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

Bechtold, Andrea G.; Scheuer, Deborah A.

doi:10.1152/ajpregu.00345.2005

Cited by 22 publications

(31 citation statements)

References 57 publications

(105 reference statements)

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“…These studies indicated that higher doses of Cort administered intracerebroventricularly produce small increases in baseline arterial pressure, whereas low doses were without effect. 26 -28 We reported previously that DHB Cort pellets increased baseline arterial pressure by 5 to 6 mm Hg after 4 days of treatment, 7,15 although in the present study there were no differences in baseline arterial pressure between groups. This was not because of a difference in duration of DHB Cort treatment, because baseline arterial pressures in rats treated with DHB Cort for 4 days (105Ϯ4 mm Hg, nϭ8) or 6 days (104Ϯ3 mm Hg, nϭ7) were not different.…”

Section: Effect Of Cort On Baseline Arterial Pressurementioning

confidence: 47%

“…In a recent study, we reported that DHB Cort treatment attenuated the gain and increased the midpoint of the arterial baroreceptor reflex. 7 Thus, it is possible that attenuation in baroreflex control of sympathetic nerve activity contributed to the effect of DHB Cort to enhance the arterial pressure response to stress observed in this study. However, if there was enhanced activation of the sympathetic nervous system, it was not universal, because the heart rate response to stress was not elevated in the DHB Cort rats.…”

Section: Mechanism Of Cort Actionmentioning

confidence: 77%

“…15 This method increases Cort levels locally in DHB areas without altering plasma Cort concentration in adrenalintact rats. 7,15 We now have shown in adrenalectomized animals that the systemic spillover of Cort from the DHB pellet is both minimal and independent of the site of pellet implantation. Thus, the systemic pellet implantation serves as an adequate control for any systemic effect of the exogenous Cort.…”

Section: Mechanism Of Cort Actionmentioning

confidence: 83%

“…7 These alterations in baroreflex function could promote the enhanced stress responses observed with elevated systemic Cort. 8,9 The DHB includes the nucleus of the solitary tract (NTS), an important cardiovascular regulatory site in the central nervous system.…”

mentioning

confidence: 99%

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Chronic Activation of Dorsal Hindbrain Corticosteroid Receptors Augments the Arterial Pressure Response to Acute Stress

Scheuer

Bechtold²,

Vernon³

2007

Hypertension

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Abstract-Augmented cardiovascular responses to acute stress can predict cardiovascular disease in humans. Chronic systemic increases in glucocorticoids produce enhanced cardiovascular responses to psychological stress; however, the site of action is unknown. Recent evidence indicates that glucocorticoids can act within the dorsal hindbrain to modulate cardiovascular function. Therefore, we tested the hypothesis that the endogenous glucocorticoid corticosterone can act in the dorsal hindbrain to enhance cardiovascular responses to restraint stress in conscious rats. Adrenal-intact animals with indwelling arterial catheters were treated for 4 or 6 days with 3-to 4-mg pellets of corticosterone or silastic (sham pellets) implanted on the dorsal hindbrain surface. Corticosterone pellets were also implanted either on the surface of the dura or subcutaneously to control for the systemic effects of corticosterone (systemic corticosterone). The integrated increase in arterial pressure during 1 hour of restraint stress was significantly (PϽ0.05) greater in dorsal hindbrain corticosterone (912Ϯ98 mm Hg per 60 minutes) relative to dorsal hindbrain sham (589Ϯ57 mm Hg per 60 minutes) or systemic corticosterone (592Ϯ122 mm Hg per 60 minutes) rats. The plasma glucose response after 10 minutes of stress was also significantly higher in dorsal hindbrain corticosterone-treated rats relative to both other groups. There were no significant between-group differences in the heart rate or corticosterone responses to stress. There were no differences in baseline values for any measured parameters. We conclude that corticosterone can act selectively in the dorsal hindbrain in rats with normal plasma corticosterone levels to augment the arterial pressure response to restraint stress. Key Words: glucocorticoids Ⅲ hypertension Ⅲ brain Ⅲ autonomic nervous system Ⅲ sympathetic nervous system Ⅲ nucleus of the solitary tract C hronic elevations in glucocorticoids increase cardiovascular disease risk. 1-3 Recent evidence suggests that glucocorticoid-mediated changes in neuroendocrine control of cardiovascular function could contribute to these adverse actions of glucocorticoids. For example, glucocorticoids reduce the sensitivity and increase the midpoint of the arterial baroreceptor reflex; similar changes in baroreflex function are positively associated with increased cardiovascular disease risk. 4 -7 Other studies have demonstrated that chronic systemic elevations in glucocorticoids increase the arterial pressure or norepinephrine response to acute stress. 8,9 Similar enhanced stress responses in humans have also been linked to increased cardiovascular disease risk. 10 However, the sites of action for stimulatory effects of glucocorticoids on cardiovascular function remain unknown.We demonstrated recently that, analogous to systemic increases in glucocorticoids, chronic treatment of the dorsal hindbrain (DHB) with the endogenous glucocorticoid corticosterone (Cort) attenuated the gain and increased the midpoint of baroreflex control of heart...

