Altered lens short-circuit current in adult cataract-prone Dahl hypertensive rats.
We assessed components of lenticular short-circuit current in adult hypertensive Dahl salt-sensitive rats (DS) during chronic control (0.4% sodium) versus high (3% sodium) dietary NaCl intake begun at the age of 4 weeks until rats were studied. We also evaluated the influence of barium, a potassium channel blocker, and ouabain, a specific inhibitor of Na+, K(+)-ATPase activity, by adding them to the anterior lens surface, thus measuring barium-sensitive, ouabain-sensitive, and barium- and ouabain-in-sensitive short-circuit currents. During control NaCl intake, short-circuit current in DS and their control group, Dahl salt-resistant rats (DR), did not differ significantly. DS were subclassified into cataract-prone rats and rats unlikely to develop cataracts on the basis of their initial pressor response to the change from a normal to high NaCl diet during the first weeks of age. Although only transparent lenses were studied, total lens short-circuit current was already markedly decreased in the cataract-prone subgroup compared with DS unlikely to develop cataracts and control DR. This was in sharp contrast to the increase in short-circuit current previously reported in Sprague-Dawley rats and now observed in control DR in response to high dietary NaCl. The decrease in lens short-circuit current in cataract-prone rats was associated with lower absolute values of barium- and ouabain-sensitive short-circuit currents as well as with low barium- and ouabain-insensitive short-circuit current. Although the barium- and ouabain-sensitive components of the short-circuit current were similar in DS unlikely to develop cataracts and DR, the barium- and ouabain-insensitive component of the short-circuit current was lower in DS unlikely to develop cataracts than values in DR. Interestingly, this component of lens short-circuit current also increased in DR during chronic high NaCl, whereas the opposite change occurred in cataract-prone DS and DS unlikely to develop cataracts. Thus, the barium- and ouabain-insensitive short-circuit current may be a mechanism that protects the normal lens from developing cataracts. Possible candidates for this short-circuit current component are voltage-dependent potassium channels, calcium-activated potassium channels, or both. Our studies show altered lens short-circuit current in response to high NaCl intake in cataract-prone DS and suggest the possibility of altered lens potassium transport during sustained hypertension but before loss of lens transparency.
Rodríguez-Sargent
C
C
San Juan VA Medical Center, Department of Pharmacology, PR 00927-5800. rodríguez-sargent,c@san juan
Estapé
E S
ES
Fernández
N
N
Irizarry
J E
JE
Cangiano
J L
JL
Candia
O A
OA
D000818:Animals; D002386:Cataract / Q000235:genetics*; D004039:Diet, Sodium-Restricted; D004351:Drug Resistance / Q000235:genetics; D004553:Electric Conductivity; D017097:Electric Impedance; D020022:Genetic Predisposition to Disease; D006973:Hypertension / Q000235:genetics* / Q000503:physiopathology*; D007908:Lens, Crystalline / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains / Q000235:genetics; D012965:Sodium Chloride / Q000494:pharmacology
D012965:Sodium Chloride