Vascular responses to orthostatic stress in patients with postural tachycardia syndrome (POTS), in patients with low orthostatic tolerance, and in asymptomatic controls

Bush, Victoria E.; Wight, Victoria L.; Brown, Clive; Hainsworth, R.

doi:10.1007/bf02281110

Cited by 49 publications

(52 citation statements)

References 15 publications

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“…In the upright position, there is normally a baroreceptor-mediated vasoconstriction, via an increase in tonic sympathetic outflow, in order to maintain blood pressure and cerebral perfusion. It has been demonstrated previously that these vascular resistance responses play a crucial role in cardiovascular control during orthostatic stress, [46][47][48] and any impairment in vascular resistance responses following SCI will predispose to orthostatic intolerance. 46,47 In the light of the alterations mentioned above, it is surprising that blood pressure control during orthostatic stress is not more severely impaired following SCI.…”

Section: Mechanisms Underlying Orthostatic Hypotension In Scimentioning

confidence: 97%

“…It has been demonstrated previously that these vascular resistance responses play a crucial role in cardiovascular control during orthostatic stress, [46][47][48] and any impairment in vascular resistance responses following SCI will predispose to orthostatic intolerance. 46,47 In the light of the alterations mentioned above, it is surprising that blood pressure control during orthostatic stress is not more severely impaired following SCI. One reason for this may be the fact that although resting supine sympathetic activity (and thus blood pressure) tends to be low after SCI, some studies do report an appropriate increase in peripheral resistance when upright in SCI individuals, despite presumed disruption of the sympathetic control.…”

Section: Mechanisms Underlying Orthostatic Hypotension In Scimentioning

confidence: 97%

“…Individuals should be advised regarding the mechanisms underlying orthostatic hypotension, and common factors likely to provoke an episode. Further advice should be given on the maintenance of plasma volume by ensuring an adequate salt and fluid intake, 47,70 and the avoidance of diuretics such as alcohol and caffeine. SCI individuals should be educated as to the symptoms of orthostatic hypotension and encouraged to assume a recumbent or semirecumbent position should they occur.…”

Section: Management Of Orthostatic Hypotension In Scimentioning

confidence: 99%

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Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

2005

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Motor and sensory deficits are well-known consequences of spinal cord injury (SCI). During the last decade, a significant number of experimental and clinical studies have focused on the investigation of autonomic dysfunction and cardiovascular control following SCI. Numerous clinical reports have suggested that unstable blood pressure control in individuals with SCI could be responsible for their increased cardiovascular mortality. The aim of this review is to outline the incidence and pathophysiological mechanisms underlying the orthostatic hypotension that commonly occurs following SCI. We describe the clinical abnormalities of blood pressure control following SCI, with particular emphasis upon orthostatic hypotension. Possible mechanisms underlying orthostatic hypotension in SCI, such as changes in sympathetic activity, altered baroreflex function, the lack of skeletal muscle pumping activity, cardiovascular deconditioning and altered salt and water balance will be discussed. Possible alterations in cerebral autoregulation following SCI, and the impact of these changes upon cerebral perfusion are also examined. Finally, the management of orthostatic hypotension will be considered.

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Section: Mechanisms Underlying Orthostatic Hypotension In Scimentioning

confidence: 97%

Section: Mechanisms Underlying Orthostatic Hypotension In Scimentioning

confidence: 97%

Section: Management Of Orthostatic Hypotension In Scimentioning

confidence: 99%

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Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

2005

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“…[22][23][24][25][26] In the AB population, it is well known that on assumption of the upright posture, there is a baroreflex-mediated peripheral vasoconstriction via an increased sympathetic outflow to maintain blood pressure and cerebral perfusion. 27,28 It is, therefore, likely that both sympathetic hypoactivity and altered baroreceptor sensitivity are the primary causes of orthostatic hypotension following cervical SCI. 29,30 However, a lack of skeletal muscle pump, 31 cardiovascular deconditioning 32 and/or altered salt and water balance 33 have also been hypothesized to contribute to hypotension.…”

