Abstract
Atrial natriuretic peptide (ANP) is known to influence NaCl transport in the medullary thick ascending limbs (MAL), where the largest NaCl reabsorption occurs among distal nephron segments in response to arginine vasopressin (AVP). In the present study, we investigated the effect of ANP on bicarbonate (HCO3 (-)) transport in the MAL using an isolated tubule perfusion technique. The HCO3 (-) concentration was measured using free-flow ultramicro-fluorometer. We first observed basal HCO3 (-) reabsorption in both long- and short-looped MALs (lMALs, and sMALs, respectively). AVP inhibited HCO3 (-) reabsorption in both lMALs and sMALs, whereas ANP did not change HCO3 (-) transport. However, in the presence of AVP, ANP restored the HCO3 (-) reabsorption inhibited by AVP both in lMAL and sMAL. The effects of ANP on HCO3 (-) transport was mimicked by cyclic GMP. The mRNA expression level of the vasopressin V2 receptor in lMALs was significantly higher than in sMALs, whereas expression of the V1a receptor was unchanged. In summary, AVP inhibits HCO3 (-) transport, and ANP counteracts the action of AVP on HCO3 (-) transport both in lMALs and sMALs.