November 1989
Volume 30, Issue 11
Free
Articles  |   November 1989
Prevention and reversal of cataracts in genetically hypertensive rats through sodium restriction.
Author Affiliations
  • C Rodríguez-Sargent
    Research Service, Veterans Hospital, San Juan, Puerto Rico 00927-5800.
  • G Berrios
    Research Service, Veterans Hospital, San Juan, Puerto Rico 00927-5800.
  • J E Irrizarry
    Research Service, Veterans Hospital, San Juan, Puerto Rico 00927-5800.
  • E S Estapé
    Research Service, Veterans Hospital, San Juan, Puerto Rico 00927-5800.
  • J L Cangiano
    Research Service, Veterans Hospital, San Juan, Puerto Rico 00927-5800.
  • M Martínez-Maldonado
    Research Service, Veterans Hospital, San Juan, Puerto Rico 00927-5800.
Investigative Ophthalmology & Visual Science November 1989, Vol.30, 2356-2360. doi:
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      C Rodríguez-Sargent, G Berrios, J E Irrizarry, E S Estapé, J L Cangiano, M Martínez-Maldonado; Prevention and reversal of cataracts in genetically hypertensive rats through sodium restriction.. Invest. Ophthalmol. Vis. Sci. 1989;30(11):2356-2360.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

We previously described the Dahl salt-sensitive rat as a potential model of cataractogenesis in which cataract formation is associated with hypertension. Cataractous lesions were characterized by a marked lenticular and aqueous humor electrolyte imbalance. In the present study the effects of chronic dietary sodium restriction on cataract formation were evaluated in salt-sensitive rats to determine whether or not modification of the hypertensive process might reduce the incidence of cataracts in this genetic model. In addition, the possibility that early cataractous lesions in adult hypertensive salt-sensitive rats might be reversed by acute sodium restriction was evaluated. Chronic dietary sodium restriction modified the development of hypertension and prevented cataract formation in salt-sensitive rats. Furthermore, acute dietary sodium restriction (1 week) completely and consistently reversed early cataractous lesions (pinpoint opacities) in adult hypertensive salt-sensitive rats. Both the prevention and reversal of cataracts were associated with normalization of the lenticular and aqueous humor parameters measured. These data suggest that cataractogenesis is not the consequence of sustained arterial hypertension, but rather that initiation of both hypertension and cataract formation in this genetic model may be the result of extracellular fluid volume state.

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