Rapid resetting of human baroreflex working range: insights from sympathetic recordings during acute hypoglycaemia.

Fagius, Jan; Berne, Christian

doi:10.1113/jphysiol.1991.sp018784

Cited by 11 publications

(6 citation statements)

References 34 publications

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“…For example: 1) transient blockade of peripheral chemoreceptors with hyperoxia temporarily increases baroreflex sensitivity in heart failure patients 2 , 2) unilateral carotid body resection in a human heart failure patient resulted in an improvement in baroreflex sensitivity 24 , 3) activation of the peripheral chemoreceptors with hypoxia decreases baroreflex sensitivity 4 . In addition, previous studies have shown antecedent hypoglycemia to reduce baroreflex sensitivity 25 and reset the baroreflex working range 26 . Our lab has recently shown the baroreflex working range is reset to higher heart rates such that systolic blood pressure is relatively maintained during hypoglycemia 5 .…”

Section: Discussionmentioning

confidence: 97%

Effect of Bilateral Carotid Body Resection on Cardiac Baroreflex Control of Blood Pressure During Hypoglycemia

et al. 2015

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Hypoglycemia results in a reduction in cardiac baroreflex sensitivity and a shift in the baroreflex working range to higher heart rates. This effect is mediated in part by the carotid chemoreceptors. Therefore, we hypothesized hypoglycemia-mediated changes in baroreflex control of heart rate would be blunted in carotid body resected patients when compared with healthy controls. Five patients with bilateral carotid body resection for glomus tumors and ten healthy controls completed a 180-minute hyperinsulinemic, hypoglycemic (~3.3 mmol.L−1) clamp. Changes in heart rate, blood pressure, and spontaneous cardiac baroreflex sensitivity were assessed. Baseline baroreflex sensitivity was not different between groups (p>0.05). Hypoglycemia resulted in a reduction in baroreflex sensitivity in both groups (Main effect of time, p<0.01) and responses were lower in resected patients when compared with controls (Main effect of group, p<0.05). Hypoglycemia resulted in large reductions in systolic (−17±7 mmHg) and mean (−14±5 mmHg) blood pressure in resected patients that were not observed in controls (Interaction of group and time, p<0.05). Despite lower blood pressures, increases in heart rate with hypoglycemia were blunted in resected patients (Interaction of group and time, p<0.01). Major novel findings from this study demonstrate that intact carotid chemoreceptors are essential for increasing heart rate and maintaining arterial blood pressure during hypoglycemia in humans. These data support a contribution of the carotid chemoreceptors to blood pressure control and highlight the potential widespread effects of carotid body resection in humans.

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Section: Discussionmentioning

confidence: 97%

Effect of Bilateral Carotid Body Resection on Cardiac Baroreflex Control of Blood Pressure During Hypoglycemia

et al. 2015

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“…Systolic blood pressure was lower in the E2 group versus the male subjects, and mean arterial pressure responses were lower in both groups of women compared with the male subjects. The baroreflex is reset with hypoglycemia (42), and although unknown, it is possible that sex further impacts the normal baroreflex response to hypoglycemia. Alternatively, men have been found to have greater responsiveness to epinephrineinduced changes in blood pressure (41) and norepinephrine-induced vasoconstriction (43), suggesting that men may simply be more sensitive to catecholamine-induced changes in blood pressure.…”

