Mineralocorticoid-Induced Hypertension in Patients with Orthostatic Hypotension

Chobanian, Aram V.; Volicer, Ladislav; Tifft, Charles P.; Gavras, Haralambos; Liang, Chang‐seng; Faxon, David P.

doi:10.1056/nejm197907123010202

Cited by 210 publications

(103 citation statements)

References 22 publications

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“…This is well in agreement with the recent study by Maule et al [20] who reported that the development of left ventricular hypertrophy in patients with MSA does not depend on years of disease and treatment for orthostatic hypotension. The pathophysiology of supine hypertension in MSA appears to be more complex, including baroreflex dysfunction, nocturnal fluid retention, adrenergic hypersensitivity, or drug treatment for orthostatic hypotension [5]. Among the causes mentioned, it was recently recognized that in patients with MSA, supine hypertension might reflect part of the pathophysiology of primary chronic autonomic failure, and residually increased sympathetic tone is a major contributor to supine hypertension regardless of pressor agent use [31].…”

Section: Discussionmentioning

confidence: 99%

White matter hyperintensities in patients with multiple system atrophy

et al. 2009

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Recent studies have reported that the majority of patients with multiple system atrophy (MSA) had hypertensive heart disease. However, the effect of autonomic failure on the brain in MSA has not been studied. We consecutively enrolled 63 patients with MSA and selected 63 age-and sex-matched healthy subjects. We performed a comparative analysis of cerebrovascular lesions between the patients with MSA and the control subjects and analyzed predisposing factors for cerebrovascular lesions in the patients with MSA. There was no significant difference in lacune and territorial infarcts between the patients with MSA and the control subjects. The median grading score of white matter hyperintensity (WMH) was significantly higher in the patients with MSA (1.0, interquartile range 0.5-2.0) than the control subjects (0.0, interquartile range 0.0-1.0; P \ 0.01). In the patients with MSA, there was strong correlation between the grading score of WMH and supine systolic blood pressure (r = 0.529, P \ 0.001) after adjusting for age. Multiple linear regression analysis showed that age and supine systolic blood pressure was significantly and independently correlated with the grading score of WMH. The present study demonstrates that patients with MSA had more severe WMH and that supine systolic pressure is a major contributing factor for the severity of WMH, suggesting that patients with MSA have target-organ damage of the brain.

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Section: Discussionmentioning

confidence: 99%

White matter hyperintensities in patients with multiple system atrophy

et al. 2009

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“…The following drugs were used: acetylcholine hydrochloride (Sigma, St. Louis, MO, USA); adenosine 5'-diphosphate (ADP; Sigma); sodium heparin (Elkin Sinn, Cherry Hill, NJ, USA); 5-hydroxytryptamine All drugs were dissolved in distilled water, except indomethacin, which was dissolved in 10 ml of distilled water containing 5 X 10" 3 M NaCO 3 and was sonicated before use. The drugs were added to the organ chambers in volumes of 500 /xl or less.…”

Section: Drugsmentioning

confidence: 99%

Endothelium-dependent vascular responses in normotensive and hypertensive Dahl rats.

Lüscher¹,

Raij²,

Vanhoutte³

1987

Hypertension

381

156

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SUMMARY Experiments were designed to study endothelium-dependent responses in salt-sensitive (DS) and salt-resistant Dahl rats (DR). The rats were fed a low sodium (0.1% NaCl) or high sodium (8% NaCl) diet for 8 weeks. Blood pressure in DS fed a high sodium diet was higher than that in the remaining animals. Aortic rings with and without endothelium were suspended for isometric tension recording. Acetylcholine, adenosine 5'-diphosphate, and thrombin induced endothelium-dependent relaxations that were significantly depressed in the aorta of DS fed a high sodium diet. The relaxations in response to sodium nitroprusside were only slightly, but significantly, depressed in DS fed a high sodium diet. Removal of the endothelium greatly enhanced the response to serotonin and norepinephrine. In rings with, but not without, endothelium taken from rats fed a high sodium diet, the tension developed in response to serotonin and norepinephrine was significantly greater than that in animals fed a low sodium diet. These experiments indicate that (1) endothelium-dependent relaxations to acetylcholine, adenosine 5'-diphosphate, and thrombin are depressed in hypertensive Dahl rats; (2) this effect probably reflects a decreased release of endothelium-derived relaxing factor(s), although structural changes might contribute; and (3) 4 Endothelium-dependent relaxations to acetylcholine are depressed in spontaneous hypertension, in aortic coarctation, and in mineralocorticoid hypertension of the rat. "7 No information is available on endothelium-dependent responses of blood vessels in salt-induced hypertension. Received April 28, 1986; accepted August 20, 1986. Dahl developed two strains of rats with different propensities toward hypertension if fed a high sodium diet: a salt-sensitive strain, which becomes hypertensive when fed a high sodium diet, and a salt-resistant strain, which does not.8 This model may have similarities with a subgroup of human hypertension in which sodium contributes to the development of high blood pressure. 9 The present study was designed to investigate whether endothelium-dependent vascular responses are altered in salt-induced hypertension of the rat. Materials and MethodsMale 6-week-old Dahl salt-sensitive (DS) and saltresistant rats (DR) weighing 257 ± 7 g were purchased from Brookhaven National Laboratories (Brookhaven, NY, USA). All rats were housed two to a cage and had free access to water. For 8 weeks both DS and DR were fed standard rat chow (Ralston-Purina, St. Louis, MO, USA) that contained either 8% NaCl or 0.1% NaCl. Four groups of rats were used in the study: DS fed 8% NaCl, DS fed 0.1% NaCl, DR fed 8% NaCl, and DR fed 0.1% NaCl. Systolic blood 157 Downloaded from http://ahajournals.org by on April 28, 2019

