Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
3R01DK040253-03S1
Application #
3240429
Study Section
Experimental Cardiovascular Sciences Study Section (ECS)
Project Start
1988-07-01
Project End
1992-08-31
Budget Start
1990-09-01
Budget End
1991-08-31
Support Year
3
Fiscal Year
1990
Total Cost
Indirect Cost

  Institution

Name
University of Tennessee Health Science Center
Department
Type
Schools of Medicine
DUNS #
941884009
City
Memphis
State
TN
Country
United States
Zip Code
38163

  Publications

Kramer, R E; Robinson, T V; Schneider, E G et al. (2000) Direct modulation of basal and angiotensin II-stimulated aldosterone secretion by hydrogen ions. J Endocrinol 166:183-94
Wang, W; Schneider, E G (1997) Potassium-induced aldosterone secretion involves a Cl(-)-dependent mechanism. Am J Physiol 272:R183-7
Hayama, N; Wang, W; Schneider, E G (1995) Osmolality-induced changes in aldosterone secretion involve a chloride-dependent process. Am J Physiol 268:R8-13
Hayama, N; Wang, W; Robinson, T V et al. (1993) Osmolality and potassium cause alterations in the volume of glomerulosa cells. Endocrinology 132:1230-4
Wang, W; Hayama, N; Robinson, T V et al. (1992) Effect of osmolality on cytosolic free calcium and aldosterone secretion. Am J Physiol 262:E68-75
Schneider, E G; Robinson, T V (1991) Insulin prevents glucose induced inhibition of angiotensin II-stimulated aldosterone secretion. Horm Metab Res 23:205-8
Kramer, R E (1991) N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) does not modify the angiotensin II-stimulated calcium signal in cultured bovine glomerulosa cells. Life Sci 48:27-35
Radke, K J; Clendenin 3rd, R E; Taylor Jr, R E et al. (1989) Calcium dependence of osmolality-, potassium-, and angiotensin II-induced aldosterone secretion. Am J Physiol 256:E760-4