Plasma adrenomedullin in patients with primary aldosteronism

Kato, Jun; Kïtamura, Kazuo; Kuwasako, Kenji; Tanaka, Miho; Ishiyama, Yuichiro; Shimokubo, Toru; Ichiki, Yoshinari; Nakamura, Shigeru; Kangawa, Kenji; Eto, Tanenao

doi:10.1016/0895-7061(95)00217-0

Cited by 41 publications

(21 citation statements)

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“…The GH subgroup, which has not been previously studied, was included because of the potential difference in etiology compared with preeclampsia. 29 Other hypertensive diseases, including essential hypertension, [11][12][13] renal failure, 11 heart failure, 12,13 and primary aldosteronism, 14 all show an increase in plasma ADM levels. In these conditions, ADM may serve to compensate for the elevation of blood pressure.…”

Section: Discussionmentioning

confidence: 99%

“…A paracrine or autocrine mode of action of ADM has been inferred from the elevated concentrations found in fetoplacental tissues. 18 We hypothesized that maternal plasma ADM levels should, as in other hypertensive disorders, 11,12,14 be higher in hypertensive pregnancies than in normotensive pregnancies and that the higher placental resistance found in preeclamptic pregnancies results not from a lack of locally produced ADM but from blunted activity of ADM on the vasculature. Therefore, we sought to evaluate maternal plasma ADM levels and the effect of ADM on placental arteries in both preeclamptic and normal pregnancies.…”

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confidence: 99%

“…9 Because of the increased levels seen in several hypertensive disorders, a potential protective antihypertensive role of ADM has been suggested. [11][12][13][14] Pregnancy is characterized by a decrease in mean arterial blood pressure despite an increase in blood volume and cardiac output of 40% to 50%. 15 Because ADM is a potent vasodilator, it has been investigated for its potential role in gestation.…”

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Effect of Adrenomedullin on Placental Arteries in Normal and Preeclamptic Pregnancies

et al. 2001

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Abstract-Adrenomedullin is a potent vasodilatory peptide with plasma levels that increase during pregnancy. Although fetoplacental adrenomedullin levels are reported to increase in preeclampsia, maternal plasma levels may be elevated or decreased, or they may resemble those in normal pregnancy. In other hypertensive conditions, adrenomedullin increases. Therefore, we hypothesized that maternal plasma adrenomedullin levels would be higher in hypertensive pregnancies than in normotensive pregnancies and that the higher placental resistance found in preeclamptic pregnancies results from blunted activity of adrenomedullin on the vasculature. Adrenomedullin concentrations in plasma from women with normotensive pregnancies, gestational hypertension, and preeclampsia were determined by radioimmunoassay. Stem villous arteries from normotensive and preeclamptic pregnancies were dissected and mounted on a wire myograph system. Arteries were first preconstricted to 80% of their maximum constriction with U46619, a thromboxane A 2 mimetic, and exposed to cumulative doses of adrenomedullin (1ϫ10 Ϫ9 to 3ϫ10 Ϫ7 mol/L). Contrary to our hypothesis, there were no significant differences in maternal plasma adrenomedullin levels among patients with normal pregnancies, gestational hypertension, and preeclampsia. Adrenomedullin significantly relaxed arteries from both normal and preeclamptic placentas, but there was no significant difference between the 2 groups. During normal pregnancy, adrenomedullin may contribute to the low placental vascular resistance. This pathway appears to be intact in preeclampsia. We conclude that the increased placental vascular resistance observed in preeclampsia is due neither to reduced adrenomedullin secretion nor to an attenuated vascular responsiveness. Moreover, unlike other hypertensive disorders, there is no compensatory rise in circulating adrenomedullin levels. (Hypertension. 2001;37:227-231.)

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Effect of Adrenomedullin on Placental Arteries in Normal and Preeclamptic Pregnancies

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“…We and one other research group have previously reported this phenomenon. 18,19 The underlying mechanism remains to be elucidated: there may be a mutual relationship between aldosterone and AM. Aldosterone stimulates AM production in rat aortic adventitia or cardiac fibroblasts; increased AM, in turn, regulates the proliferative action of aldosterone in those cells.…”

Section: Effects Of Adrenomedullin In Primary Aldosteronismmentioning

confidence: 99%

Aldosterone antisecretagogue and antihypertensive actions of adrenomedullin in patients with primary aldosteronism

