The Mechanism of Low-renin Hypertension : Aldosterone Response to Sodium Restriction and Upright Posture, Angiotensin II, ACTH and Potassium in Patients with Hypertension

Saito, Ikuo; Saruta, Takao; Nakamura, Ryuichi; Misumi, Jiro; Kondo, Kazuoki; Matsuki, Shun

doi:10.1253/jcj.40.911

Cited by 4 publications

(2 citation statements)

References 23 publications

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“…Derangements in the activity of other non-classical regulators of aldosterone secretion, such as dopamine, might also potentially contribute to change the relationship between renin and aldosterone, although there is currently no direct evidence for such an abnormality. Finally, LREH may be a heterogeneous condition, as not all patients with LREH have enhanced adrenal sensitivity to AngII [130][131][132].…”

Section: Low-renin Essential Hypertensionmentioning

confidence: 99%

Aldosterone and the Pathogenesis of Hypertension

Nyirenda¹,

Brown²,

Padfield³

2006

CHYR

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Hypertension remains a major public health problem, affecting up to 20% of the adult population in Western societies. Despite progress in treatment, the rates of blood pressure control remain suboptimal. Hypertension is a heterogeneous disorder, and in the majority of cases, with so-called "essential" hypertension, no clear single identifiable cause is found. Syndromes of excessive mineralocorticoid production or activity are among the important causes of secondary hypertension. Aldosterone is the principal mineralocorticoid in humans, and primary aldosterone excess, when associated with an aldosterone secreting adenoma (Conn's tumor), is amenable to surgical cure. Classically, patient with Conn's tumor present with spontaneous hypokalemia and have a relative excess of aldosterone production with suppression of plasma levels of renin (a proxy for angiotensin II, the major trophic substance regulating aldosterone secretion). This combination of a high aldosterone and a low renin is however more commonly associated with 'nodular hyperplasia' of the adrenal glands, a condition not improved by surgery and variably responsive to the effects of mineralocorticoid antagonists such as spironolactone. Although primary aldosteronism was previously considered to be rare, recent studies have reported prevalence rates of up to 20% among hypertensive patients. This reflects the increasing use of the plasma aldosterone concentration to renin activity ratio (ARR), rather than spontaneous hypokalemia, as a screening tool for aldosteronism. Many patients with high ARR have normokalemia and, although renin activity is low, the level of aldosterone is usually within the normal range. This group of patients may thus include those who were previously classified as having low-renin essential hypertension. Recent data suggest that disturbances in aldosterone metabolism and regulation may not be uncommon in patients with essential hypertension. Thus, relatively high serum aldosterone levels within the reference range in normotensive individuals are associated with a substantially increased risk of developing hypertension, highlighting the potential role for aldosterone in the etiology of essential hypertension. The present review addresses the physiology of aldosterone action and its role in the pathogenesis of hypertension.

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Section: Low-renin Essential Hypertensionmentioning

confidence: 99%

Aldosterone and the Pathogenesis of Hypertension

Nyirenda¹,

Brown²,

Padfield³

2006

CHYR

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“…We had been led to believe that LREH patients maintain normal basal plasma levels of aldosterone in the face of a suppressed renin system via excessive responsiveness to Ang II, at least on an ad libitum sodium intake. Early studies favored this thesis, [2][3][4][5][6] with some suggestion of heterogeneity of response, 7 although each included only small numbers of patients.…”

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confidence: 99%

Altered Adrenal Sensitivity to Angiotensin II in Low-Renin Essential Hypertension

et al. 1999

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Abstract-Low-renin essential hypertension (LREH) describes a widely recognized classification validated by clinical features, including salt-sensitive blood pressure and diuretic responsiveness. Classic physiological teaching has cited normal plasma aldosterone concentration despite suppressed renin as evidence for adrenal supersensitivity to angiotensin II (Ang II). We studied 94 patients with LREH, 242 normal-renin hypertensives, and 135 normal subjects as controls. Low-renin hypertensives did not differ significantly from the other groups in either basal or Ang II-stimulated aldosterone concentrations on a high-sodium diet. Stimulated with a low-sodium diet, LREH patients demonstrated the smallest rise in basal aldosterone secretion. Ang II responsiveness was also subnormal: the rise in aldosterone after Ang II infusion in LREH (613Ϯ39 pmol/L), although greater than in nonmodulators (180Ϯ17 pmol/L; Pϭ0.001), was less than either the patients with intact modulation (940Ϯ53 pmol/L; Pϭ0.001) or normotensives (804Ϯ50 pmol/L; PϽ0.05). Blacks with LREH demonstrated an even lower response than low-renin whites ((388Ϯ50 versus 610Ϯ47 pmol/L; Pϭ0.0001). In contrast, the rise in systolic blood pressure with Ang II infusion on a low-salt diet was greatest among LREH patients (Pϭ0.001). Patients with LREH and nonmodulators were equally salt-sensitive. These results indicate that the adrenal response in LREH is normal on a high-salt diet but becomes progressively more abnormal as sodium control mechanisms are stressed. The factors that mediate enhanced adrenal response to Ang II with sodium restriction may be defective, suggesting the existence of alternative physiological mechanisms for sodium homeostasis in the low-renin state. (Hypertension. 1999;34:388-394.)

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Alterations in Aldosterone Secretion and Metabolism in Low Renin Hypertension*

Griffing

Wilson

Melby

1990

The Journal of Clinical Endocrinology & Metabolism

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Low renin essential hypertensives (LRH) have normal plasma aldosterone levels which are inappropriately high in relation to their PRA. Posture is the major determinant for plasma aldosterone and PRA levels, but it is not known whether postural increments (delta) of plasma aldosterone and (delta) PRA are also abnormal in LRH. To evaluate this, LRH (n = 8), normal renin hypertensives (NRH; n = 9), normotensive controls (n = 18), and subjects with idiopathic hyperaldosteronism (IHA; n = 5) were studied in a metabolic unit on a controlled diet over 7 days. Overnight supine and 4-h upright PRA, plasma aldosterone, and 24-h urinary tetrahydroaldosterone (THA) and aldosterone secretion rates (ASR) were measured. The delta in plasma aldosterone after 4 h of upright posture was not different in the four groups. The ratio of delta plasma aldosterone/delta PRA, however, was elevated in both IHA and LRH compared to that in NRH and normals. THA excretion was also elevated in IHA and LRH, but LRH had a normal ASR. This resulted in a higher fractional THA excretion (THA/ASR) in LRH compared to the other three groups. These data further support enhanced adrenal angiotensin-II sensitivity in LRH. Aldosterone was preferentially metabolized to THA in LRH. Since THA has reduced biological activity, this may be a compensatory mechanism to reduce mineralocorticoid activity in LRH.

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The Mechanism of Low-renin Hypertension : Aldosterone Response to Sodium Restriction and Upright Posture, Angiotensin II, ACTH and Potassium in Patients with Hypertension

Cited by 4 publications

References 23 publications

Aldosterone and the Pathogenesis of Hypertension

Aldosterone and the Pathogenesis of Hypertension

Altered Adrenal Sensitivity to Angiotensin II in Low-Renin Essential Hypertension

Alterations in Aldosterone Secretion and Metabolism in Low Renin Hypertension*

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