Open AccessEffects of Atrial Natriuretic Peptide on Bicarbonate Transport in Long- and Short-Looped Medullary Thick Ascending Limbs of Rats
Author(s) -
Hiroshi oguchi,
Izumi Yokoyama,
Yushi Nakayama,
Takanobu Matsuzaki,
Yukiko Yasuoka,
Takeaki Inoue,
Hideki Inoue,
Tomohiko Mouri,
Katsumasa Kawahara,
Hideyuki Saya,
Kimio Tomita
Publication year - 2013
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0083146
Subject(s) - vasopressin , medicine , reabsorption , endocrinology , atrial natriuretic peptide , nephron , chemistry , bicarbonate , receptor , arginine vasopressin receptor 2 , kidney , biology , antagonist
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 (HCO 3 − ) transport in the MAL using an isolated tubule perfusion technique. The HCO 3 − concentration was measured using free-flow ultramicro-fluorometer. We first observed basal HCO 3 − reabsorption in both long- and short-looped MALs (lMALs, and sMALs, respectively). AVP inhibited HCO 3 − reabsorption in both lMALs and sMALs, whereas ANP did not change HCO 3 − transport. However, in the presence of AVP, ANP restored the HCO 3 − reabsorption inhibited by AVP both in lMAL and sMAL. The effects of ANP on HCO 3 − 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 HCO 3 − transport, and ANP counteracts the action of AVP on HCO 3 − transport both in lMALs and sMALs.