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Section: Effect Of Cort On Baseline Arterial Pressurementioning

confidence: 47%

Section: Mechanism Of Cort Actionmentioning

confidence: 77%

Section: Mechanism Of Cort Actionmentioning

confidence: 83%

mentioning

confidence: 99%

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Chronic Activation of Dorsal Hindbrain Corticosteroid Receptors Augments the Arterial Pressure Response to Acute Stress

Scheuer

Bechtold²,

Vernon³

2007

Hypertension

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“…18 Glucocorticoids also act within the brain to regulate the baroreflex function and thereby influence sympathetic tone. 19 The mineralocorticoid receptor could also have contributed to hypertension in our patient. In cases of cortisol excess, the main agonist of the receptor may be cortisol rather than aldosterone.…”

Section: How Do Acth and Glucocorticoidsmentioning

confidence: 70%

Cushing’s Disease, Hypertension, and Other Sequels

Singer

Strohm²,

Göbel³

et al. 2008

Hypertension

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Hypothalamic‐Pituitary‐Adrenal Axis—Feedback Control

Keller‐Wood

2015

Comprehensive Physiology

109

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The hypothalamo-pituitary-adrenal axis (HPA) is responsible for stimulation of adrenal corticosteroids in response to stress. Negative feedback control by corticosteroids limits pituitary secretion of corticotropin, ACTH, and hypothalamic secretion of corticotropin-releasing hormone, CRH, and vasopressin, AVP, resulting in regulation of both basal and stress-induced ACTH secretion. The negative feedback effect of corticosteroids occurs by action of corticosteroids at mineralocorticoid receptors (MR) and/or glucocorticoid receptors (GRs) located in multiple sites in the brain and in the pituitary. The mechanisms of negative feedback vary according to the receptor type and location within the brain-hypothalmo-pituitary axis. A very rapid nongenomic action has been demonstrated for GR action on CRH neurons in the hypothalamus, and somewhat slower nongenomic effects are observed in the pituitary or other brain sites mediated by GR and/or MR. Corticosteroids also have genomic actions, including repression of the pro-opiomelanocortin (POMC) gene in the pituitary and CRH and AVP genes in the hypothalamus. The rapid effect inhibits stimulated secretion, but requires a rapidly rising corticosteroid concentration. The more delayed inhibitory effect on stimulated secretion is dependent on the intensity of the stimulus and the magnitude of the corticosteroid feedback signal, but also the neuroanatomical pathways responsible for activating the HPA. The pathways for activation of some stressors may partially bypass hypothalamic feedback sites at the CRH neuron, whereas others may not involve forebrain sites; therefore, some physiological stressors may override or bypass negative feedback, and other psychological stressors may facilitate responses to subsequent stress.

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

Cited by 22 publications

References 57 publications

Chronic Activation of Dorsal Hindbrain Corticosteroid Receptors Augments the Arterial Pressure Response to Acute Stress

Chronic Activation of Dorsal Hindbrain Corticosteroid Receptors Augments the Arterial Pressure Response to Acute Stress

Cushing’s Disease, Hypertension, and Other Sequels

Hypothalamic‐Pituitary‐Adrenal Axis—Feedback Control

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