Why the study?
Do posture changes and saline infusion alter atrial natriuretic peptide levels differently in patients with Bartter's syndrome compared to healthy controls?
Do posture changes and saline infusion alter atrial natriuretic peptide levels differently in patients with Bartter's syndrome compared to healthy controls?
Atrial natriuretic peptide does not appear to play a causal role in Bartter's syndrome, as its levels and responses to physiological stimuli are similar to healthy controls.
ANP unlikely causal in Bartter's syndrome; leaves open other natriuretic pathways in renal salt handling.
In order to explore the role of atrial natriuretic peptide (ANP) in Bartter's syndrome, five patients and five healthy controls matched for age and sex were studied. The study was designed to stimulate and suppress ANP secretion by manipulation of right atrial pressure with different body positions and mild volume expansion with saline. Other vasoactive hormones were also measured, and heart rate and blood pressure were recorded at 5-min intervals. Plasma ANP levels increased after head-down tilt and returned to baseline in the upright position. Infusion of saline failed to increase plasma ANP both in the control group and in four of the patients. No significant differences were found in plasma atrial natriuretic peptide concentrations between both groups. In view of previously reported elevated plasma ANP levels, Bartter's syndrome may be heterogeneous in this respect. Plasma renin activity was higher in the patients, but plasma aldosterone, adrenaline and noradrenaline were similar in both groups. Mean arterial blood pressure was similar in both groups, but rose significantly in the upright position in the control group only, while changes in heart rate were similar in both groups. We conclude that atrial natriuretic peptide does not seem to play a causal role in our patients with Bartter's syndrome.
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Doorenbos et al. (1988) studied this question.
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