Section: Organization Of the Autonomic Nervous Systemmentioning

confidence: 99%

Peripheral vascular function in spinal cord injury: a systematic review

et al. 2012

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Background: During the past 20 years, significant advances in patient care have resulted in individuals with spinal cord injury (SCI) living longer than before. As lifespan increases, cardiovascular complications are emerging as the leading cause of mortality in this population, and individuals with SCI develop cardiovascular disease at younger ages than their able-bodied counterparts. To address this increasing clinical challenge, several recent studies investigated the central cardiovascular adaptations that occur following SCI. However, a somewhat less recognized component of cardiovascular dysfunction in this population is the peripheral vascular adaptations that also occur as a result of SCI. Study design: Literature review.Objective: To present a comprehensive overview of changes in arterial structure and function, which occur after SCI. Setting: Canada. Methods: A systematic literature review was conducted to extract studies that incorporated measures of arterial structure or function after SCI in animals or humans. Results: Individuals with SCI exhibit vascular dysfunction below the lesion that is characterized by a reduction in conduit artery diameter and blood flow, increased shear rate and leg vascular resistance, and adrenoceptor hyper-responsiveness. There is also recent alarming evidence for central arterial stiffening in individuals with SCI. Conclusion: Although physical deconditioning is the primary candidate responsible for the maladaptive remodeling of the peripheral vasculature after SCI, there is emerging evidence that blood pressure oscillations, such as those occurring in the large majority of individuals with SCI, also exacerbates vascular dysfunction in this population.

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“…[3][4][5] Even when overall blood pressure regulation is functioning properly, the balance between baroreflex regulation of heart rate and vascular tone may be perturbed. Imbalance between sympathetic activation of the heart and the vasculature has been described in heart failure patients, 6 postural tachycardia syndrome patients, 7,8 and in healthy subjects treated with norepinephrine transporter inhibitors. 9,10 Factors influencing baroreflex function may have an important bearing on human cardiovascular disease.…”

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confidence: 99%

Baroreflex Regulation of Heart Rate and Sympathetic Vasomotor Tone in Women and Men

et al. 2005

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Abstract-Gender has been reported to influence baroreflex heart rate regulation and baroreflex blood pressure buffering.We tested the hypothesis that gender influences baroreflex regulation of heart rate and sympathetic vasomotor tone. We recruited 32 normal-weight healthy subjects (17 men and 15 women). ECGs for heart rate, brachial and finger blood pressure, and muscle sympathetic nerve activity (MSNA) were measured. Baroreflex heart rate and MSNA regulation were assessed using incremental phenylephrine and nitroprusside infusions. Baseline blood pressure was similar in men and women. MSNA was 21Ϯ2.5 bursts/min in women and 19Ϯ2.8 bursts/min in men (NS). The gain of the baroreflex MSNA curves was similar in women and men (Ϫ1.9Ϯ0.2 bursts/min per mm Hg in men and Ϫ2.0Ϯ0.3 bursts/min per mm Hg in women). Baroreflex gain for heart rate regulation was 17Ϯ3.2 ms/mm Hg in women and 19Ϯ1.9 ms/mm Hg in men (NS). We conclude that baroreflex gains for heart rate and sympathetic MSNA regulation are similar in women and men. However, the probability for congruence between men and women in terms of the MSNA baroreflex curves was 0.06% for burst rate, 0.4% for burst incidence, and 0.01% for burst area. In women, the MSNA baroreflex curve may be shifted to slightly lower blood pressure such that at a given blood pressure MSNA tends to be lower. Key Words: autonomic nervous system Ⅲ baroreflex Ⅲ gender Ⅲ nervous system, sympathetic T he autonomic nervous system influences blood pressure and heart rate through adjustments in parasympathetic and sympathetic activity. Parasympathetic and sympathetic activities are tightly regulated through baroreflex mechanisms. Therefore, baroreflexes have a pivotal role in shortterm cardiovascular regulation and buffer-excessive blood pressure swings. 1,2 Among numerous other variables, baroreflexes are also involved in long-term blood pressure maintenance. [3][4][5] Even when overall blood pressure regulation is functioning properly, the balance between baroreflex regulation of heart rate and vascular tone may be perturbed. Imbalance between sympathetic activation of the heart and the vasculature has been described in heart failure patients, 6 postural tachycardia syndrome patients, 7,8 and in healthy subjects treated with norepinephrine transporter inhibitors. 9,10 Factors influencing baroreflex function may have an important bearing on human cardiovascular disease. Gender may be such a variable. Previous studies suggest that baroreflex blood pressure buffering is less effective in women than in men. 11 The balance between baroreflex-mediated heart rate and muscle sympathetic nerve activity (MSNA) changes may also be influenced by gender. The idea is supported by the observation that resting sympathetic vasomotor tone tends to be decreased in women, 12,13 whereas resting heart rate is increased. 14 -16 Furthermore, with standing, women showed an exaggerated heart rate and an attenuated sympathetic vasomotor response. 17 Moreover, previous studies suggested that baroreflex heart rate regulati...

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Vascular responses to orthostatic stress in patients with postural tachycardia syndrome (POTS), in patients with low orthostatic tolerance, and in asymptomatic controls

Cited by 49 publications

References 15 publications

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

Peripheral vascular function in spinal cord injury: a systematic review

Baroreflex Regulation of Heart Rate and Sympathetic Vasomotor Tone in Women and Men

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