Regulation of Sympathetic Nervous System Function after Cardiovascular Deconditioning

Hasser, Eileen M.; Moffitt, Julia A.

doi:10.1111/j.1749-6632.2001.tb03698.x

Cited by 53 publications

(47 citation statements)

References 49 publications

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“…In addition, hindlimb unloading in rats, which simulates the effect of spaceflight or bed rest (21,36), also produces blunted baroreflex activation of the sympathetic nervous system (14,34). These data are consistent with findings that deficits in peripheral vasoconstriction contribute importantly to orthostatic intolerance observed in susceptible individuals after spaceflight or bed rest (5,31,66).…”

supporting

confidence: 79%

“…The purpose of the current study was to test the hypothesis that exposure to a period of simulated microgravity or bed rest results in attenuated hypotension-induced increases in circulating concentrations of vasopressin and plasma renin activity (PRA). We used the hindlimb-unloaded (HU) rat in the current experiments because it has been shown to mimic responses observed after spaceflight and bed rest (4,21,27,36). To test our hypothesis, we measured plasma levels of vasopressin and PRA in re-…”

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confidence: 99%

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Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats

Mueller¹,

Sullivan²,

Grindstaff³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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. Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats. Am J Physiol Regul Integr Comp Physiol 291: R46 -R52, 2006. First published February 9, 2006 doi:10.1152/ajpregu.00622.2005.-Cardiovascular deconditioning occurs in astronauts after spaceflight or in individuals subjected to bed rest. It is characterized by an increased incidence of orthostatic intolerance. The mechanisms responsible for orthostatic intolerance are likely multifactorial and may include hypovolemia, autonomic dysfunction, and vascular and cardiac alterations. The arterial baroreflex is an important compensatory mechanism in the response to an orthostatic stress. In a previous study, we demonstrated that arterial baroreflex mediated sympathoexcitation was blunted in hindlimb-unloaded (HU) rats, a model of cardiovascular deconditioning. The arterial baroreflex also contributes to the regulation of vasoactive hormones including vasopressin and angiotensin II. In the present study, we tested the hypothesis that the neurohumoral response to hypotension is also attenuated in rats after 14 days of hindlimb unloading. To test this hypothesis, the vasodilator diazoxide (15 or 25 mg/kg) or saline (0.9%) was administered to produce hypotension or control conditions, respectively, in conscious HU and control rats. Plasma samples were collected and assayed for vasopressin and plasma renin activity (PRA). Diazoxide (25 mg/kg) produced significant increases in vasopressin and PRA compared with saline controls. HU rats exhibited significantly higher levels of vasopressin at rest and the increase in vasopressin levels during hypotension was enhanced by hindlimb unloading. Neither resting nor hypotension-induced PRA was altered by hindlimb unloading. These data suggest that although baroreflex-mediated sympathoexcitation is blunted by hindlimb unloading, hypotension-induced vasopressin release is enhanced and hypotension-induced PRA is unaffected. Increased circulating vasopressin may serve to compensate for blunted baroreflex regulation of sympathetic nervous activity produced by hindlimb unloading or may actually contribute to it. neurohumoral control; antidiuretic hormone; renin-angiotensin system ASTRONAUTS RETURNING FROM space, or individuals recovering from prolonged bed rest often experience symptoms of orthostatic intolerance (5,8,16,31,54,65). To delineate the possible mechanisms mediating orthostatic intolerance, individuals have been categorized as presyncopal or nonpresyncopal (17, 31, 66), finishers and nonfinishers (5), or simply, orthostatic tolerant and intolerant (54). No matter what nomenclature is used, the common characteristic among these individuals is an inability to maintain arterial pressure during an orthostatic challenge.Compensations for orthostatic stress include baroreflexmediated increases in heart rate in an attempt to maintain cardiac output, as well as increases in total peripheral resistance to maintain adequate arterial pressure (47). Initially, vasoconstriction is accomplished through a...

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confidence: 79%

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confidence: 99%

Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats

Mueller¹,

Sullivan²,

Grindstaff³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Thus, an increase in blood pressure in vessels above the heart appears to be a consequence of μG, requiring the adaptation of the vascular system [52]. The vascular adaptation to μG likely involves a response of factors known to regulate blood pressure, including: (1) control of plasma volume [37]; (2) modulation of baro-and cardiopulmonary reflexes inducing the decrease of cardiac function [19]; and finally (3) adaptation of intrinsic properties of vascular endothelial and smooth muscle cells (VSMC). We have focused our study on this last factor and used the hindlimb unloaded (HU) rat model as it simulates the biological effects of μG; especially, modulations of vascular reactivity were described in this model [7,28,39,53].…”

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confidence: 99%

Up-regulation of ryanodine receptor expression increases the calcium-induced calcium release and spontaneous calcium signals in cerebral arteries from hindlimb unloaded rats

