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Mineralocorticoid receptor activation contributes to the supine hypertension of autonomic failure

Primary autonomic failure is characterized by disabling orthostatic hypotension, but at least half of these patients have paradoxical supine hypertension. Renin-angiotensin mechanisms were not initially thought to contribute to this hypertension because plasma renin activity is often undetectable in... Full description

Journal Title: Hypertension (Dallas Tex. 1979), 2016-02, Vol.67 (2), p.424-429
Main Author: Arnold, Amy C
Other Authors: Okamoto, Luis E , Gamboa, Alfredo , Black, Bonnie K , Raj, Satish R , Elijovich, Fernando , Robertson, David , Shibao, Cyndya A , Biaggioni, Italo
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: United States
ID: ISSN: 0194-911X
Link: https://www.ncbi.nlm.nih.gov/pubmed/26644241
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recordid: cdi_proquest_miscellaneous_1760859754
title: Mineralocorticoid receptor activation contributes to the supine hypertension of autonomic failure
format: Article
creator:
  • Arnold, Amy C
  • Okamoto, Luis E
  • Gamboa, Alfredo
  • Black, Bonnie K
  • Raj, Satish R
  • Elijovich, Fernando
  • Robertson, David
  • Shibao, Cyndya A
  • Biaggioni, Italo
subjects:
  • Administration, Oral
  • Aged
  • Autonomic Nervous System - drug effects
  • Autonomic Nervous System - physiopathology
  • Blood Pressure - drug effects
  • Blood Pressure - physiology
  • Blood Pressure Determination
  • Cross-Over Studies
  • Dose-Response Relationship, Drug
  • Double-Blind Method
  • Female
  • Follow-Up Studies
  • Humans
  • Hypertension - drug therapy
  • Hypertension - etiology
  • Hypertension - physiopathology
  • Male
  • Middle Aged
  • Mineralocorticoid Receptor Antagonists - administration & dosage
  • Pure Autonomic Failure - complications
  • Pure Autonomic Failure - drug therapy
  • Pure Autonomic Failure - physiopathology
  • Spironolactone - administration & dosage
  • Spironolactone - analogs & derivatives
  • Supine Position - physiology
  • Treatment Outcome
ispartof: Hypertension (Dallas, Tex. 1979), 2016-02, Vol.67 (2), p.424-429
description: Primary autonomic failure is characterized by disabling orthostatic hypotension, but at least half of these patients have paradoxical supine hypertension. Renin-angiotensin mechanisms were not initially thought to contribute to this hypertension because plasma renin activity is often undetectable in autonomic failure. Plasma aldosterone levels are normal, however, and we recently showed that plasma angiotensin II is elevated and acts at AT1 (angiotensin type 1) receptors to contribute to hypertension in these patients. Because aldosterone and angiotensin II can also bind mineralocorticoid receptors to elevate blood pressure, we hypothesized that mineralocorticoid receptor activation plays a role in the hypertension of autonomic failure. To test this hypothesis, we determined the acute effects of the mineralocorticoid receptor antagonist eplerenone (50 mg, oral) versus placebo on supine blood pressure in a randomized, double-blind, crossover study. Medications were given at 8:00 pm with blood pressure recorded every 2 hours for 12 hours. Ten primary autonomic failure patients with supine hypertension completed this study (7 pure autonomic failure, 2 multiple system atrophy, 1 parkinson's disease; 7 male; 70±2 years of age). Eplerenone maximally reduced supine systolic blood pressure by 32±6 mm Hg at 8 hours after administration (versus 8±10 mm Hg placebo, P=0.016), with no effect on nocturia (12-hour urine volume: 985±134 mL placebo versus 931±94 mL eplerenone, P=0.492; nocturnal weight loss: -1.19±0.15 kg placebo versus -1.18±0.15 kg eplerenone, P=0.766). These findings suggest that inappropriate mineralocorticoid receptor activation contributes to the hypertension of autonomic failure, likely independent of canonical mineralocorticoid effects, and provides rationale for use of eplerenone in these patients.
language: eng
source:
identifier: ISSN: 0194-911X
fulltext: no_fulltext
issn:
  • 0194-911X
  • 1524-4563
url: Link


