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Medizinische Poliklinik and the Department of Clinical Chemistry, University of Berne Berne, Switzerland Department of Pharmacology, University of Heidelberg Heidelberg, West Germany
Address all correspondence and requests for reprints to: Peter Weidmann,M.D., Medizinische Universitaets-Poliklinik, Freiburgstrasse 3,3010 Berne, Switzerland.
Endogenous plasma concentrations of human atrial natriuretic peptide (
hANP) as well as effects of synthetic
hANP on some cardiovascular, endocrine, and renal excretory parameters were investigated in 10 normal subjects during sodium (Na+) intakes of 17, 140, and 310 mmol/day, respectively. Plasma hANP was slightly but not significantly higher after 5 days of normal or high sodium intake than after 5 days of low sodium intake [54 ± 13, 46 ± 8, and 37 ± 5 (mean ± SEM) pg/ml, respectively].
hANP infused at 0.1µg/kg-min during all Na+ intakes produced a similar fall in diastolic blood pressure (P < 0.001) and rise in heart rate (P < 0.001), a comparable percent increase in plasma norepinephrine (P < 0.001), and a reduction in plasma cortisol and aldosterone (P < 0.01-0.001) despite raised renin activity (P < 0.05-0.001) and unchanged plasma electrolytes.
hANP-induced plasma volume contraction, diuresis, and natriuresis were greater during high than low Na+ intake (P < 0.01-0.001). Therefore, in normal man different Na+ intakes are accompanied by marked modifications in renal excretory responsiveness to
hANP. Regardless of sodium intake,
hANP can promote BP reduction and hemoconcentration, elicit reflex (?) sympathetic activation, and depress basal circulating aldosterone and cortisol levels in the face of an activated renin system.
* This work was supported in part by the Swiss National Foundation and a research grant from the Ciba-Geigy Corp. (Basel, Switzerland).
Received August 9, 1985.
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