Atrial natriuretic factor inhibits metoclopramide stimulated aldosterone release in man.

Lang, Chim C.; Rahman, Abdul Rashid Abdul; Struthers, Allan D.

doi:10.1111/j.1365-2125.1991.tb05612.x

Cited by 3 publications

(1 citation statement)

References 25 publications

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“…30 It is therefore possible that training augmented the effect of ACTH on aldosterone production during standing; however, the relationship of ACTH pulsations to adrenal responsiveness is complex and beyond the scope of this study. Since dopamine suppresses aldosterone secretion, while atrial natriuretic factor (ANF) is an antagonist of aldosterone secretion, 31–33 training-induced changes in dopamine and/or ANF levels also have contributed to the increased aldosterone-to-renin ratio in POTS patients. Unfortunately, we did not measure ACTH, dopamine, and ANF.…”

Section: Discussionmentioning

confidence: 99%

Exercise Training Versus Propranolol in the Treatment of the Postural Orthostatic Tachycardia Syndrome

et al. 2011

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We have recently found that exercise training is effective in the treatment of the Postural Orthostatic Tachycardia Syndrome (POTS). Whether this non-drug treatment is superior to “standard” drug therapies, such as β-blockade, is unknown. We tested the hypothesis that exercise training but not β-blockade treatment improves symptoms, hemodynamics, and renal-adrenal responses in POTS patients. Nineteen patients (18 women, 1 man) completed a double-blind drug trial (propranolol or placebo) for 4 weeks, followed by 3 months of exercise training. Fifteen age-matched healthy individuals (14 women, 1 man) served as controls. A 2-hour standing test was performed before and after drug treatment and training. Hemodynamics, catecholamines, plasma renin activity, and aldosterone were measured supine and during 2-hour standing. We found that both propranolol and training significantly lowered standing heart rate. Standing cardiac output was lowered after propranolol treatment (P=0.01), but was minimally changed after training. The aldosterone-to-renin ratio during 2-hour standing remained unchanged after propranolol treatment [4.1±1.7 (SD) pre vs. 3.9±2.0 post, P=0.46), but modestly increased after training (5.2±2.9 vs. 6.5±3.0, P=0.05). Plasma catecholamines were not affected by propranolol or training. Patient quality of life, assessed using the 36-item Short Form Health Survey, was improved after training (physical functioning score 33±10 pre vs. 50±9 post; social functioning score 37±9 vs. 48±6, both P<0.01), but not after propranolol treatment (34±10 vs. 36±11, P=0.63; 39±7 vs. 39±5, P=0.73). These results suggest that for patients with POTS, exercise training is superior to propranolol at restoring upright hemodynamics, normalizing renal-adrenal responsiveness, and improving quality of life.

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Section: Discussionmentioning

confidence: 99%