Section: Figmentioning

confidence: 99%

Estrogen Blunts Neuroendocrine and Metabolic Responses to Hypoglycemia

et al. 2003

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This study tested the hypothesis that estrogen is the mechanism responsible for the sexual dimorphism present in the neuroendocrine and metabolic responses to hypoglycemia. Postmenopausal women receiving (E2; n ‫؍‬ 8) or not receiving (NO E2; n ‫؍‬ 9) estrogen replacement were compared with age-and BMI-matched male subjects (n ‫؍‬ 8) during a single-step 2-h hyperinsulinemic-hypoglycemic clamp. Plasma insulin (599 ؎ 28 pmol/l) and glucose (2.9 ؎ 0.03 mmol/l) levels were similar among all groups during the glucose clamp. In response to hypoglycemia, epinephrine (2.8 ؎ 0.6 vs. 5.8 ؎ 0.8 and 4.4 ؎ 0.5 nmol/l), glucagon (57 ؎ 8 vs. 77 ؎ 8 and 126 ؎ 18 ng/l), and endogenous glucose production (2 ؎ 2 vs. 10 ؎ 2 and 6 ؎ 3 mol ⅐ kg ؊1 ⅐ min ؊1 ) were significantly lower in E2 vs. both NO E2 and male subjects (P < 0.05). These reduced counterregulatory responses resulted in significantly greater glucose infusion rates (16 ؎ 2 vs. 6 ؎ 2 and 6 ؎ 3 mol ⅐ kg ؊1 ⅐ min ؊1 ; P < 0.01) in E2 vs. both NO E2 and male subjects. Pancreatic polypeptide was significantly lower (P < 0.05) in both the E2 and NO E2 groups compared with the male subjects (136 ؎ 20 and 136 ؎ 23 vs. 194 ؎ 16 pmol/l). Last, glycerol (36 ؎ 3 vs. 47 ؎ 5 mol/l; P < 0.05), lactate (1.4 ؎ 0.1 vs. 1.8 ؎ 0.2 mmol/l; P < 0.05), and muscle sympathetic nerve activity (19 ؎ 4 to 27 ؎ 4 vs. 27 ؎ 5 to 42 ؎ 6 bursts/min; P < 0.05) responses to hypoglycemia were all significantly lower in E2 vs. NO E2 subjects. We conclude that estrogen appears to play a major role in the sexual dimorphism present in counterregulatory responses to hypoglycemia in healthy humans. Diabetes 52:1749 -1755, 2003 M en and women respond differently to an acute bout of hypoglycemia. We have previously shown that healthy and type 1 diabetic women, compared with men, have lower catecholamine, glucagon, cortisol, growth hormone, endogenous glucose production (EGP), and lactate responses, and they have increased glycerol responses to hypoglycemia (1,2). This sexual dimorphism also appears to be present in a wide variety of physiological stresses. For example, women have been found to have reduced neuroendocrine and increased lipolytic responses to exercise (3-5) and reduced sympathetic nervous system responses to cognitive stress (6).The physiological mechanism(s) responsible for sexually dimorphic responses to stress in humans remains unknown, although it seems likely that one or more of the reproductive hormones may be responsible. Animal studies suggest that estrogen may play an important role. Estrogen administration has been shown to independently reduce catecholamine levels, either by increasing norepinephrine degradation in the brain (and thereby reducing sympathetic system drive) (7) or by decreasing secretion from the adrenal medulla (8,9). Metabolically, estrogen has been found to increase lipolysis (10), glycogen deposition (11), and glucose uptake during exercise in rats (10). Recent studies in mice even suggest that estrogen, specifically estrone sulfate, may have a direct effect on reduc...

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“…there is a rise in pulse pressure; Hilsted et al 1984). With a detailed study of the beat‐to‐beat relationship between MSNA and diastolic blood pressure, we could demonstrate an acute resetting of the arterial (high pressure) baroreflex working range during hypoglycaemia and subsequent glucose counter‐regulation (Fagius & Berne 1991). The blood pressure levels at which bursts of MSNA occurred were altered but the baroreflex sensitivity remained unchanged.…”

Section: Muscle Sympathetic Nerve Activitymentioning

confidence: 99%

Sympathetic nerve activity in metabolic control – some basic concepts

Fagius

2003

Acta Physiologica Scandinavica

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A role for the sympathetic nervous system in hypertension has been looked for in relation to the 'metabolic syndrome' with associations between body weight, insulin sensitivity and hypertension. By use of microneurography human sympathetic responses to hypoglycaemia, normoglycaemic hyperinsulinaemia and food intake have been studied. A strong but differentiated influence of insulin-induced hypoglycaemia comprises increase in muscle sympathetic nerve activity (MSNA) and the sudomotor part of skin sympathetic nerve activity (SSNA), whereas vasoconstrictor SSNA is inhibited. Responses to infusion of 2-deoxy-D-glucose are identical, suggesting central nervous system glucopenia and not insulin to be the causative factor. Insulin infusion during normoglycaemia evokes a moderate increase in MSNA; SSNA and blood pressure does not change. After glucose ingestion MSNA displays a sustained increase, which is only partly elicited by insulin. A significant albeit weaker increase occurs after pure protein or fat meals, and after glucose ingestion in C-peptide-negative diabetic patients, with no insulin secretion. In healthy elderly people the MSNA response to food intake is weak, because of a high outflow already at rest; this is suggested to explain postprandial hypotension in the elderly, a paradoxical mechanism behind clinical autonomic failure. A pathophysiological role of MSNA in the metabolic syndrome with hypertension has been speculated. An association between obesity and elevated level of MSNA at rest is established; observed relationships to chronic insulin levels and hypertension are less unanimous. The adipose tissue regulating hormone leptin has become one focus of interest in ongoing attempts to elucidate a possible role of the human sympathetic nervous system in the 'metabolic syndrome' and hypertension.

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Rapid resetting of human baroreflex working range: insights from sympathetic recordings during acute hypoglycaemia.

Cited by 11 publications

References 34 publications

Effect of Bilateral Carotid Body Resection on Cardiac Baroreflex Control of Blood Pressure During Hypoglycemia

Effect of Bilateral Carotid Body Resection on Cardiac Baroreflex Control of Blood Pressure During Hypoglycemia

Estrogen Blunts Neuroendocrine and Metabolic Responses to Hypoglycemia

Sympathetic nerve activity in metabolic control – some basic concepts

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