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Connecting tubule glomerular feedback in hypertension
Hong Wang1, Martin A D'Ambrosio, Jeffrey L Garvin
1Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI 48202. ocarret1@hfhs.org.
Hypertension (Dallas, Tex. : 1979)
|August 21, 2013
Summary
Dahl salt-sensitive rats exhibit impaired tubule glomerular feedback (TGF) and increased connecting TGF (CTGF) compared to hypertensive rats. High salt intake exacerbates these issues, leading to higher glomerular pressure and injury in Dahl SS rats.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Renal Pathophysiology
Background:
- Dahl salt-sensitive (SS) rats show increased glomerular injury with high salt intake compared to spontaneously hypertensive rats.
- Glomerular capillary pressure, a key factor in injury, is regulated by tubule glomerular feedback (TGF) and connecting TGF (CTGF).
Purpose of the Study:
- To investigate differences in TGF response and resetting between Dahl SS rats and spontaneously hypertensive rats.
- To determine the role of increased CTGF in the impaired renal response to high salt in Dahl SS rats.
Main Methods:
- In vivo micropuncture techniques were used to measure stop-flow pressure, a surrogate for glomerular capillary pressure.
- Tubule glomerular feedback (TGF) response, TGF resetting, and CTGF were quantified in normal and high-salt conditions.
- CTGF was assessed by inhibiting its action with benzamil.
Main Results:
- Dahl SS rats demonstrated significantly lower TGF responses and greater TGF resetting compared to spontaneously hypertensive rats under both normal and high-salt conditions.
- Connecting TGF (CTGF) was significantly higher in Dahl SS rats and was further enhanced by a high-salt diet.
- CTGF was found to antagonize TGF, with a greater contribution in Dahl SS rats.
Conclusions:
- Dahl SS rats exhibit a blunted TGF response and enhanced CTGF compared to spontaneously hypertensive rats.
- Increased CTGF significantly contributes to TGF resetting and is exacerbated by high salt intake.
- These mechanisms may explain the heightened glomerular capillary pressure and injury observed in Dahl SS hypertension during high salt consumption.
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