Abnormal regulation of proximal tubule renin mRNA in the Dahl/Rapp salt- sensitive rat

Julia E. Tank, Orson W. Moe, William L. Henrich

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Background. The precise pathogenesis of salt-sensitive hypertension in the Dahl rat is unknown. Abnormalities in renal hemodynamics and NaCl handling have been implicated, and may relate to changes in the activity of the intrarenal renin-angiotensin system. Methods. Circulating, juxtaglomerular and intrarenal (glomerular and proximal tubular) renin were studied in Dahl/Rapp salt-sensitive and salt-resistant rats fed with a normal (0.5%) or high (4%) NaCl diet. Circulating and juxtaglomerular renin were assessed by measurement of plasma renin activity and renin secretory rates. Glomerular and proximal tubular renin mRNA were assessed by microdissection and quantitative competitive RT-PCR. Results. Circulating and juxtaglomerular renin were suppressed by high dietary NaCl in salt-sensitive rats (plasma renin activity, 0.5%, 10.9 ± 0.7 vs. 4%, 7.9 ± 0.3 ng/ml/hr, P < 0.05; renin secretory rate, 0.5% 220 ± 32 vs. 4%, 58 ± 5 ng/mg/hr, P < 0.05). Glomerular renin mRNA was also suppressed by the higher salt diet in salt- sensitive animals (0.5%, 411 ± 84 vs. 4%, 67 ± 22 x 103 copies/glomerulus, P < 0.05). In contrast, proximal tubular renin was not suppressed by a high NaCl diet in salt-sensitive animals (0.5%, 13.9 ± 2.7 vs. 4%, 12.1 ± 3.6 x 103 copies/mm tubule, P = NS), but was suppressed in salt-resistant rats (0.5%, 9.5 ± 2.8 vs. 4%, 3.2 ± 1.2 x 103 copies/mm, P < 0.05). Conclusions. Failure to suppress proximal tubular renin in response to high dietary NaCl may result in increased local generation of angiotensin II and enhanced proximal tubular NaCl absorption, and thereby contribute to the generation of salt sensitive hypertension.

Original languageEnglish (US)
Pages (from-to)1608-1616
Number of pages9
JournalKidney International
Volume54
Issue number5
DOIs
StatePublished - 1998

Fingerprint

Inbred Dahl Rats
Renin
Salts
Messenger RNA
Secretory Rate
Diet
Hypertension
Microdissection
Renin-Angiotensin System
Angiotensin II

Keywords

  • Angiotensin II
  • Glomerulus
  • Hypertension
  • Renin-angiotensin system
  • Sodium chloride

ASJC Scopus subject areas

  • Nephrology

Cite this

Abnormal regulation of proximal tubule renin mRNA in the Dahl/Rapp salt- sensitive rat. / Tank, Julia E.; Moe, Orson W.; Henrich, William L.

In: Kidney International, Vol. 54, No. 5, 1998, p. 1608-1616.

Research output: Contribution to journalArticle

Tank, Julia E. ; Moe, Orson W. ; Henrich, William L. / Abnormal regulation of proximal tubule renin mRNA in the Dahl/Rapp salt- sensitive rat. In: Kidney International. 1998 ; Vol. 54, No. 5. pp. 1608-1616.
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abstract = "Background. The precise pathogenesis of salt-sensitive hypertension in the Dahl rat is unknown. Abnormalities in renal hemodynamics and NaCl handling have been implicated, and may relate to changes in the activity of the intrarenal renin-angiotensin system. Methods. Circulating, juxtaglomerular and intrarenal (glomerular and proximal tubular) renin were studied in Dahl/Rapp salt-sensitive and salt-resistant rats fed with a normal (0.5{\%}) or high (4{\%}) NaCl diet. Circulating and juxtaglomerular renin were assessed by measurement of plasma renin activity and renin secretory rates. Glomerular and proximal tubular renin mRNA were assessed by microdissection and quantitative competitive RT-PCR. Results. Circulating and juxtaglomerular renin were suppressed by high dietary NaCl in salt-sensitive rats (plasma renin activity, 0.5{\%}, 10.9 ± 0.7 vs. 4{\%}, 7.9 ± 0.3 ng/ml/hr, P < 0.05; renin secretory rate, 0.5{\%} 220 ± 32 vs. 4{\%}, 58 ± 5 ng/mg/hr, P < 0.05). Glomerular renin mRNA was also suppressed by the higher salt diet in salt- sensitive animals (0.5{\%}, 411 ± 84 vs. 4{\%}, 67 ± 22 x 103 copies/glomerulus, P < 0.05). In contrast, proximal tubular renin was not suppressed by a high NaCl diet in salt-sensitive animals (0.5{\%}, 13.9 ± 2.7 vs. 4{\%}, 12.1 ± 3.6 x 103 copies/mm tubule, P = NS), but was suppressed in salt-resistant rats (0.5{\%}, 9.5 ± 2.8 vs. 4{\%}, 3.2 ± 1.2 x 103 copies/mm, P < 0.05). Conclusions. Failure to suppress proximal tubular renin in response to high dietary NaCl may result in increased local generation of angiotensin II and enhanced proximal tubular NaCl absorption, and thereby contribute to the generation of salt sensitive hypertension.",
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T1 - Abnormal regulation of proximal tubule renin mRNA in the Dahl/Rapp salt- sensitive rat

AU - Tank, Julia E.

