Urodilatin resists proteolytic degradation by kidney cortex enzymes that rapidly inactivate atrial natriuretic peptide, suggesting a distinct metabolic profile.
Urodilatin may exhibit prolonged renal activity versus ANP; leaves open human therapeutic relevance pending clinical studies.
Atrial natriuretic peptide (CDD/ANP-99-126) is rapidly inactivated by a membrane preparations from dog kidney cortex. Inactivation occurs by cleavage of the ring structure in the position between Cys-105 and Phe-106. A unique proteolytic product separated by HPLC on reverse-phase column appears as a single peak which elutes prior the intact peptide. In contrast, CDD/ANP-95-126 (urodilatin) which is released from the kidney is not destroyed by proteolysis using an identical membrane preparation.
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Gagelmann et al. (1988) studied this question.
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