Renal Na,K-ATPase in genetic hypertension
M Ferrandi1, G Tripodi, S Salardi
1Prassis-Sigma Tau Research Institute, Settimo M.se, Milan, Italy.
Hypertension (Dallas, Tex. : 1979)
|December 1, 1996
Summary
Milan hypertensive rats exhibit faster renal sodium transport, leading to hypertension. This is linked to increased Na-K pump activity and expression, potentially due to a genetic alteration in adducin.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Molecular Biology
Background:
- Milan hypertensive rats (MHS) develop hypertension due to primary renal alterations.
- Both apical and basolateral sodium transport are accelerated in MHS renal tubules.
- This suggests altered transepithelial sodium transport contributes to hypertension in MHS.
Purpose of the Study:
- To investigate alterations in renal Na,K-ATPase activity and expression in prehypertensive MHS.
- To determine if changes in Na,K-ATPase precede hypertension development in MHS.
Main Methods:
- Measured Na,K-ATPase activity, Rb+ occlusion, and subunit protein/mRNA levels in renal outer medulla microsomes.
- Compared young (prehypertensive) and adult (hypertensive) MHS with age-matched Milan normotensive rats (MNS).
Main Results:
- Na,K-ATPase activity was significantly higher in both young and adult MHS.
- This increase was due to a greater number of active pump sites.
- Elevated alpha 1 and beta 1 mRNA levels preceded hypertension onset in MHS.
Conclusions:
- Increased renal Na,K-ATPase activity and expression are primary events in MHS hypertension.
- The upregulation of the Na-K pump is linked to a genetic alteration of adducin.
- These findings highlight a novel molecular mechanism in renal sodium handling and hypertension development.
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