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titleMineralocorticoid receptor activation contributes to the supine hypertension of autonomic failure
creatorArnold, Amy C ; Okamoto, Luis E ; Gamboa, Alfredo ; Black, Bonnie K ; Raj, Satish R ; Elijovich, Fernando ; Robertson, David ; Shibao, Cyndya A ; Biaggioni, Italo
creatorcontribArnold, Amy C ; Okamoto, Luis E ; Gamboa, Alfredo ; Black, Bonnie K ; Raj, Satish R ; Elijovich, Fernando ; Robertson, David ; Shibao, Cyndya A ; Biaggioni, Italo
descriptionPrimary autonomic failure is characterized by disabling orthostatic hypotension, but at least half of these patients have paradoxical supine hypertension. Renin-angiotensin mechanisms were not initially thought to contribute to this hypertension because plasma renin activity is often undetectable in autonomic failure. Plasma aldosterone levels are normal, however, and we recently showed that plasma angiotensin II is elevated and acts at AT1 (angiotensin type 1) receptors to contribute to hypertension in these patients. Because aldosterone and angiotensin II can also bind mineralocorticoid receptors to elevate blood pressure, we hypothesized that mineralocorticoid receptor activation plays a role in the hypertension of autonomic failure. To test this hypothesis, we determined the acute effects of the mineralocorticoid receptor antagonist eplerenone (50 mg, oral) versus placebo on supine blood pressure in a randomized, double-blind, crossover study. Medications were given at 8:00 pm with blood pressure recorded every 2 hours for 12 hours. Ten primary autonomic failure patients with supine hypertension completed this study (7 pure autonomic failure, 2 multiple system atrophy, 1 parkinson's disease; 7 male; 70±2 years of age). Eplerenone maximally reduced supine systolic blood pressure by 32±6 mm Hg at 8 hours after administration (versus 8±10 mm Hg placebo, P=0.016), with no effect on nocturia (12-hour urine volume: 985±134 mL placebo versus 931±94 mL eplerenone, P=0.492; nocturnal weight loss: -1.19±0.15 kg placebo versus -1.18±0.15 kg eplerenone, P=0.766). These findings suggest that inappropriate mineralocorticoid receptor activation contributes to the hypertension of autonomic failure, likely independent of canonical mineralocorticoid effects, and provides rationale for use of eplerenone in these patients.
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descriptionPrimary autonomic failure is characterized by disabling orthostatic hypotension, but at least half of these patients have paradoxical supine hypertension. Renin-angiotensin mechanisms were not initially thought to contribute to this hypertension because plasma renin activity is often undetectable in autonomic failure. Plasma aldosterone levels are normal, however, and we recently showed that plasma angiotensin II is elevated and acts at AT1 (angiotensin type 1) receptors to contribute to hypertension in these patients. Because aldosterone and angiotensin II can also bind mineralocorticoid receptors to elevate blood pressure, we hypothesized that mineralocorticoid receptor activation plays a role in the hypertension of autonomic failure. To test this hypothesis, we determined the acute effects of the mineralocorticoid receptor antagonist eplerenone (50 mg, oral) versus placebo on supine blood pressure in a randomized, double-blind, crossover study. Medications were given at 8:00 pm with blood pressure recorded every 2 hours for 12 hours. Ten primary autonomic failure patients with supine hypertension completed this study (7 pure autonomic failure, 2 multiple system atrophy, 1 parkinson's disease; 7 male; 70±2 years of age). Eplerenone maximally reduced supine systolic blood pressure by 32±6 mm Hg at 8 hours after administration (versus 8±10 mm Hg placebo, P=0.016), with no effect on nocturia (12-hour urine volume: 985±134 mL placebo versus 931±94 mL eplerenone, P=0.492; nocturnal weight loss: -1.19±0.15 kg placebo versus -1.18±0.15 kg eplerenone, P=0.766). These findings suggest that inappropriate mineralocorticoid receptor activation contributes to the hypertension of autonomic failure, likely independent of canonical mineralocorticoid effects, and provides rationale for use of eplerenone in these patients.
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2Autonomic Nervous System - drug effects
3Autonomic Nervous System - physiopathology
4Blood Pressure - drug effects
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6Blood Pressure Determination
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8Dose-Response Relationship, Drug
9Double-Blind Method
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11Follow-Up Studies
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13Hypertension - drug therapy
14Hypertension - etiology
15Hypertension - physiopathology
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17Middle Aged
18Mineralocorticoid Receptor Antagonists - administration & dosage
19Pure Autonomic Failure - complications
20Pure Autonomic Failure - drug therapy
21Pure Autonomic Failure - physiopathology
22Spironolactone - administration & dosage
23Spironolactone - analogs & derivatives
24Supine Position - physiology
25Treatment Outcome
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titleMineralocorticoid receptor activation contributes to the supine hypertension of autonomic failure
authorArnold, Amy C ; Okamoto, Luis E ; Gamboa, Alfredo ; Black, Bonnie K ; Raj, Satish R ; Elijovich, Fernando ; Robertson, David ; Shibao, Cyndya A ; Biaggioni, Italo
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abstractPrimary autonomic failure is characterized by disabling orthostatic hypotension, but at least half of these patients have paradoxical supine hypertension. Renin-angiotensin mechanisms were not initially thought to contribute to this hypertension because plasma renin activity is often undetectable in autonomic failure. Plasma aldosterone levels are normal, however, and we recently showed that plasma angiotensin II is elevated and acts at AT1 (angiotensin type 1) receptors to contribute to hypertension in these patients. Because aldosterone and angiotensin II can also bind mineralocorticoid receptors to elevate blood pressure, we hypothesized that mineralocorticoid receptor activation plays a role in the hypertension of autonomic failure. To test this hypothesis, we determined the acute effects of the mineralocorticoid receptor antagonist eplerenone (50 mg, oral) versus placebo on supine blood pressure in a randomized, double-blind, crossover study. Medications were given at 8:00 pm with blood pressure recorded every 2 hours for 12 hours. Ten primary autonomic failure patients with supine hypertension completed this study (7 pure autonomic failure, 2 multiple system atrophy, 1 parkinson's disease; 7 male; 70±2 years of age). Eplerenone maximally reduced supine systolic blood pressure by 32±6 mm Hg at 8 hours after administration (versus 8±10 mm Hg placebo, P=0.016), with no effect on nocturia (12-hour urine volume: 985±134 mL placebo versus 931±94 mL eplerenone, P=0.492; nocturnal weight loss: -1.19±0.15 kg placebo versus -1.18±0.15 kg eplerenone, P=0.766). These findings suggest that inappropriate mineralocorticoid receptor activation contributes to the hypertension of autonomic failure, likely independent of canonical mineralocorticoid effects, and provides rationale for use of eplerenone in these patients.
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doi10.1161/HYPERTENSIONAHA.115.06617
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