Endocrine responses to 7 days of head‐down bed rest and orthostatic tests in men and women

Millet, Catherine; Custaud, Marc‐Antoine; Maillet, A.; Allevard, A. M.; Duvareille, Monique; Gauquelin‐Koch, Guillemette; Gharib, Claude; Fortrat, Jacques‐Olivier

doi:10.1046/j.1365-2281.2001.00315.x

Cited by 38 publications

(42 citation statements)

References 34 publications

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“…Alterations in the regulation of the renin-angiotensin system have been reported previously after spaceflight and bed rest. In fact, most bed rest studies have noted an enhancement of PRA (18,33,55), especially in response to an orthostatic challenge (32,33,64). The reasons for the lack of difference in the present study are unknown but may be due to offsetting effects of hindlimb unloading on different aspects of the regulation of plasma renin, including renin release regulated by renal sympathetic nerves (9).…”

Section: Discussionmentioning

confidence: 51%

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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Section: Discussionmentioning

confidence: 51%

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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“…But at hour 41, when hormonal measurements were done, all volunteers had normal potassium levels. A biphasic pattern of hormonal activation has been observed in head down tilt, another model used to simulate effects of weightlessness (Nixon et al 1979) that produces a transient increase in plasma aldosterone (Millet et al 2001). After the initial fall of plasma aldosterone with water immersion, a subsequent rise might have caused hypokalemia in two of our divers.…”

Section: Discussionmentioning

confidence: 80%

Adrenomedullin and elements of orthostatic competence after 41 h of voluntary submersion in water as measured in four healthy males

et al. 2006

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Four men established a new score (Guinness Book of Records) by staying submersed in thermoneutral water (average diving depth 2.5 m) for 41 h without sleeping. The aim of this study is to measure circulating hormones together with plasma mass density and total protein concentration as indices of plasma volume change to test the hypotheses that (1) blood volume and related hormones are influenced by prolonged water submersion the same way as observed after short-term water immersion, and (2) plasma adrenomedullin levels change in an opposite fashion as with orthostatic stimulation. We also studied effects on cortisol and testosterone levels. Water submersion led to a 19% increase in plasma protein concentration and a 2.5 g/l rise in plasma mass density, corresponding to a 15.6+/-1.1% plasma volume decrease (P=0.00). We therefore individually corrected (c) the observed post-submersion hormone values for plasma volume contraction. Based on this correction, we found a rise of plasma adrenomedullin from 7.9+/-0.9 to 12.5(c)+/-2.3 pg/ml. Aldosterone rose from 123+/-14 to 186(c)+/-24 ng/ml (P=0.029); plasma renin activity increased in all four persons but the type I error was >0.05. Plasma testosterone decreased from 3.5+/-0.4 to 2.2(c)+/-0.6 ng/ml (P=0.009) while plasma cortisol stayed unchanged. The daily salivary cortisol rhythm was preserved. We conclude that long-term water submersion has endocrine as well as plasma volume effects that are opposite to those seen after short-term immersion, and which increases plasma adrenomedullin. Circadian cortisol rhythm seems to be conserved even under extreme circumstances as those of this study.

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“…In addition to being a direct vasoconstrictor, angiotensin II increases norepinephrine release from adrenergic nerve terminals and augments the postsynaptic response (29, 30a). Plasma renin activity (PRA) normally increases in response to an orthostatic challenge (12,26,27,41), but this response may be attenuated in some POTS patients (18,21). Jacob et al (18) observed that a subgroup of POTS patients had significantly decreased supine and standing PRA compared with healthy subjects.…”

Section: Discussionmentioning

confidence: 99%

Baroreflex control of muscle sympathetic nerve activity in postural orthostatic tachycardia syndrome

Swift

Charkoudian

Dotson³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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-Postural orthostatic tachycardia syndrome (POTS) is characterized by excessive tachycardia during orthostasis. To test the hypothesis that patients with POTS have decreased sympathetic neural responses to baroreflex stimuli, we measured heart rate (HR) and muscle sympathetic nerve activity (MSNA) responses to three baroreflex stimuli including vasoactive drug boluses (modified Oxford technique), Valsalva maneuver, and head-up tilt (HUT) in POTS patients and healthy control subjects. The MSNA response to the Valsalva maneuver was significantly greater in the POTS group (controls, 26 Ϯ 7 vs. POTS, 48 Ϯ 6% of baseline MSNA/mmHg; P ϭ 0.03). POTS patients also had an exaggerated MSNA response to 30°HUT (controls, 123 Ϯ 24 vs. POTS, 208 Ϯ 30% of baseline MSNA; P ϭ 0.03) and tended to have an exaggerated response to 45°HUT (controls, 137 Ϯ 27 vs. POTS, 248 Ϯ 58% of baseline MSNA; P ϭ 0.10). Sympathetic baroreflex sensitivity calculated during administration of the vasoactive drug boluses also tended to be greater in the POTS patients; however, this did not reach statistical significance (P ϭ 0.15). Baseline MSNA values during supine rest were not different between the groups (controls, 23 Ϯ 4 vs. POTS, 16 Ϯ 5 bursts/100 heartbeats; P ϭ 0.30); however, resting HR was significantly higher in the POTS group (controls, 58 Ϯ 3 vs. POTS, 82 Ϯ 4 beats/min; P ϭ 0.0001). Our results suggest that POTS patients have exaggerated MSNA responses to baroreflex challenges compared with healthy control subjects, although resting supine MSNA values did not differ between the groups. intolerance; blood pressure; heart rate; Valsalva maneuver; head-up tilt POSTURAL ORTHOSTATIC TACHYCARDIA syndrome (POTS) is a chronic, potentially debilitating condition that often occurs in otherwise healthy individuals who are most often young women. Patients with this condition (also known as idiopathic orthostatic intolerance) exhibit excessive tachycardia [increase in heart rate (HR) of Ͼ30 beats/min] during head-up tilt (HUT) in the absence of significant orthostatic hypotension. They also develop dizziness, fatigue, headache, and/or anxiety with standing or HUT (24,34). Although POTS has become better recognized clinically in recent years, the mechanisms underlying the pathophysiology of this condition remain unclear.In humans, normal baroreflex physiology involves increased HR, increased vascular sympathetic nerve activity, and peripheral vasoconstriction in response to decreased venous return during upright posture (31). These normal responses result in maintenance of arterial pressure with the upright posture and an absence of symptoms such as those reported by POTS patients. It is not clear whether the excessive tachycardia with orthostasis in POTS patients is the cause or the consequence of one or more abnormal steps in the baroreflex pathway. For example, evidence is conflicting regarding baroreflex control of HR in patients with orthostatic intolerance. Some researchers have reported decreased sensitivity of baroreflex control of HR in these ...

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Endocrine responses to 7 days of head‐down bed rest and orthostatic tests in men and women

Cited by 38 publications

References 34 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

Adrenomedullin and elements of orthostatic competence after 41 h of voluntary submersion in water as measured in four healthy males

Baroreflex control of muscle sympathetic nerve activity in postural orthostatic tachycardia syndrome

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