Key result
Administration of ANP-specific antiserum significantly impaired the return to normal sodium balance and augmented kaliuresis in DOCA-treated rats, suggesting ANP mediates mineralocorticoid escape.
Why the study?
Does passive immunization with ANP-specific antiserum impair the natriuretic response during mineralocorticoid escape in DOCA-treated rats?
Does passive immunization with ANP-specific antiserum impair the natriuretic response during mineralocorticoid escape in DOCA-treated rats?
Passive immunization with ANP-specific antiserum impairs the return to normal sodium balance in DOCA-treated rats, suggesting plasma ANP plays a key role in mineralocorticoid escape.
Supports ANP mediation of mineralocorticoid escape in rats; leaves open translation to human physiology or therapy.
To elucidate the physiological role of atrial natriuretic peptide (ANP) in plasma during mineralocorticoid escape, we investigated the effects of passive immunization with ANP-specific antiserum on deoxycorticosterone (DOCA)-treated rats. Sodium was retained in excess of intake during the first day after treatment with DOCA, and sodium balance returned to control values by the second day, whereas the excretion of potassium exceeded the intake during all days after DOCA treatment. These changes in electrolyte balance were associated with a significant increase in plasma levels of ANP. Administration of ANP-specific antiserum significantly impaired the return to normal sodium balance as well as the augmented kaliuresis that were observed on the second day after injection of DOCA. No significant effect was observed on either sodium or potassium balance after the injection of normal rabbit serum. These results suggest that plasma ANP plays an important role in mineralocorticoid escape.
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Zeng et al. (1991) studied Mineralocorticoid escape. ANP-specific antiserum vs. Normal rabbit serum was evaluated on Return to normal sodium balance and augmented kaliuresis. Administration of ANP-specific antiserum significantly impaired the return to normal sodium balance and augmented kaliuresis in DOCA-treated rats, suggesting ANP mediates mineralocorticoid escape.
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