Renal functional derangements in hypertension

B. G. Zimmerman, W. J. Arendshorst, G. F. DiBona, T. H. Hostetter, D. W. Ploth, Leopoldo Raij

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

The altered function and hemodynamic characteristics of the kidney or kidneys of the experimental hypertensive animals reported here may participate in the etiology and/or maintenance of the hypertensive state. A depression of GFR and enhanced sodium reabsorption in the SHR owing to hemodynamic, membrane permeability, and neural influences appear to be important in this form of experimental hypertension. In Goldblatt hypertension the renin-angiotensin system causes both vasoconstriction and increased proximal fluid reabsorption in the contralateral kidney of the two-kidney, one-clip Goldblatt hypertensive rat and dog. These factors could lead to the establishment of a long-term pressor influence in these animals. Protein in the diet has been clearly shown to worsen the glomerular lesions seen in several forms of experimental hypertension - those caused by reduced renal mass, DOCA-salt, and constriction of the renal artery. However, only in the DOCA-salt model does protein seem to accentuate the increase in blood pressure. On the other hand, glomerular damage seen in these hypertension models is also partly a function of the increased pressure. In the salt-sensitive Dahl rat with glomerulonephritis, sodium through its hypertensive effect contributes to renal damage. In these rats glomerular injury is aggravated by high dietary protein but is not prevented by protein restriction.

Original languageEnglish
Pages (from-to)2661-2664
Number of pages4
JournalFederation Proceedings
Volume45
Issue number12
StatePublished - Dec 1 1986
Externally publishedYes

Fingerprint

Hypertension
Kidney
Desoxycorticosterone Acetate
Salts
Hemodynamics
Sodium
Inbred Dahl Rats
Renovascular Hypertension
Proteins
Dietary Proteins
Renal Artery
Renin-Angiotensin System
Glomerulonephritis
Vasoconstriction
Surgical Instruments
Constriction
Permeability
Maintenance
Dogs
Diet

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Zimmerman, B. G., Arendshorst, W. J., DiBona, G. F., Hostetter, T. H., Ploth, D. W., & Raij, L. (1986). Renal functional derangements in hypertension. Federation Proceedings, 45(12), 2661-2664.

Renal functional derangements in hypertension. / Zimmerman, B. G.; Arendshorst, W. J.; DiBona, G. F.; Hostetter, T. H.; Ploth, D. W.; Raij, Leopoldo.

In: Federation Proceedings, Vol. 45, No. 12, 01.12.1986, p. 2661-2664.

Research output: Contribution to journalArticle

Zimmerman, BG, Arendshorst, WJ, DiBona, GF, Hostetter, TH, Ploth, DW & Raij, L 1986, 'Renal functional derangements in hypertension', Federation Proceedings, vol. 45, no. 12, pp. 2661-2664.
Zimmerman BG, Arendshorst WJ, DiBona GF, Hostetter TH, Ploth DW, Raij L. Renal functional derangements in hypertension. Federation Proceedings. 1986 Dec 1;45(12):2661-2664.
Zimmerman, B. G. ; Arendshorst, W. J. ; DiBona, G. F. ; Hostetter, T. H. ; Ploth, D. W. ; Raij, Leopoldo. / Renal functional derangements in hypertension. In: Federation Proceedings. 1986 ; Vol. 45, No. 12. pp. 2661-2664.
@article{97d87c30a8b74993af1fdf4fb6dadbc5,
title = "Renal functional derangements in hypertension",
abstract = "The altered function and hemodynamic characteristics of the kidney or kidneys of the experimental hypertensive animals reported here may participate in the etiology and/or maintenance of the hypertensive state. A depression of GFR and enhanced sodium reabsorption in the SHR owing to hemodynamic, membrane permeability, and neural influences appear to be important in this form of experimental hypertension. In Goldblatt hypertension the renin-angiotensin system causes both vasoconstriction and increased proximal fluid reabsorption in the contralateral kidney of the two-kidney, one-clip Goldblatt hypertensive rat and dog. These factors could lead to the establishment of a long-term pressor influence in these animals. Protein in the diet has been clearly shown to worsen the glomerular lesions seen in several forms of experimental hypertension - those caused by reduced renal mass, DOCA-salt, and constriction of the renal artery. However, only in the DOCA-salt model does protein seem to accentuate the increase in blood pressure. On the other hand, glomerular damage seen in these hypertension models is also partly a function of the increased pressure. In the salt-sensitive Dahl rat with glomerulonephritis, sodium through its hypertensive effect contributes to renal damage. In these rats glomerular injury is aggravated by high dietary protein but is not prevented by protein restriction.",
author = "Zimmerman, {B. G.} and Arendshorst, {W. J.} and DiBona, {G. F.} and Hostetter, {T. H.} and Ploth, {D. W.} and Leopoldo Raij",
year = "1986",
month = "12",
day = "1",
language = "English",
volume = "45",
pages = "2661--2664",
journal = "Federation Proceedings",
issn = "0014-9446",
number = "12",