Morel

Dabertrand

Porte

et al. 2013

Pflugers Arch - Eur J Physiol

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Microgravity induces a redistribution of blood volume. Consequently, astronauts' body pressure is modified so that the upright blood pressure gradient is abolished, thereby inducing a modification in cerebral blood pressure. This effect is mimicked in the hindlimb unloaded rat model. After a duration of 8 days of unloading, Ca 2+ signals activated by depolarization and inositol-1,4,5-trisphosphate intracellular release were increased in cerebral arteries. In the presence of ryanodine and thapsigargin, the depolarization-induced Ca 2+ signals remained increased in hindlimb suspended animals, indicating that Ca 2+ influx and Ca 2+ -induced Ca 2+ release mechanism were both increased. Spontaneous Ca 2+ waves and localized Ca 2+ events were also investigated. Increases in both amplitude and frequency of spontaneous Ca 2+ waves were measured in hindlimb suspension conditions. After pharmacological segregation of Ca 2+ sparks and Ca 2+ sparklets, their kinetic parameters were characterized. Hindlimb suspension induced an increase in the frequencies of both Ca 2+ localized events, suggesting an increase of excitability. Labeling with bodipy compounds suggested that voltage-dependent Ca 2+ channels and ryanodine receptor expressions were increased. Finally, the expression of the ryanodine receptor subtype 1 (RyR1) was increased in hindlimb unloading conditions. Taken together, these results suggest that RyR1 expression and voltage-dependent Ca 2+ channels activity are the focal points of the regulation of Ca 2+ signals activated by vasoconstriction in rat cerebral arteries with an increase of the voltage-dependent Ca 2+ influx.

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“…Male HU rats exhibit a blunted ability to reflexly increase sympathetic nerve activity compared with control rats (34). This effect is likely due to an adaptation within the central nervous system, because aortic baroreceptor afferent sensitivity is not altered by HU (36) and changes in neuronal activation at the rostral ventrolateral medulla are involved (24,35). This alteration in baroreflex control of sympathetic nerve activity in male rats after HU affected both renal and lumbar sympathetic nerve activity (34), suggesting that it may be a generalized effect across sympathetic outputs to different vascular beds.…”

mentioning

confidence: 99%

Hindlimb unloading and female gender attenuate baroreflex-mediated sympathoexcitation

Foley¹,

Mueller²,

Hasser³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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-Exposure to a period of microgravity or bed rest produces several physiological adaptations. These changes, which include an increased incidence of orthostatic intolerance, have an impact when people return to a 1G environment or resume an upright posture. Compared with males, females appear more susceptible to orthostatic intolerance after exposure to real or simulated microgravity. Decreased arterial baroreflex compensation may contribute to orthostatic intolerance. We hypothesized that female rats would exhibit a greater reduction in arterial baroreflex function after hindlimb unloading (HU) compared with male rats. Mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were recorded in conscious animals after 13-15 days of HU. Baseline HR was elevated in female rats, and HU increased HR in both genders. Consistent with previous results in males, baroreflex-mediated activation of RSNA was blunted by HU in both genders. Maximum RSNA in response to decreases in MAP was reduced by HU (male control 513 Ϯ 42%, n ϭ 11; male HU 346 Ϯ 38%, n ϭ 13; female control 359 Ϯ 44%, n ϭ 10; female HU 260 Ϯ 43%, n ϭ 10). Maximum baroreflex increase in RSNA was lower in females compared with males in both control and HU rats. Both female gender and HU attenuated baroreflex-mediated increases in sympathetic activity. The combined effects of HU and gender resulted in reduced baroreflex sympathetic reserve in females compared with males and could contribute to the greater incidence of orthostatic intolerance in females after exposure to spaceflight or bed rest. simulated microgravity; sympathetic nervous system; bed rest; deconditioning; hindlimb unweighting PROLONGED EXPOSURE TO MICROGRAVITY or bed rest results in a series of adaptations and changes including a central shift in body fluids, followed by a reduction in total blood and plasma volume, and muscle atrophy (46). Upon return to a 1G environment or to normal activity, individuals display resting tachycardia, decreased exercise capacity, and increased incidence of orthostatic intolerance (6,17,19). The mechanisms that account for these changes are still unresolved, although cardiac atrophy (39), altered vascular reactivity (17, 32), hypovolemia (47), and altered baroreflex control of sympathetic nerve activity (11, 18, 48) have been suggested, and all potentially contribute. In addition, females appear to be less tolerant of the negative effects of returning from spaceflight or a period of bed rest, because females exhibit a greater incidence of orthostatic intolerance after spaceflight compared with men (23, 48). The mechanisms that account for the greater susceptibility of women to the effects of microgravity and bed rest are unknown.The physiological response to an orthostatic challenge requires several compensatory mechanisms to maintain blood pressure and cerebral perfusion, including baroreflex-mediated increases in heart rate (HR) and vascular resistance (40). The arterial baroreceptor reflex is the primary controller of beat-tobe...

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Regulation of Sympathetic Nervous System Function after Cardiovascular Deconditioning

Cited by 53 publications

References 49 publications

Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats

Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats

Up-regulation of ryanodine receptor expression increases the calcium-induced calcium release and spontaneous calcium signals in cerebral arteries from hindlimb unloaded rats

Hindlimb unloading and female gender attenuate baroreflex-mediated sympathoexcitation

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