Abstract

Quantitative adjustments in the rat of renal sodium excretion constitute the major defense of man's extracellular fluid volume against the potentially disruptive effects of variations in the intake and extrarenal loss of sodium. Derangements of this renal homeostatic mechanism are a hallmark of diseases characterized by the formation of ascites and/or edema. Although effective therapeutic means are available for manipulating the rate of sodium excretion in the majority of edematous patients, considerable ignorance remains as to the mechanisms responsible for the retention of sodium.
The aim of the studies under current investigation are: (1) To provide new information concerning the intrarenal regulation of sodium excretion in the rat using conventional clearance and microperfusion-micropuncture techniques and (2) To provide new information concerning the effects of experimentally induced alterations in renal hemodynamics on sodium and water handling by both the intact and isolated kidney of the rat. Such information will prove useful for an understanding of the normal mechanisms controlling sodium excretion, as well as for an understanding of the mechanisms of pathological sodium retention frequently encountered in clinical medicine.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
5R01DK035930-02
Application #
3234218
Study Section
(SSS)
Project Start
1984-12-01
Project End
1988-11-30
Budget Start
1985-12-01
Budget End
1986-11-30
Support Year
2
Fiscal Year
1986
Total Cost
Indirect Cost

  Institution

Name
Brigham and Women's Hospital
Department
Type
DUNS #
071723621
City
Boston
State
MA
Country
United States
Zip Code
02115

  Publications

Totsune, K; Mackenzie, H S; Totsune, H et al. (1998) Upregulation of atrial natriuretic peptide gene expression in remnant kidney of rats with reduced renal mass. J Am Soc Nephrol 9:1613-9
Kojima, R; Randall, J; Brenner, B M et al. (1996) Osmotic stress protein 94 (Osp94). A new member of the Hsp110/SSE gene subfamily. J Biol Chem 271:12327-32
Zhang, P L; Mackenzie, H S; Totsune, K et al. (1995) Renal effects of high-dose natriuretic peptide receptor blockade in rats with congestive heart failure. Circ Res 77:1240-5
King, A J (1995) Nitric oxide and the renal hemodynamic response to proteins. Semin Nephrol 15:405-14
Mackenzie, H S; Azuma, H; Rennke, H G et al. (1995) Renal mass as a determinant of late allograft outcome: insights from experimental studies in rats. Kidney Int Suppl 52:S38-42
Heemann, U W; Azuma, H; Tullius, S G et al. (1994) The contribution of reduced functioning mass to chronic kidney allograft dysfunction in rats. Transplantation 58:1317-22
Zhang, P L; Mackenzie, H S; Troy, J L et al. (1994) Effects of an atrial natriuretic peptide receptor antagonist on glomerular hyperfiltration in diabetic rats. J Am Soc Nephrol 4:1564-70
Mackenzie, H S; Tullius, S G; Heemann, U W et al. (1994) Nephron supply is a major determinant of long-term renal allograft outcome in rats. J Clin Invest 94:2148-52
Zhang, P L; Jimenez, W; Mackenzie, H S et al. (1994) HS-142-1, a potent antagonist of natriuretic peptides in vitro and in vivo. J Am Soc Nephrol 5:1099-105
Zhang, P L; Mackenzie, H S; Troy, J L et al. (1994) Effects of natriuretic peptide receptor inhibition on remnant kidney function in rats. Kidney Int 46:414-20

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