Glucocorticoid-induced hypertension

Goodwin, Julie E.; Geller, David S.

doi:10.1007/s00467-011-1928-4

Cited by 125 publications

(81 citation statements)

References 60 publications

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“…Numerous studies indicate that glucocorticoids act in the periphery to increase vascular tone and reactivity (16). Fewer studies have investigated the central nervous system actions of glucocorticoids on blood pressure regulation, and the results have been equivocal (15,52,53,56,57).…”

mentioning

confidence: 97%

Elevated corticosterone in the dorsal hindbrain increases plasma norepinephrine and neuropeptide Y, and recruits a vasopressin response to stress

Daubert

Looney

Clifton

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Repeated stress and chronically elevated glucocorticoids cause exaggerated cardiovascular responses to novel stress, elevations in baseline blood pressure, and increased risk for cardiovascular disease. We hypothesized that elevated corticosterone (Cort) within the dorsal hindbrain (DHB) would: 1) enhance arterial pressure and neuroendocrine responses to novel and repeated restraint stress, 2) increase c-Fos expression in regions of the brain involved in sympathetic stimulation during stress, and 3) recruit a vasopressin-mediated blood pressure response to acute stress. Small pellets made of 10% Cort were implanted on the surface of the DHB in male Sprague-Dawley rats. Blood pressure was measured by radiotelemetry. Cort concentration was increased in the DHB in Cort-treated compared with Sham-treated rats (60 ± 15 vs. 14 ± 2 ng Cort/g of tissue, P < 0.05). DHB Cort significantly increased the integrated arterial pressure response to 60 min of restraint stress on days 6, 13, and 14 following pellet implantation (e.g., 731 ± 170 vs. 1,204 ± 68 mmHg/60 min in Sham- vs. Cort-treated rats, day 6, P < 0.05). Cort also increased baseline blood pressure by day 15 (99 ± 2 vs. 108 ± 3 mmHg for Sham- vs. Cort-treated rats, P < 0.05) and elevated baseline plasma norepinephrine and neuropeptide Y concentrations. Cort significantly enhanced stress-induced c-Fos expression in vasopressin-expressing neurons in the paraventricular nucleus of the hypothalamus, and blockade of peripheral vasopressin V1 receptors attenuated the effect of DHB Cort to enhance the blood pressure response to restraint. These data indicate that glucocorticoids act within the DHB to produce some of the adverse cardiovascular consequences of chronic stress, in part, by a peripheral vasopressin-dependent mechanism.

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mentioning

confidence: 97%

Elevated corticosterone in the dorsal hindbrain increases plasma norepinephrine and neuropeptide Y, and recruits a vasopressin response to stress

Daubert

Looney

Clifton

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Cortisol and aldosterone bind to the mineralocorticoid receptor [51,52]. The abundance of cortisol in apparent mineralocorticoid excess results in mineralocorticoid receptor activation in aldosterone-specific tissues, such as the kidney, causing excessive sodium reabsorption leading to volume expansion and the development of hypertension.…”

Section: α-Reductase Inhibition May Contribute To Vascular Diseasementioning

confidence: 99%

5α-Reductase inhibitors alter steroid metabolism and may contribute to insulin resistance, diabetes, metabolic syndrome and vascular disease: a medical hypothesis

Traish

Guay

Zitzmann³

2014

Hormone Molecular Biology and Clinical Investigation

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5α-reductases, a unique family of enzymes with a wide host of substrates and tissue distributions, play a key role in the metabolism of androgens, progestins, mineralocorticoids and glucocorticoids. These enzymes are the rate-limiting step in the synthesis of a host of neurosteroids, which are critical for central nervous system function. Androgens and glucocorticoids modulate mitochondrial function, carbohydrate, protein and lipid metabolism and energy balance. Thus, the inhibition of these regulatory enzymes results in an imbalance in steroid metabolism and clearance rates, which leads to altered physiological processes. In this report, we advance the hypothesis that inhibition of 5α-reductases by finasteride and dutasteride alters not only steroid metabolism but also interferes with the downstream actions and signaling of these hormones. We suggest that finasteride and dutasteride inhibit 5α-reductase activities and reduce the clearance of glucocorticoids and mineralocorticoids, potentiating insulin resistance, diabetes and vascular disease.

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“…Todavia, a dexametasona utilizada em grande quantidade está relacionada à síndrome de Cushing iatrogênica, caracterizada pela "face de lua", surgimento de estrias, ganho de peso com acúmulo de gordura central. Além destes efeitos, a utilização indiscriminada de glicocorticoides promove alterações negativas no metabolismo da glicose 2,3 , miopatia e fraqueza muscular [4][5][6] , hipertensão arterial 7,8 , osteoporose 9,10 e maior suscetibilidade a infecções oportunistas 11 . Nesse sentido, buscam-se métodos alternativos que possam reduzir/atenuar os efeitos adversos decorrentes do uso crônico da dexametasona.…”

Section: Introductionunclassified

Efeitos Do Exercício Resistido De Alta Intensidade Em Ratos Que Receberam Dexametasona

Rodrigues

Abrahin

Sousa

et al. 2016

Rev Bras Med Esporte

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RESUMOIntrodução: A dexametasona administrada cronicamente promove alterações deletérias no metabolismo dos carboidratos. Objetivo: Avaliar os efeitos do exercício resistido de alta intensidade sobre a sensibilidade à insulina, tolerância à glicose e força muscular de ratos submetidos ao uso crônico de dexametasona. Métodos: Foram utilizados 40 ratos machos divididos randomicamente em quatro grupos: 1) Controle Sedentário (CS); 2) Controle Treinado (CT); 3) Dexametasona Sedentário (DS) e 4) Dexametasona Treinado (DT). O exercício resistido foi realizado em aparelho de agachamento composto por três séries, 10 repetições, com intensidade de 75% de 1 RM durante quatro semanas. Concomitantemente, os grupos DS e DT recebiam diariamente dexametasona intraperitoneal (0,2 g/kg) e os grupos CS e CT recebiam somente solução salina (0,9%). Ao final do protocolo foram realizados testes de tolerância à glicose, sensibilidade à insulina e teste de força máxima. Resultados: Nos grupos treinados (CT e DT) houve aumento da força muscular de 14,78% e 36,87% respectivamente, sem ganho significativo nos grupos sedentários. No teste de tolerância à glicose, os grupos treinados (CT e DT) apresentaram amplitudes atenuadas da glicose plasmática quando comparados aos grupos sedentários (CS e DS). No teste de sensibilidade à insulina, o grupo DT apresentou menor área sob a curva em relação ao grupo DS. Conclusão: O exercício resistido de alta intensidade melhora a sensibilidade à insulina, tolerância à glicose e a força muscular em ratos que receberam a dexametasona.Descritores: treinamento de resistência; resistência à insulina; hiperglicemia. ABSTRACT

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Glucocorticoid-induced hypertension

Cited by 125 publications

References 60 publications

Elevated corticosterone in the dorsal hindbrain increases plasma norepinephrine and neuropeptide Y, and recruits a vasopressin response to stress

Elevated corticosterone in the dorsal hindbrain increases plasma norepinephrine and neuropeptide Y, and recruits a vasopressin response to stress

5α-Reductase inhibitors alter steroid metabolism and may contribute to insulin resistance, diabetes, metabolic syndrome and vascular disease: a medical hypothesis

Efeitos Do Exercício Resistido De Alta Intensidade Em Ratos Que Receberam Dexametasona

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