2010

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Adrenomedullin (AM) is located in the zona glomerulosa of the adrenal cortex and is considered to suppress aldosterone release. To determine the effect of AM in primary aldosteronism (PA), we infused AM (2.5 pmol kg À1 min À1 ) for 27 h, followed by a 15-h recovery period, in a control group (essential hypertensives with plasma aldosterone levels p100 pg ml À1 , n¼7) and in a PA group (n¼5). The control group was also infused with vehicle. Hemodynamic, hormonal, oxidative and inflammatory responses were studied. AM infusion caused similar and steady decreases in blood pressure and several markers for arteriosclerosis (for example, pulse wave velocity) in both groups. Interestingly, AM infusion suppressed aldosterone release to values within the normal range in the PA group (300.0 ± 58.4 to 111.6 ± 13.5 pg ml À1 , Po0.01). In the control group, aldosterone release suppression was significant but limited (81.7 ± 9.1 to 47.9 ± 9.9 pg ml À1 , Po0.01). The adrenocorticotropic hormone-cortisol system was not changed by AM infusion. Brain natriuretic peptide was cumulatively increased by prolonged AM infusion in both groups, probably because of cardiac overload. AM did not affect oxidative markers. In addition, a mild but significant increase in C-reactive protein (CRP) mediated by interleukin-6 was observed during AM infusion in every participant, without exception. This pathway might participate in CRP elevation in cardiovascular disease. In summary, AM seems to have an essential role in the suppression of aldosterone release in PA. AM may be an important modulator in PA, and intermediate-term Keywords: adrenomedullin; aldosterone; C-reactive protein; humans; primary aldosteronism INTRODUCTION Adrenomedullin (AM) is a potent hypotensive peptide found ubiquitously in tissues and organs, especially in cardiovascular tissues, the kidneys, lungs and endocrine glands. AM has multiple functions in a wide range of tissues and acts mainly as a vasodilatory and proliferation-inhibitory factor. 1 AM was initially identified in the adrenal medulla, but similar densities of AM were detected in the zona glomerulosa of the adrenal cortex, where AM suppresses aldosterone release. 2,3 In addition, expression of AM and its receptor was detected in Conn's adenoma cells, and AM exerted aldosterone antisecretagogue action and proliferative effects on cultured Conn's adenoma cells. 4 These findings suggest that endogenous AM may be an important modulator of aldosterone release in normal and pathogenic hyperaldosteronism. In addition, AM antagonized aldosterone-induced vascular or cardiac remodeling 5,6 and suppressed aldosterone-induced oxidative stress in a malignant hypertensive model. 7 The characteristics that define this compound, from its release to alterations in target organs, suggest that AM may be an endogenous anti-aldosterone factor, especially in the cardiovascular system.

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“…9 Recently, it was reported that patients with hypertension show high levels of plasma AM compared with normotensive control subjects. [10][11][12][13] Nevertheless, the exact physiopathological role of AM in human hypertension remain to be established.…”

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High plasma adrenomedullin concentrations in patients with high-renin essential hypertension

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et al. 2002

J Renin Angiotensin Aldosterone Syst

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Adrenomedullin (AM) is a novel peptide, first isolated from human phaeochromocytoma, which elicits a long-lasting vasorelaxant activity. Recently, it has been reported that endothelial cells produce AM and that immunoreactive AM plasma levels may be elevated in human arterial hypertension, although the exact pathophysiological role of AM remains to be established.The aim of our study was to determine the relationship between the components of the reninangiotensin-aldosterone system (RAAS) and plasma AM levels in patients with low-, medium-or highrenin essential hypertension.The study groups included 10 patients with lowrenin essential hypertension (average age 42+15 years), nine patients with medium-renin essential hypertension (46+13 years), 11 patients with high-renin essential hypertension (42+14 years) and 12 healthy subjects (43+11 years).Our results demonstrated that the mean AM values of all patients with essential hypertension were 10.85+3.14 pg/ml; there was a statistical correlation (r=0.705; p<0.001) between plasma renin activity (PRA) and AM levels in hypertensives.In patients with high-renin essential hypertension, plasma AM levels (14.2+2.2 pg/ml) were significantly higher (p<0.001) than those of healthy subjects (8.7+2.1 pg/ml), patients with medium-renin essential hypertension (8.5+1.4 pg/ml), and patients with low-renin essential hypertension (9.1+1.5 pg/ml). There was no statistical difference in AM concentrations between medium-and low-renin hypertensive patients. In conclusion, we have found that, in hypertensive patients, plasma AM levels were increased only in high-renin individuals, suggesting a role of AM in this particular form of human essential hypertension. IntroductionAdrenomedullin (AM) is a novel peptide first isolated from human phaeochromocytoma.

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Plasma adrenomedullin in patients with primary aldosteronism

Cited by 41 publications

References 14 publications

Effect of Adrenomedullin on Placental Arteries in Normal and Preeclamptic Pregnancies

Effect of Adrenomedullin on Placental Arteries in Normal and Preeclamptic Pregnancies

Aldosterone antisecretagogue and antihypertensive actions of adrenomedullin in patients with primary aldosteronism

High plasma adrenomedullin concentrations in patients with high-renin essential hypertension

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