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Urinary sodium excretion in chronic caval dogs after combined infusions of mannitol and ANP.

We studied the natriuretic effects of a combined mannitol and atrial natriuretic peptide (ANP) infusion in chronic caval dogs (TIVC) either responsive or unresponsive to an initial ANP infusion (75 ng.kg-1.min-1). The increment in urinary Na+ excretion (delta UNaV) to the initial ANP infusion in 11 TIVC responders was 127 and 1 mu eq/min in 7 nonresponders. A modest mannitol dose was then infused so as to augment distal Na+ delivery to the distal nephron but not flood the terminal inner medullary collecting duct (IMCD) with enormous quantities of salt and water. After mannitol, UNaV was 26 +/- 8 mu eq/min in TIVC responders and 24 +/- 4 mu eq/min in nonresponders. In these two groups of dogs, delta UNaV after manitol was 13 and 10 mu eq/min, respectively, from the previous experimental phase. During this stable mannitol-induced modest natriuresis, ANP was reinfused at initial dose levels. In TIVC responders, delta UNaV was 186 mu eq/min, a value greater than that obtained initially (P < 0.05), and delta UNaV in nonresponders was now 52 mu eq/min (P < 0.05). Because control and postmanitol UNaV was equivalent for each group, in the face of similar levels of glomerular filtration rate, blood pressure, and renal perfusion, it is difficult to conclude that only augmented delivery of Na+ to the IMCD converted TIVC nonresponders into responding dogs after mannitol and ANP. Other modulating factors may be involved.