LEAD, HYPERTENSION, AND THE RENIN-ANGIOTENSIN SYSTEM IN RATS

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  • 1 January 1982
    • journal article
    • research article
    • Vol. 99  (3) , 354-362
Abstract
Rats were exposed continuously to Pb in utero and after birth by giving their mothers, during pregnancy and lactation, drinking water containing 0, 100 or 500 ppm Pb (as Pb acetate) and then continuing this regimen after weaning. Male rats receiving 100 ppm developed a significant elevation of systolic blood pressure (152 .+-. 3.7 mm Hg vs. 135 .+-. 5.6 for controls) at 3 1/2 mo. and remained hypertensive until sacrifice at 6 mo; 500 ppm rats remained normotenisive. Both 100 and 500 ppm females remained normotensive. At 6 mo, PRA [plasma renin activity] was significantly reduced in the 100 ppm male group, but was normal in the 500 ppm group. There were dose-dependent decreases in the AII[angiotensin II]/PRA ratio and in renal renin. Pulmonary converting enzyme activity was not changed by Pb exposure. Blood [Pb] was 40 and 71 .mu.g/dl, respectively and kidney [Pb] was 4.8 and 22.9 .mu.g/g. Renal histology was normal in the 100 ppm group. Doses of Pb which produced blood [Pb] seen many people were capable of inducing modest hypertension in male rats; higher doses failed to do so. The hypertension was associated with a reduction in PRA and AII and was unlikely to be due to hyperactivity of the RAS [renin-angiotensin system].

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