP in the ID-HTN group, suggesting heightened cardiopulmonary BRS. The ID-HTN group also had a trend toward increased diastolic BP response during LBNP, and had significantly greater increases in BP during the cold pressor test. Conclusion: Patients with ID-HTN have augmented cardiopulmonary BRS that may contribute to increased SNS activation and BP response during HD.

8.
Artículo en Inglés | MEDLINE | ID: mdl-30303706

RESUMEN

Posttraumatic stress disorder (PTSD) is characterized by increased sympathetic nervous system (SNS) activity, blunted parasympathetic nervous system (PNS) activity, and impaired baroreflex sensitivity (BRS) that contribute to accelerated cardiovascular disease (CVD). PTSD patients also have chronic stress-related elevations in resting blood pressure (BP), often in the prehypertensive range; yet, it is unclear if elevated resting blood pressure (ERBP) augments these autonomic derangements in PTSD. We hypothesized that compared to normotensive PTSD (N-PTSD), those with ERBP (E-PTSD) have further increased SNS, decreased PNS activity and impaired BRS at rest, and exaggerated SNS reactivity, PNS withdrawal, and pressor responses during stress. In 16 E-PTSD and 17 matched N-PTSD, we measured continuous BP, ECG, muscle sympathetic nerve activity (MSNA), and heart rate variability (HRV) markers reflecting cardiac PNS activity (standard deviation of R-R intervals (SDNN), root mean square of differences in successive R-R intervals (RMSSD), and high frequency power (HF)) during five minutes of rest and three minutes of mental arithmetic. Resting MSNA (p=0.943), sympathetic BRS (p=0.189) and cardiovagal BRS (p=0.332) were similar between groups. However, baseline SDNN (56±6 vs 78±8ms, p=0.019), RMSSD (39±6 vs 63±9 ms, p=0.018), and HF (378±103 vs 693±92 ms2, p=0.015) were lower in E-PTSD vs. N-PTSD. During mental stress, the systolic blood pressure response (p=0.011) was augmented in E-PTSD. While MSNA reactivity was not different (p>0.05), the E-PTSD group had an exaggerated reduction in HRV during mental stress (p<0.05). PTSD with ERBP have attenuated resting cardiac PNS activity, coupled with exaggerated BP reactivity and PNS withdrawal during stress.

10.
Am J Physiol Heart Circ Physiol ; 315(1): H141-H149, 2018 Jul 01.
Artículo en Inglés | MEDLINE | ID: mdl-29652544

RESUMEN

Patients with posttraumatic stress disorder (PTSD) have elevated sympathetic nervous system reactivity and impaired sympathetic and cardiovagal baroreflex sensitivity (BRS). Device-guided slow breathing (DGB) has been shown to lower blood pressure (BP) and sympathetic activity in other patient populations. We hypothesized that DGB acutely lowers BP, heart rate (HR), and improves BRS in PTSD. In 23 prehypertensive veterans with PTSD, we measured continuous BP, ECG, and muscle sympathetic nerve activity (MSNA) at rest and during 15 min of DGB at 5 breaths/min ( n = 13) or identical sham device breathing at normal rates of 14 breaths/min (sham; n = 10). Sympathetic and cardiovagal BRS was quantified using pharmacological manipulation of BP via the modified Oxford technique at baseline and during the last 5 min of DGB or sham. There was a significant reduction in systolic BP (by -9 ± 2 mmHg, P < 0.001), diastolic BP (by -3 ± 1 mmHg, P = 0.019), mean arterial pressure (by -4 ± 1 mmHg, P = 0.002), and MSNA burst frequency (by -7.8 ± 2.1 bursts/min, P = 0.004) with DGB but no significant change in HR ( P > 0.05). Within the sham group, there was no significant change in diastolic BP, mean arterial pressure, HR, or MSNA burst frequency, but there was a small but significant decrease in systolic BP ( P = 0.034) and MSNA burst incidence ( P = 0.033). Sympathetic BRS increased significantly in the DGB group (-1.08 ± 0.25 to -2.29 ± 0.24 bursts·100 heart beats-1·mmHg-1, P = 0.014) but decreased in the sham group (-1.58 ± 0.34 to -0.82 ± 0.28 bursts·100 heart beats-1·mmHg-1, P = 0.025) (time × device, P = 0.001). There was no significant difference in the change in cardiovagal BRS between the groups (time × device, P = 0.496). DGB acutely lowers BP and MSNA and improves sympathetic but not cardiovagal BRS in prehypertensive veterans with PTSD. NEW & NOTEWORTHY Posttraumatic stress disorder is characterized by augmented sympathetic reactivity, impaired baroreflex sensitivity, and an increased risk for developing hypertension and cardiovascular disease. This is the first study to examine the potential beneficial effects of device-guided slow breathing on hemodynamics, sympathetic activity, and arterial baroreflex sensitivity in prehypertensive veterans with posttraumatic stress disorder.

