Lenticular rubidium uptake and plasma renin activity in weanling cataract-prone salt-sensitive rats.

Author:

Rodríguez-Sargent C1,Estapé E S1,Rodríguez-Santiago A1,Ramos V L1,Irizarry J E1,Cangiano J L1,Martínez-Maldonado M1

Affiliation:

1. Research Service, San Juan Veterans Hospital, Puerto Rico 00927-5800.

Abstract

Our earlier studies of cataracts in Dahl salt-sensitive (DS) rats suggested the possibility of altered lens ion transport as a contributing factor in cataractogenesis in this genetic model. We also observed that those weanling DS rats with the greatest pressor response to a high salt diet eventually developed cataracts, and that changes in salt intake modified cataract formation. In the present studies, we measured lens 86Rb uptake as an index of sodium-potassium adenosine triphosphatase [(Na+,K+)-ATPase] activity in weanling DS rats before the development of cataracts or sustained hypertension. Additionally, plasma renin activity was measured to indirectly assess our hypothesis that the difference between cataract-prone DS rats and DS rats unlikely to develop cataracts might be a difference in degree of salt sensitivity. At the age of 4 weeks, 50 DS and 25 salt-resistant (DR) rats were given a high sodium diet for 2 weeks, at which time the rats were divided into three groups based on the systolic blood pressure response, that is, cataract-prone DS rats with systolic blood pressure equal to or greater than 155 mm Hg, DS rats unlikely to develop cataracts with systolic blood pressure less than or equal to 125 mm Hg, and DR rats. Lens and aqueous humor Na+ and K+, lens dry weight, and water content were not significantly different among the three groups of weanling rats. Plasma renin activity was lowest in cataract-prone DS rats and low in DS rats unlikely to develop cataracts when compared with values in DR rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Internal Medicine

Reference11 articles.

1. Cataracts and hypertension in salt-sensitive rats. A possible ion transport defect.

2. Lens Opacities Associated with Experimental Calcium Deficiency*

3. CORTICOSTEROIDS AND CATARACTS

4. Mechanism of development of hereditary cataract in mice;Iwata S;Invest Ophthalmol Vis Sci,1971

5. Mechanisms initiating cataract formation: Proctor Lecture;Kinoshita JH;Invest Ophthalmol Vis Sci,1974

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