}

TY - JOUR

T1 - Renal functional derangements in hypertension

AU - Zimmerman, B. G.

AU - Arendshorst, W. J.

AU - DiBona, G. F.

AU - Hostetter, T. H.

AU - Ploth, D. W.

AU - Raij, Leopoldo

PY - 1986/12/1

Y1 - 1986/12/1

N2 - The altered function and hemodynamic characteristics of the kidney or kidneys of the experimental hypertensive animals reported here may participate in the etiology and/or maintenance of the hypertensive state. A depression of GFR and enhanced sodium reabsorption in the SHR owing to hemodynamic, membrane permeability, and neural influences appear to be important in this form of experimental hypertension. In Goldblatt hypertension the renin-angiotensin system causes both vasoconstriction and increased proximal fluid reabsorption in the contralateral kidney of the two-kidney, one-clip Goldblatt hypertensive rat and dog. These factors could lead to the establishment of a long-term pressor influence in these animals. Protein in the diet has been clearly shown to worsen the glomerular lesions seen in several forms of experimental hypertension - those caused by reduced renal mass, DOCA-salt, and constriction of the renal artery. However, only in the DOCA-salt model does protein seem to accentuate the increase in blood pressure. On the other hand, glomerular damage seen in these hypertension models is also partly a function of the increased pressure. In the salt-sensitive Dahl rat with glomerulonephritis, sodium through its hypertensive effect contributes to renal damage. In these rats glomerular injury is aggravated by high dietary protein but is not prevented by protein restriction.

AB - The altered function and hemodynamic characteristics of the kidney or kidneys of the experimental hypertensive animals reported here may participate in the etiology and/or maintenance of the hypertensive state. A depression of GFR and enhanced sodium reabsorption in the SHR owing to hemodynamic, membrane permeability, and neural influences appear to be important in this form of experimental hypertension. In Goldblatt hypertension the renin-angiotensin system causes both vasoconstriction and increased proximal fluid reabsorption in the contralateral kidney of the two-kidney, one-clip Goldblatt hypertensive rat and dog. These factors could lead to the establishment of a long-term pressor influence in these animals. Protein in the diet has been clearly shown to worsen the glomerular lesions seen in several forms of experimental hypertension - those caused by reduced renal mass, DOCA-salt, and constriction of the renal artery. However, only in the DOCA-salt model does protein seem to accentuate the increase in blood pressure. On the other hand, glomerular damage seen in these hypertension models is also partly a function of the increased pressure. In the salt-sensitive Dahl rat with glomerulonephritis, sodium through its hypertensive effect contributes to renal damage. In these rats glomerular injury is aggravated by high dietary protein but is not prevented by protein restriction.

UR - http://www.scopus.com/inward/record.url?scp=0023025394&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023025394&partnerID=8YFLogxK

M3 - Article

C2 - 3770216

AN - SCOPUS:0023025394

VL - 45

SP - 2661

EP - 2664

JO - Federation Proceedings

JF - Federation Proceedings

SN - 0014-9446

IS - 12

ER -