Project: Research project

Project Details


The renin-angiotensin system (RAS) and kallikrein-kinin system (KKS) may
control renal salt and water excretion by acting intrarenally. Preliminary
data show that, in vitro, angiotensin II (AII) directly alters proximal
tubule Na transport, and that lysyl-bradykinin (LBK) inhibits ADH action in
the cortical collecting tubule (CCT). This proposal will further address
these questions: 1) Does AII specifically stimulate NaCl transport? If
so, is this effect on electroneutral, electrogenic, or passive NaCl
transport? What is the role of calcium in AII's action? 2) Does AII alter
ion and water transport in the CCT, and, if so, are calcium cAMP or
prostaglandins involved? 3) Does LBK effect Na, K, Cl, or HCO3 transport
in the CCT? If so, are prostaglandins involved? 4) Which cell type in the
CCT responds to LBK? These studies have significant potential clinical relevance. The normal
natriuresis and diuresis seen with elevated perfusion pressure ("pressure
natriuresis") is abnormal in some patients with essential hypertension.
The RAS and KKS are probably important in the normal response, and may play
a role in the abnormal one. The applicant is committed to developing a productive career in academic
medicine and membrane transport research. The present environment is ideal
for such growth. The Department of Medicine and the Renal Division
actively and carefully foster growth of new faculty. Most importantly, the
applicant's laboratory is located within a multidisciplinary group of
established epithelial transport investigators. The cross-fertilization of
ideas and the standards of scientific excellence present in this
environment should permit the applicant to rapidly achieve independence.
Effective start/end date12/31/8912/31/89


  • Medicine(all)
  • Nephrology


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