11.
Sleep ; 41(6)2018 Jun 01.
Artículo en Inglés | MEDLINE | ID: mdl-29522186

RESUMEN

Study Objectives: Chronic insomnia affects up to 15 per cent of adults. Recent cross-sectional and prospective epidemiological studies report an association between insomnia and hypertension, including incident hypertension, yet mechanisms underlying the association remain unknown. We hypothesized that participants with chronic insomnia would have elevated sympathetic neural outflow, blunted baroreflex sensitivity, and augmented sympathetic neural and cardiovascular reactivity to stress when compared with good-sleeper controls. Methods: Twelve participants with chronic insomnia (11 women, 1 man) and 12 controls (8 women, 4 men) underwent one night of laboratory polysomnography, two weeks of at-home wrist actigraphy, and one night of controlled laboratory sleep prior to a comprehensive morning autonomic function test. The autonomic function test consisted of simultaneous recordings of muscle sympathetic nerve activity (MSNA; microneurography), beat-to-beat blood pressure (finger plethysmography), and heart rate (electrocardiogram) during a 10 min supine baseline and a 2 min cold pressor test. Results: Baseline blood pressure, heart rate, and MSNA were not different between groups, but sympathetic baroreflex sensitivity was significantly blunted in participants with insomnia (-2.1 ± 1.0 vs. -4.3 ± 1.3 bursts/100 heartbeats/mm Hg; p < 0.001). During the cold pressor test, systolic arterial pressure reactivity (Δ21 ± 11 vs. Δ14 ± 8 mm Hg; time × group = 0.04) and total MSNA reactivity (Δ127%, 54%-208% vs. Δ52%, 30%-81%; time × group = 0.02) were augmented in chronic insomnia. Conclusions: Participants with chronic insomnia demonstrated impaired sympathetic baroreflex function and augmented neural cardiovascular responsiveness to stress, when compared with controls. These findings support growing evidence of cardiovascular risk and physiological hyperarousal in chronic insomnia. Clinical Trial Registration: NCT02048878. https://clinicaltrials.gov/ct2/show/NCT02048878.

12.
J Appl Physiol (1985) ; 124(1): 201-207, 2018 01 01.
Artículo en Inglés | MEDLINE | ID: mdl-28970198

RESUMEN

Black adults have a higher risk of hypertension compared with non-Hispanic white (NHW) adults, but physiological mechanisms underlying this predisposition remain unclear. This study compared muscle sympathetic nerve activity (MSNA) responses to mental stress in a group of young black and NHW participants. We hypothesized that the sympathoexcitation associated with mental stress would be greater in black adults compared with NHW participants. Thirty-five male adults (19 black, 23 ± 1 yr; 16 NHW, 22 ± 1 yr) were examined during 5-min supine baseline and 5 min of mental stress (via mental arithmetic). Baseline mean arterial pressure (80 ± 2 vs. 82 ± 1 mmHg), heart rate (61 ± 4 vs. 61 ± 2 beats/min), MSNA (13 ± 1 vs. 15 ± 2 bursts/min), and sympathetic baroreflex sensitivity (-1.1 ± 0.4 vs. -1.5 ± 0.3 bursts·100 heart beats-1·mmHg-1) were not significantly different between NHW and black adults ( P > 0.05), respectively. MSNA reactivity to mental stress was significantly higher in NHW compared with black adults (time × race, P = 0.006), with a particularly divergent responsiveness during the first minute of mental stress in NHW (Δ4 ± 1 burst/min) and black (Δ-2 ± 2 burst/min; P = 0.022) men. Blood pressure and heart rate reactivity to mental stress were similar between groups. In summary, black participants demonstrated a lower MSNA responsiveness to mental stress compared with NHW adults. These findings suggest that, despite a higher prevalence of hypertension, black subjects do not appear to have higher neural and cardiovascular responsiveness to mental stress compared with NHW. NEW & NOTEWORTHY Black men have a blunted muscle sympathetic nerve activity response to mental stress compared with non-Hispanic white (NHW) men, especially at the onset of mental stress when muscle sympathetic nerve activity decreased in blacks and increased in NHW men. Thus, despite a high prevalence of hypertension in blacks, normotensive NHW men display a greater peripheral sympathetic neural reactivity to mental stress than black men.

