Effects of fetal ovine adrenalectomy on sympathetic  and baroreflex responses at birth

Segar, Jeffrey L.; Natta, Timothy Van; Fg, Smith

doi:10.1152/ajpregu.00056.2002

Cited by 13 publications

(13 citation statements)

References 37 publications

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“…Previous studies from this and other laboratories have demonstrated that systemic glucocorticoid administration can increase the arterial pressure midpoint and decrease the gain of baroreflex control of heart rate and renal sympathetic nerve activity (37,40,(42)(43)(44). However, the sites of action of Cort to modulate baroreflex function have not been determined.…”

Section: Discussionmentioning

confidence: 91%

“…Many of these risk factors are also associated with dysregulation of autonomic function (2, 14, 36). However, the mechanisms by which glucocorticoids modulate arterial pressure regulation, particularly with respect to the effects of glucocorticoids on central pathways controlling autonomic function, remain poorly understood.Studies in animals indicate that systemic elevations in glucocorticoids can modulate the function of the arterial baroreceptor reflex (12,37,40,(42)(43)(44). The arterial baroreceptor reflex is an autonomic reflex that is important for the shortterm, and possibly long-term, regulation of arterial pressure (3,29,32,50).…”

mentioning

confidence: 99%

“…Studies from our laboratory have demonstrated that systemic administration of corticosterone (Cort) modulates baroreflex control of both renal sympathetic nerve activity and heart rate to increase the arterial pressure midpoint and decreases the reflex gain independent of changes in arterial pressure in rats (37,40). Studies from Segar et al (42)(43)(44) demonstrate that glucocorticoids increase the midpoint and reduce the gain of the arterial baroreflex during the perinatal period. These results support the hypothesis that glucocorticoids actively modulate the baroreceptor reflex, suggesting one mechanism by which glucocorticoids may contribute to the development of cardiovascular disease.…”

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confidence: 99%

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Glucocorticoids act in the dorsal hindbrain to modulate baroreflex control of heart rate

Bechtold¹,

Scheuer²

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Bechtold, Andrea G., and Deborah A. Scheuer. Glucocorticoids act in the dorsal hindbrain to modulate baroreflex control of heart rate. Am J Physiol Regul Integr Comp Physiol 290: R1003-R1011, 2006. First published November 3, 2005 doi:10.1152/ajpregu.00345.2005.-Systemic corticosterone (Cort) modulates arterial baroreflex control of both heart rate and renal sympathetic nerve activity. Because baroreceptor afferents terminate in the dorsal hindbrain (DHB), an area with dense corticosteroid receptor expression, we tested the hypothesis that prolonged activation of DHB Cort receptors increases the midpoint and reduces the gain of arterial baroreflex control of heart rate in conscious rats. Small (3-4 mg) pellets of Cort (DHB Cort) or Silastic (DHB Sham) were placed on the surface of the DHB, or Cort was administered systemically by placing a Cort pellet on the surface of the dura (Dura Cort). Baroreflex control of heart rate was determined in conscious male Sprague Dawley rats on each of 4 days after initiation of treatment. Plots of arterial pressure vs. heart rate were analyzed using a four-parameter logistic function. After 3 days of treatment, the arterial pressure midpoint for baroreflex control of heart rate was increased in DHB Cort rats (123 Ϯ 2 mmHg) relative to both DHB Sham (108 Ϯ 3 mmHg) and Dura Cort rats (109 Ϯ 2 mmHg, P Ͻ 0.05). On day 4, baseline arterial pressure was greater in DHB Cort (112 Ϯ 2 mmHg) compared with DHB Sham (105 Ϯ 2 mmHg) and Dura Cort animals (106 Ϯ 2 mmHg, P Ͻ 0.05), and the arterial pressure midpoint was significantly greater than mean arterial pressure in the DHB Cort group only. Also on day 4, maximum baroreflex gain was reduced in DHB Cort (2.72 Ϯ 0.12 beats ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ) relative to DHB Sham and Dura Cort rats (3.51 Ϯ 0.28 and 3.37 Ϯ 0.27 beats ⅐ min Ϫ1 ⅐ mmHg Ϫ1 , P Ͻ 0.05). We conclude that Cort acts in the DHB to increase the midpoint and reduce the gain of the heart rate baroreflex function. corticosterone; nucleus of the solitary tract; glucocorticoid receptors; brain; stress ELEVATED GLUCOCORTICOIDS INCREASE the risk for cardiovascular disease (13,20,46,58,59). Accumulating evidence further indicates that altered glucocorticoid activity or sensitivity, even in the absence of elevated plasma glucocorticoid levels, may play a role in the etiology of human essential hypertension, a primary risk factor for cardiovascular disease (27,47,56,57). Altered glucocorticoid activity has also been implicated in the pathogenesis of metabolic syndrome, a condition whose symptoms include obesity, elevated blood pressure, and insulin resistance or diabetes (55). Genetic factors appear to increase sensitivity to the adverse cardiovascular effects of glucocorticoids, since several recently identified polymorphisms of the human glucocorticoid receptor (GR) gene have been linked to hypertension and cardiovascular disease (25,26,34,35). Complementing the data from humans, a glucocorticoid-dependent mechanism of hypertension has been demonstrated in several rat strains, including s...

