Circadian blood pressure variation in patients with renovascular hypertension or primary aldosteronisn

Imai, Yutaka; Abe, Keishi; Sasaki, Shin; Munakata, Masanori; Minami, Naoyoshi; Sakuma, Hiromichi; Hashimoto, Junichiro; Yabe, Tamami; Watanabe, Noriko; Sakuma, Masayoshi; Tsunoda, Kazuo; Saito, Hiroshi; Imai, Keiko; Yoshinaga, Kaoru

doi:10.3109/10641969209038198

Cited by 17 publications

(9 citation statements)

References 34 publications

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“…[1][2][3][4][5][6] However, these observations are of limited value because either a small number of studied subjects have been used in previous reports (especially in the case of pheochromocytoma) or controversial results have been published regarding the circadian BP pattern in primary aldosteronism and also in pheochromocytoma. 1,2,[7][8][9][10][11][12][13][14] Until now, no study has been focused on differences in diurnal BP variations between the steroid-and catecholamine-induced hypertension.…”

Section: Introductionmentioning

confidence: 99%

Diurnal blood pressure variationin pheochromocytoma, primary aldosteronism and Cushing's syndrome

et al. 2004

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We examined circadian blood pressure (BP) variation (expressed as a relative night-time BP decline) in subjects with primary aldosteronism (78 patients), pheochromocytoma (n ¼ 45) and Cushing's syndrome (n ¼ 18). Subjects with aldosterone-producing adenoma (n ¼ 21) and pheochromocytoma (n ¼ 27) were also investigated after the tumour removal. In all, 65 patients with essential hypertension served as a control group. The night-time BP decline was significantly attenuated in all three forms of endocrine hypertension compared to the control group (primary aldosteronism Po0.0001, pheochromocytoma Po0.0001 for systolic and diastolic BP and Cushing's syndrome Po0.0001/o0.001 vs essential hypertension). In the case of pheochromocytoma, the absence of the night-time BP decrease was more prominent compared to the primary aldosteronism group (P ¼ 0.003/0.001) and for the diastolic BP also in comparison with the Cushing's syndrome group (P ¼ 0.03). Tumour removal led in both groups to the restoration of the previously altered circadian rhythm (aldosterone-producing adenoma: P ¼ 0.0005/0.0009; pheochromocytoma: P ¼ 0.001/0.0007). Our study demonstrates a blunted circadian BP variation in all forms of adrenal hypertension in comparison with essential hypertension. This reduction of the night-time BP decrease was more prominent in pheochromocytoma than in primary aldosteronism or Cushing's syndrome.

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Section: Introductionmentioning

confidence: 99%

Diurnal blood pressure variationin pheochromocytoma, primary aldosteronism and Cushing's syndrome

et al. 2004

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“…[3][4][5] For example, autonomic failure, 6 Shy-Drager syndromes, 7 catecholamine excess states, 8 chronic renal failure, 9 Cushing's syndrome, 10 and diabetes mellitus 11 are all associated with an attenuation of the nocturnal BP decline. However, there are conflicting reports 8,[12][13][14][15][16][17] on whether patients with primary hyperaldosteronism have a normal circadian BP profile.…”

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confidence: 99%

Circadian Blood Pressure Variation in Hypertensive Patients With Primary Hyperaldosteronism

Mansoor

White

1998

Hypertension

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Abstract-A less-than-normal decline in nocturnal blood pressure (BP) has been associated with excessive hypertensive complications. This is concerning because secondary hypertension is often associated with this so-called nondipper BP profile. A nondipping pattern is more frequently found in the presence of pheochromocytoma, Cushing's syndrome, and sleep apnea syndrome, but the prevalence is unclear in patients with primary hyperaldosteronism. We therefore studied ambulatory BP profiles in 16 hypertensive patients with primary hyperaldosteronism and an equal number of essential hypertensive subjects. The awakeϪsleep BP difference of the hyperaldosteronism patients was similar to that of essential hypertensives (15/14Ϯ3/2 versus 14/9Ϯ3/2 mm Hg, PϭNS). The prevalence of dippers and nondippers (according to two distinct criteria) in the two groups was similar. Repeat ambulatory BP monitoring in 12 subjects with primary hyperaldosteronism after specific intervention (3 after surgical removal of an adrenal adenoma and 9 after commencement and titration of spironolactone therapy) showed highly significant reductions in office BP (22/10Ϯ6/4 mm Hg, PϽ.05) and awake and sleep BP. However, the extent of nocturnal BP decline was unchanged between the two studies (17/16Ϯ3/3 versus 16/12Ϯ2/2 mm Hg, PϭNS). There was no correlation between the awakeϪsleep difference and serum or urinary aldosterone levels or the aldosterone-to-renin ratio. In this study, we did not detect any differences in the awakeϪsleep differences between a group of hypertensives with primary hyperaldosteronism and a control group of essential hypertensives. (Hypertension. 1998;31:843-847.)Key Words: blood pressure, ambulatory Ⅲ hyperaldosteronism Ⅲ blood pressure variability Ⅲ hypertension, secondary T he circadian BP profile is likely a result of the complex interaction of neurological and hormonal circadian changes and the superimposed effects of physical and mental activity and posture.1,2 As part of this variation, there is a long-standing observation that BP decreases in the majority of normotensive and hypertensive subjects during sleep.3 Therefore, a terminology has come into practice for subjects with normal sleep BP decline who are labeled dippers and those with a less-thanexpected decline are called nondippers. These categories are not clearly defined, and the extent of BP reduction during sleep is affected by several factors such as age, sleep quality, and underlying comorbidity.3-5 For example, autonomic failure, Shy-Drager syndromes, 7 catecholamine excess states, 8 chronic renal failure, 9 Cushing's syndrome, 10 and diabetes mellitus 11 are all associated with an attenuation of the nocturnal BP decline. However, there are conflicting reports 8,12-17 on whether patients with primary hyperaldosteronism have a normal circadian BP profile.The issue of whether the BP profile is altered in subjects with primary hyperaldosteronism is a relevant one because the nondipper profile is associated with excess hypertensive complications. 18 -22 We theref...

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“…20,31-33 PA is also well known as a typical form of sodium-sensitive secondary hypertension. 34 Several groups have described a disturbed circadian rhythm of BP in PA, 20,35 while, in contrast, other reports showed that the circadian rhythm of BP was unchanged in PA. [36][37][38] However, many of these reports 20,35,36,38 included patients with PA that was caused by adenoma as well as PA caused by idiopathic hyperaldosteronism, and some of the reports 20,36,38 studied PA patients who were taking antihypertensive drugs. We studied eight patients with PA caused by unilateral adenoma (Conn's syndrome), and found no nocturnal fall in BP (158 Ϯ 24/95 Ϯ 11 mmHg during daytime vs 158 Ϯ 21/95 Ϯ 10 mmHg during night-time [systolic/diastolic BP, mean Ϯ SD].…”

Section: Introductionmentioning

confidence: 94%

Circadian rhythm of blood pressure and cardiovascular risk in sodium-sensitive hypertension

Uzu

1999

Clinical and Experimental Nephrology

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Circadian blood pressure variation in patients with renovascular hypertension or primary aldosteronisn

Cited by 17 publications

References 34 publications

Diurnal blood pressure variationin pheochromocytoma, primary aldosteronism and Cushing's syndrome

Diurnal blood pressure variationin pheochromocytoma, primary aldosteronism and Cushing's syndrome

Circadian Blood Pressure Variation in Hypertensive Patients With Primary Hyperaldosteronism

Circadian rhythm of blood pressure and cardiovascular risk in sodium-sensitive hypertension

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