13.
Am J Physiol Heart Circ Physiol ; 311(2): H426-32, 2016 08 01.
Artículo en Inglés | MEDLINE | ID: mdl-27371684

RESUMEN

A number of recent studies have highlighted large interindividual variability of muscle sympathetic nerve activity (MSNA) responsiveness to mental stress in humans. The purpose of this study was to examine blood pressure (BP) and MSNA responsiveness to mental stress in a large and generalizable cohort of young adults with and without family history of hypertension (FHH). We hypothesized that subjects with FHH would demonstrate greater sympathoexcitation to mental stress than subjects without FHH. A total of 87 subjects (55 men and 32 women, 18-40 yr of age) from recently published (n = 45) and ongoing (n = 42) studies were examined; 57 subjects (19 with FHH and 38 without FHH) had complete MSNA recordings at baseline. Heart rate (HR), BP, and MSNA were recorded during 5 min of supine rest and 5 min of mental stress (mental arithmetic). Resting MSNA and HR were not statistically different between subjects with and without FHH (P > 0.05), whereas resting mean arterial pressure was higher in subjects with FHH (86 ± 2 vs. 80 ± 1 mmHg, P < 0.05). Mental stress increased MSNA in subjects with FHH (Δ5 ± 1 bursts/min), but not in subjects without FHH [Δ1 ± 1 burst/min, P < 0.01 (time × group)]. Mental stress increased mean arterial pressure (Δ12 ± 1 and Δ10 ± 1 mmHg, P < 0.001) and HR (Δ19 ± 2 and Δ16 ± 2 beats/min, P < 0.001) in subjects with and without FHH, but these increases were not different between groups [P ≥ 0.05 (time × group)]. MSNA and BP reactivity to mental stress were not correlated in either group. In conclusion, FHH was associated with heightened MSNA reactivity to mental stress, despite a dissociation between MSNA and BP responsiveness.


Asunto(s)
Presión Arterial , Hijo de Padres Discapacitados , Frecuencia Cardíaca , Hipertensión , Músculo Esquelético/inervación , Estrés Psicológico/fisiopatología , Sistema Nervioso Simpático/fisiopatología , Adolescente , Adulto , Presión Sanguínea , Femenino , Humanos , Masculino , Adulto Joven
14.
Am J Physiol Regul Integr Comp Physiol ; 310(7): R602-11, 2016 Apr 01.
Artículo en Inglés | MEDLINE | ID: mdl-26818059

