Previous studies have shown that in proximal and distal tubule nephron segments, peritubular ANG II stimulates sodium chloride transport. However, ANG II inhibits chloride transport in the medullary thick ascending limb (mTAL). Because ANG II and catecholamines are both stimulated by a decrease in extracellular fluid volume, the purpose of this study was to examine whether there was an interaction between ANG II and catecholamines to mitigate the inhibition in chloride transport by ANG II. In isolated perfused rat mTAL, 10-8 M bath ANG II inhibited transport (from a basal transport rate of 165.6 ± 58.8 to 58.8 ± 29.4 pmol•mm-1 •min-1; P < 0.01). Bath norepinephrine stimulated chloride transport (from a basal transport rate of 298.1 ± 31.7 to 425.2 ± 45.8 pmol · mm-1 · min-1; P < 0.05) and completely prevented the inhibition in chloride transport by ANG II. The stimulation of chloride transport by norepinephrine was mediated entirely by its β-adrenergic effect; however, both the β- and α-adrenergic agonists isoproterenol and phenylephrine prevent the ANG II-mediated inhibition in chloride transport. In the presence of 10-5 M propranolol, the effect of norepinephrine to prevent the inhibition of chloride transport by ANG II was still present. These data are consistent with an interaction of both α- and β-catecholamines and ANG II on net chloride transport in the mTAL.
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|State||Published - Apr 2010|
ASJC Scopus subject areas
- Physiology (medical)