The Nitric Oxide System and Cortisol‐induced Hypertension in Humans

Kelly, John J.; Tam, Sim H; Williamson, Paula; Lawson, J A; Whitworth, Judith A.

doi:10.1111/j.1440-1681.1998.tb02349.x

Cited by 77 publications

(56 citation statements)

References 6 publications

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“…The lower cortisol levels in females are in accordance with the perception of an ongoing and unavoidable stress situation, but is however not associated with an increase in blood pressure levels or increased vascular responsiveness. 22,28 The lower testosterone and higher prolactin levels in females are in accordance with vasoconstriction and therefore with increased DBP reactivity and TPR reactivity. 40 This may interfere with blood pressure, and these parameters are therefore associated with the high rate of hypertension in stratum 3 subjects.…”

Section: Malesmentioning

confidence: 93%

“…The nitric oxide system may also play a role in cortisol-induced hypertension. 28,29 It is also reported that cortisol is not a direct determinant of blood pressure, but cortisol may regulate other key components of vascular risk such as low high-density lipoprotein (HDL) cholesterol and fat distribution. 30 Heightened prolactin levels are also associated with powerless situation stress.…”

Section: Introductionmentioning

confidence: 99%

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Prolactin, testosterone and cortisol as possible markers of changes in cardiovascular function associated with urbanization

et al. 2002

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People living in large informal settlements in South Africa showed a significant increase in cardio/cerebrovascular disease. This study was undertaken to compare the cardiovascular and endocrine parameters of urbanized and rural black female and males. The hormone levels such as prolactin, cortisol and testosterone may also change with urbanization and could make a contribution to the high rate of hypertension. For this study, 1202 black subjects were selected from 37 randomly selected rural and urbanized settlements. Resting blood pressure was recorded with a Finapres apparatus. Cardiac output, stroke volume, heart rate, total peripheral vascular resistance and compliance had been obtained with the Fast Modelflow software program. An acute laboratory stressor (hand dynamometer exercise) was applied to challenge the cardiovascular system and the measurements were repeated. Blood sampling was done and hormone levels were determined by biochemical analyses. For females, significant lower levels of cortisol were found in the urban strata in comparison with the rural strata. The testosterone levels were significantly lower and the prolactin levels significantly higher for females in the informal settlements compared with the rural strata. It is noticeable that most cardiovascular parameters showed the highest changes with the application of the stressor in the informal settlement strata and the lowest in people living on farms for both male and female. The prolactin levels in males are significantly higher in the informal settlement stratum. Subjects living in informal settlements showed a noticeable endocrine pattern of ongoing stress that can be associated with changes in the cardiovascular parameters with urbanization. This can partly explain the reported high rate of cardio/cerbrovascular disease in black South Africans living in informal settlements.

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Section: Malesmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Prolactin, testosterone and cortisol as possible markers of changes in cardiovascular function associated with urbanization

et al. 2002

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“…1,3 Cortisol treatment also causes suppression of the nitric oxide system as evidenced by reduced plasma nitrate/nitrite concentrations. 5 In the context of these observations, Correspondence 6,7 EPO-induced hypertension has also been demonstrated to be due in part to nitric oxide resistance. 8 The aim of the current study was to examine the role of EPO as a possible mediator of cortisolinduced hypertension.…”

Section: Introductionmentioning

confidence: 99%

Role of erythropoietin in cortisol-induced hypertension

2000

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The mechanism of cortisol-induced hypertension remains unknown. We investigated a possible role of erythropoietin (EPO) as a mediator of hypertension in healthy male subjects treated with cortisol. In Study 1, blood pressure (BP) and serum EPO concentrations were measured on alternate days in nine subjects treated with 80 mg of cortisol per day for 5 days. In Study 2 the same parameters were measured in eight subjects randomised to cortisol (80 mg/day) or placebo and 10 subjects randomised to cortisol (200 mg/day) or placebo for 5 days. In Study 1, cortisol caused a significant increase in systolic BP (SBP) (115 ؎ 2 vs 126 ؎ 2 mm Hg, control vs day 5, P Ͻ 0.001) and serum EPO

