The proposed research is designed to determine the physiological and pathophysiological factors involved in the interaction between dietary sodium intake and environmental stress in relation to the pathogenesis of hypertension. A major focus is that dietary sodium intake modulates the efferent renal sympathetic nerve activity (ERSNA) response to environmental stress and that the resultant changes in renal hemodynamic and excretory function contribute importantly to the development, maintenance and exacerbation of hypertension. Using techniques for measurements of ERSNA and renal function in conscious hypertensive rate models, the interaction between genetic and environmental (dietary sodium/potassium intake, environmental stress) factors will be examined.
Specific Aim 1 will determine if the sensitivity of central nervous system alpha-2 adrenoceptors involved in the regulation of the ERSNA response to environmental stress is affected by changes in dietary sodium intake.
Specific Aims 2 and 3 will determine if acute exposure to environmental stress increases ERSNA and decreases urinary sodium excretion in Dahl R/S and Borderline Hypertensive Rats (BHR).
Specific Aim 4 will determine if high dietary sodium intake modulates the ERSNA and renal hemodynamic/excretory response to environmetal stress in BHR.
Specific Aim 5 will determine if the enhanced ERSNA and renal hemodynamic/excretory responses to environmental stress in SHR on a high dietary sodium intake are dependent on increases in total body sodium and fluid volumes.
Specific Aim 6 will determine if dietary potassium supplementation modulates the ERSNA and renal hemodynamic/excretory responses to environmental stress in experimental forms of hypertension.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL040222-04
Application #
3357346
Study Section
Special Emphasis Panel (SRC (08))
Project Start
1987-09-30
Project End
1992-07-31
Budget Start
1990-08-01
Budget End
1991-07-31
Support Year
4
Fiscal Year
1990
Total Cost
Indirect Cost
Name
University of Iowa
Department
Type
Schools of Medicine
DUNS #
041294109
City
Iowa City
State
IA
Country
United States
Zip Code
52242
DiBona, G F; Jones, S Y (1994) Role of endogenous peripheral opioid mechanisms in renal function. J Am Soc Nephrol 4:1792-7
DiBona, G F; Sawin, L L (1994) Reflex regulation of renal nerve activity in cardiac failure. Am J Physiol 266:R27-39
DiBona, G F (1994) Hemodynamic support: volume management and pharmacological cardiovascular support. Semin Nephrol 14:33-40
Hinojosa-Laborde, C; Jones, S Y; DiBona, G F (1994) Hemodynamics and baroreflex function in rats with nephrotic syndrome. Am J Physiol 267:R953-64
Goligorsky, M S; DiBona, G F (1993) Pathogenetic role of Arg-Gly-Asp-recognizing integrins in acute renal failure. off. Proc Natl Acad Sci U S A 90:5700-4
Kapusta, D R; Obih, J C; Dibona, G F (1993) Central mu opioid receptor-mediated changes in renal function in conscious rats. J Pharmacol Exp Ther 265:134-43
Kopp, U C; DiBona, G F (1993) Neural regulation of renin secretion. Semin Nephrol 13:543-51
DiBona, G F; Jones, S Y (1993) Cardiac volume receptor reflex in borderline hypertensive rats. Hypertension 21:222-6
DiBona, G F; Jones, S Y (1992) Effect of acute NaCl depletion on NaCl-sensitive hypertension in borderline hypertensive rats. J Hypertens 10:125-9
Petersen, J S; DiBona, G F (1992) Ganglionic blockade with tetraethylammonium in conscious rats. Hypertension 19:814-7

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