Project: Research project

Project Details


The original aims of this grant were to investigate the effects of
vasoactive peptides (angiotensin and bradykinin) on renal tubule
ion and water transport. In work funded by this grant we have
found the following. 1) Bradykinin, via prostaglandins, inhibits
the hydroosmotic effect of vasopressin in the cortical collecting
tubule at a pre-cyclic AMP level, probably at adenylate cyclase,
but has no effect on Na transport. 2) Beta-adrenergic agonists
via cAMP stimulate both Cl-HCO3 and Cl self-exchange in the
cortical collecting tubule. 3) Cl exit across the basolateral
membrane in this segment occurs conductively. 4) The red cell
anion exchange protein, band 3, is present at the basolateral
membrane of a subpopulation of collecting tubule cells, where it
probably mediates Cl-HCO3 exchange.

In the next two years we will investigate three hypothetical
mechanisms by which beta-agonists and cAMP stimulate anion
transport: 1) cAMP stimulates H+ secretion by stimulating the
insertion of H+ pump-bearing vesicles into the cytoplasmic
membrane; 2) cAMP increases a basolateral Cl conductance; 3)
cAMP causes the insertion of a Cl-HCO3 exchanger into the
cytoplasmic membrane. Secondly, we plan to redirect our goals
slightly to the subject of chronic regulation of anion transport by
in vivo acid-base disturbances. Using the combined techniques
of tubule microperfusion and cytochemistry, we will address two
opposing hypothetical mechanisms for reversal of cortical
collecting duct HC03 transport: 1) transport elements within a
given anion-transporting cell reverse their polarity; or 2)
transport of anions is regulated up or down within two different
types of vectorally-fixed anion-transporting cells.
Effective start/end date12/31/891/1/90


  • Nephrology
  • Medicine(all)


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