RESUMEN

Positive airway pressure (PAP) treatment has been shown to have a modest effect on ambulatory blood pressure (BP) in patients with obstructive sleep apnea (OSA). However, there is a paucity of data on the effect of PAP therapy on rapid, yet significant, BP swings during sleep, particularly in obesity hypoventilation syndrome (OHS). The present study hypothesizes that PAP therapy will improve nocturnal BP on the first treatment night (titration PAP) in OHS patients with underlying OSA, and that these improvements will become more significant with 6 wk of PAP therapy. Seventeen adults (7 men, 10 women; age 50.4 ± 10.7 years, BMI 49.3 ± 2.4 kg/m(2)) with OHS and clinically diagnosed OSA participated in three overnight laboratory visits that included polysomnography and beat-to-beat BP monitoring via finger plethysmography. Six weeks of PAP therapy, but not titration PAP, lowered mean nocturnal BP. In contrast, when nocturnal beat-to-beat BPs were aggregated into bins consisting of at least three consecutive cardiac cycles with a >10 mmHg BP surge (i.e., Δ10-20, Δ20-30, Δ30-40, and Δ>40 mmHg), titration, and 6-wk PAP reduced the number of BP surges per hour (time × bin, P < 0.05). PAP adherence over the 6-wk period was significantly correlated to reductions in nocturnal systolic (r = 0.713, P = 0.001) and diastolic (r = 0.497, P = 0.043) BP surges. Despite these PAP-induced improvements in nocturnal beat-to-beat BP surges, 6 wk of PAP therapy did not alter daytime BP. In conclusion, PAP treatment reduces nocturnal beat-to-beat BP surges in OHS patients with underlying OSA, and this improvement in nocturnal BP regulation was greater in patients with higher PAP adherence.


Asunto(s)
Presión Sanguínea , Síndrome de Hipoventilación por Obesidad/fisiopatología , Síndrome de Hipoventilación por Obesidad/terapia , Respiración con Presión Positiva/métodos , Apnea Obstructiva del Sueño/fisiopatología , Apnea Obstructiva del Sueño/terapia , Chicago , Femenino , Frecuencia Cardíaca , Humanos , Masculino , Persona de Mediana Edad , Síndrome de Hipoventilación por Obesidad/diagnóstico , Apnea Obstructiva del Sueño/diagnóstico , Resultado del Tratamiento
15.
Am J Physiol Regul Integr Comp Physiol ; 309(11): R1380-6, 2015 Dec 01.
Artículo en Inglés | MEDLINE | ID: mdl-26400186

RESUMEN

Mental stress consistently increases arterial blood pressure, but this reliable pressor response is often associated with highly variable muscle sympathetic nerve activity (MSNA) responsiveness between individuals. Although MSNA has been shown to be reproducible within individuals at rest and during the cold pressor test (CPT), intraindividual reproducibility of MSNA responsiveness to mental stress has not been adequately explored. The purpose of this study was to examine MSNA reactivity to mental stress across three experimental sessions. Sixteen men and women (age 21 ± 1 yr) performed two experimental sessions within a single laboratory visit and a third experimental session 1 mo later. Each experimental session consisted of a mental stress trial via mental arithmetic and a CPT trial. Blood pressure, heart rate (HR), and MSNA were measured, and the consistencies of these variables were determined using intraclass correlation (Cronbach's α coefficient). MSNA, mean arterial pressure (MAP), and HR were highly reproducible across the baselines preceding mental stress (Cronbach's α ≥ 0.816, P ≤ 0.001) and CPT (Cronbach's α ≥ 0.782, P ≤ 0.001). Across the three mental stress trials, changes in MSNA (Cronbach's α = 0.875; P = 0.001), MAP (Cronbach's α = 0.749; P < 0.001), and HR (Cronbach's α = 0.919; P < 0.001) were reproducible. During CPT, changes in MSNA (Cronbach's α = 0.805; P = 0.008), MAP (Cronbach's α = 0.878; P < 0.001), and HR (Cronbach's α = 0.927; P < 0.001) remained consistent across the three sessions. In conclusion, our findings demonstrate that MSNA reactivity to mental stress is consistent within a single laboratory visit and across laboratory sessions conducted on separate days.


Asunto(s)
Sistema Cardiovascular/inervación , Músculo Esquelético/inervación , Nervio Peroneo/fisiopatología , Estrés Psicológico/fisiopatología , Sistema Nervioso Simpático/fisiopatología , Presión Sanguínea , Frío , Electrocardiografía , Electromiografía , Femenino , Frecuencia Cardíaca , Humanos , Masculino , Conceptos Matemáticos , Contracción Muscular , Valor Predictivo de las Pruebas , Reproducibilidad de los Resultados , Esfigmomanometros , Estrés Psicológico/psicología , Factores de Tiempo , Adulto Joven
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