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1 Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520, USA
* To whom correspondence should be addressed. E-mail: tong.wang{at}yale.edu.
It has been well documented that low concentrations of angiotensin II (10-11 to 10-10M) stimulate, whereas high concentrations of Ang II (10-8 to 10-5M) inhibit Na+ transport in proximal tubules of rat and rabbit kidneys. Measured Ang II concentration in proximal tubular fluid is in the nanomolar range. In the present study, we investigated the role of protein kinase C (PKC), intracellular Ca2+ and cAMP in modulating the effects of luminal Ang II on Na+ absorption by microperfusion techniques in rabbit S2 proximal tubules in vitro. We confirmed that Ang II (10-9 M) had no change on fluid absorption (Jv); however, fluid absorption increased significantly when 10-9 M Ang II and TMB-8, a blocker of intracellular calcium mobilization, were added together. In contrast, Ang II significantly decreased Jv when PKC was inhibited. When 10-9 M AngII was present together with H-7 and TMB-8, no significant change of Jv occurred. Inhibition of endogenous cAMP activity by a PKA inhibitor did not change either basal or Ang II stimulated fluid absorption. Our results indicate that Ang II regulates Na+ absorption by a cAMP-independent mechanism and that PKC and intracellular calcium both play a critical role in modulating the effects of physiological concentration of AII on proximal tubule transport. The balance between these two cytosolic messengers modulates the effects of AII on fluid absorption in the proximal tubule.
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