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“…18 It is postulated that mineralocorticoids elevate blood pressure mainly by increasing total peripheral resistance and vascular reactivity to catecholamines in humans, with a tendency to suppress circulating catecholamines. 19 ' 20 In addition, neither measurements of plasma catecholamine levels nor analysis of the cardiovascular responses to sympatholytic agents in patients with PA have afforded any evidence of enhanced peripheral sympathetic activity mineralocorticoid-excess hypertension. 21 These findings and our recent preliminary findings, which show an increase of MSNA after adrenalectomy in PA patients (unpublished observation from our laboratory), are in line with the results indicating that sympathetic nerve activity was rather suppressed in PA patients.…”

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confidence: 99%

Muscle sympathetic nerve activity in renovascular hypertension and primary aldosteronism.

et al. 1991

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Previous studies, including our own, have demonstrated that muscle sympathetic nerve activity (MSNA) is increased in patients with essential hypertension compared with normotensive subjects. However, the features of sympathetic nerve activity are still unknown in secondary hypertension. We examined MSNA in eight patients with renovascular hypertension and in 11 patients with primary aldosteronism. Twenty patients with essential hypertension and 20 normotensive subjects who were age-matched to the patients with renovascular hypertension and those with primary aldosteronism were also studied. The MSNA of a bundle of the tibial nerve was recorded by microneurography in supine subjects and expressed as both burst rate (bursts/min) and burst incidence (bursts/100 heart beats). Plasma renin activity and the plasma concentration of angiotensin II and aldosterone were also measured. MSNA was increased in the patients with renovascular hypertension compared with the patients with primary aldosteronism and those with essential hypertension and the normotensive subjects (p<0.01 for each). MSNA was decreased in the patients with primary aldosteronism compared with those with essential hypertension (p<0.01), and it was smaller than in the normotensive subjects (p<0.l). Furthermore, MSNA, plasma renin activity, and the plasma concentration of angiotensin II decreased significantly in five patients with renovascular hypertension 4-10 days after successful percutaneous renal angioplasty. Thus, the changes in MSNA seem to characterize the patbophysiology of renovascular hypertension and primary aldosteronism. Activation of the renin-angiotensin system may be involved in the increase in the central outflow of sympathetic nerve activity, thus exacerbating hypertension in patients with renovascular hypertension. (Hypertension 1991;17:1057-1062) N eurogenic mechanisms have often been implicated in the pathogenesis of hypertension. Although the plasma concentration of norepinephrine has been used as a rough index of overall sympathetic nerve activity, its pathophysiological implications need careful evaluation since the plasma concentration of norepinephrine is determined by many factors, such as the reuptake and metabolic degradation of norepinephrine and its spillover from the nerve endings.1 ' 2 Accordingly, we have investigated sympathetic tone by directly recording the muscle sympathetic nerve activity (MSNA) contained in a bundle of the tibial nerve using a microneurographic technique in the conscious human.3 -8 Our previous studies have demonstrated that the baroreflex control of sympathetic

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Mineralocorticoid-Induced Hypertension in Patients with Orthostatic Hypotension

Cited by 210 publications

References 22 publications

White matter hyperintensities in patients with multiple system atrophy

White matter hyperintensities in patients with multiple system atrophy

Endothelium-dependent vascular responses in normotensive and hypertensive Dahl rats.

Muscle sympathetic nerve activity in renovascular hypertension and primary aldosteronism.

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