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“…4 In humans, cortisol-increases in blood pressure occur in association with reductions in plasma nitrate/nitrite concentrations, but no change in plasma arginine or symmetric or asymmetric dimethyl arginine has been observed, indicating that the reductions in nitrate could not be explained by changes in substrate availability or endogenous nitric oxide synthase inhibitors. 5 More recently, using bilateral forearm plethysmography, we have found impaired cholinergic vasodilatation after cortisol administration. Cortisol did not affect the response to sodium nitroprusside, and although N G -monomethyl-L-arginine inhibited cholinergic vasodilation in placebo-treated subjects, it had no additional effect in the presence of cortisol.…”

mentioning

confidence: 99%

l -Arginine Transport in Humans With Cortisol-Induced Hypertension

et al. 2003

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Abstract-A deficient L-arginine-nitric oxide system is implicated in cortisol-induced hypertension. We investigate whether abnormalities in L-arginine uptake contribute to this deficiency. Eight healthy men were recruited. Hydrocortisone acetate (50 mg) was given orally every 6 hours for 24 hours after a 5-day fixed-salt diet (150 mmol/d).Crossover studies were performed 2 weeks apart. Thirty milliliters of blood was obtained for isolation of peripheral blood mononuclear cells after each treatment period. L-Arginine uptake was assessed in mononuclear cells incubated with L-arginine (1 to 300 mol/L), incorporating 100 nmol/L [ 3 H]-L-arginine for a period of 5 minutes at 37°C. Forearm Key Words: cortisol Ⅲ hypertension, mineralocorticoid Ⅲ nitric oxide Ⅲ arginine Ⅲ human C ortisol, the major naturally occurring human glucocorticoid, is implicated in the pathogenesis of some forms of essential hypertension, 1 but the mechanisms by which cortisol raises blood pressure are not fully defined. Cardiac output is increased but is not essential for the increase, 2 and sympathetic activity is, if anything, decreased. 3 A role for the nitric oxide system in cortisol-induced hypertension has been implicated in animal models of cortisol-induced hypertension; L-arginine, the substrate precursor to nitric oxide, prevents and reverses the development of adrenocorticotropin-induced hypertension in rats. 4 In humans, cortisol-increases in blood pressure occur in association with reductions in plasma nitrate/nitrite concentrations, but no change in plasma arginine or symmetric or asymmetric dimethyl arginine has been observed, indicating that the reductions in nitrate could not be explained by changes in substrate availability or endogenous nitric oxide synthase inhibitors. 5 More recently, using bilateral forearm plethysmography, we have found impaired cholinergic vasodilatation after cortisol administration. Cortisol did not affect the response to sodium nitroprusside, and although N G -monomethyl-L-arginine inhibited cholinergic vasodilation in placebo-treated subjects, it had no additional effect in the presence of cortisol. 6 Taken together, these results are consistent with a role for abnormalities of the nitric oxide system in cortisol-induced hypertension in humans.In the current study, we explored whether cortisol reduces the cellular uptake of L-arginine and whether this mechanism might provide an explanation for the decreased synthesis or secretion of nitric oxide. The study was performed in healthy adult men against a background of a restricted-nitrate diet. L-Arginine transport was assessed in peripheral blood mononuclear cells isolated from these subjects as well as in vivo in the forearm vascular bed. Methods SubjectsHealthy (or disease-free) men were recruited by advertisement. All underwent a physical medical examination and had their medical history recorded. Persons with a history of major illness, including diabetes, cardiovascular disease, respiratory illness, and any contraindication to corticosteroid therapy...

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The Nitric Oxide System and Cortisol‐induced Hypertension in Humans

Cited by 77 publications

References 6 publications

Prolactin, testosterone and cortisol as possible markers of changes in cardiovascular function associated with urbanization

Prolactin, testosterone and cortisol as possible markers of changes in cardiovascular function associated with urbanization

Role of erythropoietin in cortisol-induced hypertension

l -Arginine Transport in Humans With Cortisol-Induced Hypertension

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