AU - Moe, Orson W.

AU - Henrich, William L.

PY - 1998

Y1 - 1998

N2 - Background. The precise pathogenesis of salt-sensitive hypertension in the Dahl rat is unknown. Abnormalities in renal hemodynamics and NaCl handling have been implicated, and may relate to changes in the activity of the intrarenal renin-angiotensin system. Methods. Circulating, juxtaglomerular and intrarenal (glomerular and proximal tubular) renin were studied in Dahl/Rapp salt-sensitive and salt-resistant rats fed with a normal (0.5%) or high (4%) NaCl diet. Circulating and juxtaglomerular renin were assessed by measurement of plasma renin activity and renin secretory rates. Glomerular and proximal tubular renin mRNA were assessed by microdissection and quantitative competitive RT-PCR. Results. Circulating and juxtaglomerular renin were suppressed by high dietary NaCl in salt-sensitive rats (plasma renin activity, 0.5%, 10.9 ± 0.7 vs. 4%, 7.9 ± 0.3 ng/ml/hr, P < 0.05; renin secretory rate, 0.5% 220 ± 32 vs. 4%, 58 ± 5 ng/mg/hr, P < 0.05). Glomerular renin mRNA was also suppressed by the higher salt diet in salt- sensitive animals (0.5%, 411 ± 84 vs. 4%, 67 ± 22 x 103 copies/glomerulus, P < 0.05). In contrast, proximal tubular renin was not suppressed by a high NaCl diet in salt-sensitive animals (0.5%, 13.9 ± 2.7 vs. 4%, 12.1 ± 3.6 x 103 copies/mm tubule, P = NS), but was suppressed in salt-resistant rats (0.5%, 9.5 ± 2.8 vs. 4%, 3.2 ± 1.2 x 103 copies/mm, P < 0.05). Conclusions. Failure to suppress proximal tubular renin in response to high dietary NaCl may result in increased local generation of angiotensin II and enhanced proximal tubular NaCl absorption, and thereby contribute to the generation of salt sensitive hypertension.

AB - Background. The precise pathogenesis of salt-sensitive hypertension in the Dahl rat is unknown. Abnormalities in renal hemodynamics and NaCl handling have been implicated, and may relate to changes in the activity of the intrarenal renin-angiotensin system. Methods. Circulating, juxtaglomerular and intrarenal (glomerular and proximal tubular) renin were studied in Dahl/Rapp salt-sensitive and salt-resistant rats fed with a normal (0.5%) or high (4%) NaCl diet. Circulating and juxtaglomerular renin were assessed by measurement of plasma renin activity and renin secretory rates. Glomerular and proximal tubular renin mRNA were assessed by microdissection and quantitative competitive RT-PCR. Results. Circulating and juxtaglomerular renin were suppressed by high dietary NaCl in salt-sensitive rats (plasma renin activity, 0.5%, 10.9 ± 0.7 vs. 4%, 7.9 ± 0.3 ng/ml/hr, P < 0.05; renin secretory rate, 0.5% 220 ± 32 vs. 4%, 58 ± 5 ng/mg/hr, P < 0.05). Glomerular renin mRNA was also suppressed by the higher salt diet in salt- sensitive animals (0.5%, 411 ± 84 vs. 4%, 67 ± 22 x 103 copies/glomerulus, P < 0.05). In contrast, proximal tubular renin was not suppressed by a high NaCl diet in salt-sensitive animals (0.5%, 13.9 ± 2.7 vs. 4%, 12.1 ± 3.6 x 103 copies/mm tubule, P = NS), but was suppressed in salt-resistant rats (0.5%, 9.5 ± 2.8 vs. 4%, 3.2 ± 1.2 x 103 copies/mm, P < 0.05). Conclusions. Failure to suppress proximal tubular renin in response to high dietary NaCl may result in increased local generation of angiotensin II and enhanced proximal tubular NaCl absorption, and thereby contribute to the generation of salt sensitive hypertension.

KW - Angiotensin II

KW - Glomerulus

KW - Hypertension

KW - Renin-angiotensin system

KW - Sodium chloride

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