Cataracts and Hypertension in Salt-Sensitive Rats A Possible Ion Transport Defect

• Published in: Hypertension (Dallas, Tex. 1979) Vol. 9; no. 3; pp. 304 - 308
• Main Authors: ARGENT, CARMEN RODRÍGUEZ-S, CANGIANO, JOSÉ L, CABÁN, GRACIA BERRÍOS, MARRERO, EVELIO, MARTŃEZ-MALDONADO, MANUEL
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Heart Association, Inc 01.03.1987; Hagerstown, MD Lippincott
• Subjects: Animals; Aqueous Humor - analysis; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Biological Transport, Active; Blood and lymphatic vessels; Calcium - blood; Cardiology. Vascular system; Cataract - complications; Diabetes Mellitus, Experimental - complications; Disease Models, Animal; Electrolytes - analysis; Experimental diseases; Female; Hypertension - complications; Lens diseases; Medical sciences; Ophthalmology; Potassium - metabolism; Rats; Rats, Inbred Strains; Sodium - metabolism; Sodium Chloride - pharmacology; Sodium-Potassium-Exchanging ATPase - metabolism; Hypertension; Vertebrata; Cataract; Eye disease; Experimental disease; Sensitivity; Mammalia; Rat; Sodium; Rodentia; Ion transport; Cardiovascular disease
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.HYP.9.3.304

In previous unrelated studies, we observed a 35 to 50% incidence of cataract formation in several groups of Dahl salt-sensitive hypertensive rats (DS) over a 4-year period. In the present study we evaluated longitudinal changes in blood pressure In DS in which cataracts eventually developed and those in which cataracts did not develop when all animals were maintained on a high sodium diet. Lenses were evaluated by slit-lamp microscopy to determine if cataractous lesions were similar among rats, to classify lesion types, and to define the age at which cataracts were detectable in DS. The possible participation of several cataractogenic risk factors as major Influences on cataract formation also was evaluated. Finally, aqueous humor concentrations and lenticular content of sodium and potassium were determined to evaluate the possibility that a defect in ion transport at the lens epithelium and ciliary body might play a role in cataractogenesis in DS, since ion transport defects have been shown to lead to lens opaciflcatlon in other models of genetic and experimental cataracts. Parallel studies were performed in Dahl salt-resistant control rats (DR). A high incidence of cataract formation was found in DS. Although systolic blood pressure was not consistently greater in adult DS with cataracts compared with values in age-matched DS without cataracts, the initial pressor response to a high salt diet was greatest in weanling DS in which cataractous lesions later developed. Slit-lamp analysis revealed that cataracts in this genetic model were cortical, with one mixed cortical, nuclear lesion. Posterior subcapsular lesions were not observed, suggesting that lesions were not steroidinduced. Serum ultrafiltrable calcium concentration was similar among DS with and without cataracts and normotensive DR, indicating that hypocalcemia was not involved in cataractogenesis. Analysis of aqueous humor showed high potassium concentration and low sodium concentration in DS with cataracts, suggesting a possible ion transport defect in the ciliary processes or lens epithelium (or both). In addition, increased lenticular water and sodium content, as well as decreased potassium content, indicated that mature cataracts in DS were associated with altered sodium and potassium transport. Although aqueous humor sodium concentration and lenticular sodium content were not altered in DS without cataracts, lenticular potassium content was decreased while aqueous humor potassium concentration was increased compared with values in control DR. These data suggesting a decreased transmembrane potassium gradient in DS without cataracts also suggest that a specific defect in potassium transport may precede the development of cataracts in this genetic model. The finding of a potential genetic model of cataracts in which cataractogenesis is associated with hypertension suggests a possible link between hypertension and cataract formation.