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Section: Discussionmentioning

confidence: 91%

mentioning

confidence: 99%

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confidence: 99%

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Glucocorticoids act in the dorsal hindbrain to modulate baroreflex control of heart rate

Bechtold¹,

Scheuer²

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…It is not known whether insulin secretion was altered in the present study. It is possible that betamethasone treatment prematurely developed sympathetic suppression of insulin secretion, since previous studies have shown that glucocorticoids have a maturational effect on the sympathetic response at birth (Segar et al 1998(Segar et al , 2001(Segar et al , 2002. We have previously shown, however, that offspring treated with prenatal glucocorticoids exhibit exaggerated insulin responses to a glucose bolus at 1 year of postnatal age, rather than inhibited insulin secretion (Moss et al 2001).…”

Section: Discussionmentioning

confidence: 93%

Repeated maternal glucocorticoid administration and the developing liver in fetal sheep

Sloboda¹,

Newnham²,

Challis³

2002

Journal of Endocrinology

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Prenatal glucocorticoid exposure has been associated with a reduction in birth weight and postnatal alterations in glucose homeostasis and hypothalamic-pituitary-adrenal (HPA) axis function. The mechanisms underlying these responses are unknown, although changes in fetal hepatic development may play an important role. The fetal liver produces key regulators of fuel metabolism and of the developing HPA axis that are altered by glucocorticoids. The local availability of glucocorticoids is regulated, in part, by corticosteroid-binding protein (CBG), glucocorticoid receptors (GR) and by the enzyme 11 -hydroxysteroid dehydrogenase (11 HSD), but the effects of maternal glucocorticoid administration on the expression of these genes in the fetal liver are unknown. 11 HSD1 is the predominant form of this enzyme present in the liver and is responsible for the conversion of cortisone to cortisol. To determine if prenatal glucocorticoid exposure alters fetal hepatic regulation of CBG, 11 HSD1 and GRs, we treated pregnant ewes with betamethasone (0·5 mg/kg) intramuscularly at 104, 111 and 118 days of gestation (term 150 days). Animals were killed at 125 or 146 days of gestation. Maternal betamethasone administration did not alter mean cord plasma glucose but significantly decreased cord plasma insulin levels (P<0·05) at 125 days of gestation. At 146 days of gestation, cord plasma glucose levels were significantly increased without alterations in insulin levels following maternal betamethasone treatment (P<0·05). Maternal betamethasone administration resulted in a significant increase in fetal hepatic 11 HSD1 mRNA and protein levels at 125 days of gestation (P<0·05). CBG mRNA levels were significantly elevated over control at 125 days although levels of CBG protein were not significantly different. GR protein levels were not statistically different at either 125 or 146 days of gestation following glucocorticoid administration. These data suggest that prenatal betamethasone exposure in the ovine fetus results in alterations in cord glucose and insulin levels as well as alterations in hepatic 11 HSD1 mRNA and protein expression. These changes in 11 HSD1 increase the potential to generate local cortisol from circulating cortisone. We speculate that this could affect expression of glucocorticoid-dependent hepatic enzymes involved with the regulation of glucose production and HPA responsiveness.

