Key result
Patients with nonmodulating hypertension exhibited higher plasma norepinephrine levels during upright posture (P<0.05) and lower aldosterone levels both supine (P<0.05) and upright (P<0.01).
Why the study?
Do patients with nonmodulating hypertension have abnormal norepinephrine and aldosterone responses to upright posture compared to normal subjects and other hypertensive groups?
Observational
Do patients with nonmodulating hypertension have abnormal norepinephrine and aldosterone responses to upright posture compared to normal subjects and other hypertensive groups?
p-value: p=< 0.05
Patients with nonmodulating hypertension exhibit heightened norepinephrine and blunted aldosterone responses to upright posture, extending the known abnormalities of the renin-angiotensin-aldosterone axis in this subgroup.
Should not yet change management of nonmodulating hypertension; leaves open prognostic value and therapeutic targeting of these responses.
The subgroup of patients with nonmodulating hypertension demonstrates a number of abnormalities of the renin-angiotensin-aldosterone axis. We previously identified abnormalities in plasma and urinary dopamine in nonmodulators and posited that this may be in part due to a generalized defect in sympathetic nervous system activity. In the present study we assessed the state of activation of the renin-angiotensin system and the sympathetic nervous system in normal subjects and patients with modulating, nonmodulating, and low renin essential hypertension during sodium depletion and change from supine to upright posture. Levels of plasma norepinephrine were higher in non-modulators during the posture study (P < 0.05). PRA rose with upright posture in all groups, but low renin subjects had a blunted response. Nonmodulators and low renin subjects had lower aldosterone levels both supine (P< 0.05) and upright (P< 0.01). However, the aldosterone/PRA increment ratio was increased in low renin subjects (P< 0.01), whereas it was decreased in nonmodulators. Twenty-four-hour urine collections for catecholamine determinations were obtained in a subgroup of the subjects, with nonmodulators showing higher levels of norepinephrine excretion which approached significance (P = 0.08). In vitro experiments using rat and human adrenal glomerulosa cells showed that norepinephrine does not affect aldosterone secretion per se. These observations extend the series of abnormalities observed in nonmodulating hypertension. However, it is likely that the alterations in norepinephrine levels during sodium depetion and upright posture are a secondary event and not linked to the altered aldosterone production in these patients.
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Conlin et al. (1992) conducted an observational in Essential hypertension. Nonmodulating hypertension vs. Normal subjects, modulating hypertension, and low renin hypertension was evaluated on Plasma norepinephrine and aldosterone levels during posture change (p=< 0.05). Patients with nonmodulating hypertension exhibited higher plasma norepinephrine levels during upright posture (P<0.05) and lower aldosterone levels both supine (P<0.05) and upright (P<0.01).
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