Abstract
Two lines of Dahl rats, one resistant to salt-induced hypertension (DR) and one susceptible to salt-induced hypertension (DS) were subchronically exposed to SO 2 (50 ppm, 6 hr/d, 5 d/wk for 31 weeks) or ozone (2.0 ppm, 6 hr/d, 5 d/wk for 20 weeks). Subgroups of rats were maintained on either high or low salt diets. In rats not expected to develop hypertension, exposure to SO 2 caused a slight but consistent decrease in blood pressure. In DS rats on a high salt diet exposure to SO 2 resulted in an increase in blood pressure over that of their air exposed counterparts. All exposure-related differences in blood pressure disappeared after the last exposure to SO 2. Exposure to ozone was fatal to all DS rats, regardless of the amount of salt in the diet. The DR rats were more resistant to ozone, with most animals surviving the 20-week exposure. Ozone-exposed rats exhibited a decrease in both growth rate and blood pressure in all groups when compared to their air-exposed counterparts. It is not known if exposure-related blood pressure differences would persist after ending ozone exposures. After brief exposures, ozone caused increased lung weights in both groups, but there were no consistent changes in pulmonary nonprotein sulfhydryl groups. Hepatic nonprotein sulfhydryl levels were consistently, but not significantly, lower in ozone-exposed rats.
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