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“…In general, stressors can elicit responses from both the SAM and hypothalamic pituitary adrenal (HPA) axes. Animal studies also have demonstrated that ACTH and glucocorticoids contribute to cardiovascular regulation through modulation of the baroreceptor sensitivity and sympathetic activity (26,27). Effects for the HPA axis are usually quantified by differences in subjects' salivary cortisol levels before and after exposure to stressors.…”

Section: Discussionmentioning

confidence: 99%

Autonomic Alterations in Cocaine-Exposed Neonates Following Orthostatic Stress

et al. 2007

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ABSTRACT:We investigated the effects of prenatal cocaine exposure (PCE) on heart rate (HR) and heart rate variability (HRV) in the presence of orthostatic stress among near-and full-term neonates. PCE infants (n ϭ 21) and controls (n ϭ 23) were enrolled within 120 h of birth. ECG was recorded for an hour during quiet sleep, 30 min in supine position and then 30 min in an inclined position. Linear mixed models were used to analyze HR and HRV in the time domain and wavelet and power spectrum analyses in the frequency domain. PCE infants had tachycardia both before (p ϭ 0.091) and after tilting (p ϭ 0.015), but with a clear interaction between PCE and orthostatic stress (p ϭ 0.049). Compared with controls, PCE infants had a delayed and prolonged reaction to orthostatic stress. There was also a pronounced interaction with regard to log-transformed SDDRR, a measure of HRV (p ϭ 0.049). Controls experienced an instantaneous increase in log (SDDRR) followed by a prompt return to normal levels, while PCE infants had a gradual increase that did not dissipate quickly. Frequency-domain analyses also distinguished between the cocaine-exposed infants and the controls. Results suggest that the effects of PCE on the development of sympathetic and parasympathetic systems could lead to altered cardiovascular function. H eart rate (HR) and heart rate variability (HRV) are increasingly used to detect a variety of pathophysiologic alterations in the autonomic nervous system (ANS) regulation of cardiac control mechanisms (1). Infants who succumb to sudden infant death syndrome have higher HR and reduced HRV compared with other infants; one speculation is that autonomic disturbances may lead to cardiac instability or may indicate ANS alterations with the potential to affect other vital functions (2). Moreover, the circadian range of HR and certain quantities related to blood pressure (BP) are predictors of neonatal cardiovascular events (3). Hence, power spectrum analysis (PSA) of HRV has been used to assess fetal viability and maturity of the ANS (4,5).Cocaine use by pregnant women has continued to be a prevalent public health problem. Prenatal cocaine exposure (PCE) may lead to abruptio placentae, premature delivery, intrauterine growth restriction, congenital malformations, and fetal death (6 -8). However, controversy exists regarding the influences of PCE on the ANS control mechanism and on neonatal cardiovascular function. Some studies (9 -11), have found elevated HR and reduced HRV in infants with PCE. On the other hand, Regalado et al. (12) found reduced HR and increased HRV following PCE, while another study focusing on the nonlinear dynamics of HRV (13) found no significant differences between PCE infants and controls in spectral power distribution, approximate entropy, correlation dimension, or nonlinear predictability. Spectral analyses in particular have not yielded a consensus about the nature of PCEinduced autonomic alterations. Higher HRV was attributed to increased spectral power across all frequency bands in quiet sl...

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Effects of fetal ovine adrenalectomy on sympathetic and baroreflex responses at birth

Cited by 13 publications

References 37 publications

Glucocorticoids act in the dorsal hindbrain to modulate baroreflex control of heart rate

Glucocorticoids act in the dorsal hindbrain to modulate baroreflex control of heart rate

Repeated maternal glucocorticoid administration and the developing liver in fetal sheep

Autonomic Alterations in Cocaine-Exposed Neonates Following Orthostatic Stress

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