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Plasma renin is increased in young rats exposed to lead in utero and during nursing
Insights
Lead exposure in pregnant and lactating rats stimulated basal plasma renin activity (PRA) but blunted responses to stimuli. Higher doses reduced angiotensin II levels, highlighting timing-dependent lead effects on the renin-angiotensin system.
Area of Science:
- Toxicology
- Endocrinology
- Physiology
Background:
- Lead (Pb) exposure is a significant public health concern.
- The renin-angiotensin system (RAS) plays a crucial role in blood pressure regulation.
- Timing of exposure can influence the toxicological effects of lead.
Purpose of the Study:
- To investigate the impact of developmental lead exposure on the renin-angiotensin system in rats.
- To determine how different doses of lead affect plasma renin activity and related hormones.
- To assess the influence of exposure timing on lead's effects on the RAS.
Main Methods:
- Rats were exposed to varying concentrations of lead (0-500 ppm) in drinking water from gestation through lactation.
- Blood lead concentrations were measured at 1 month of age.
- Plasma renin activity (PRA), renal renin concentration, and plasma angiotensin II levels were assessed.
Main Results:
- All lead-exposed groups showed elevated basal PRA compared to controls.
- Pentobarbital anesthesia and laparotomy increased PRA, but this response was attenuated in the 100 ppm lead group.
- Renal renin concentration increased at higher lead doses (100 and 500 ppm).
- The ratio of plasma angiotensin II to PRA was reduced at the highest lead dose (500 ppm).
Conclusions:
- Developmental lead exposure stimulates basal renin secretion in young rats.
- Lead exposure partially inhibits the renin-angiotensin system's response to stimuli.
- The timing of lead exposure significantly modifies its effects on the renin-angiotensin system.
Abstract:
Rats were exposed continuously to Pb in utero and after birth by giving their mothers, during pregnancy and lactation, drinking water containing 0, 5, 25, 100, or 500 ppm Pb (as Pb acetate); they were sacrificed at 1 month of age, at which time their mean blood Pb concentrations were, respectively, approximately 3, 9, 19, 30, and 70 micrograms/dl. All Pb-exposed groups sacrificed by decapitation had elevated mean plasma renin activities (PRA), relative to controls. Pentobarbarbital-anesthesia and laparotomy markedly increased PRA in the 0, 100, and 500 ppm groups, but the increase was significantly less in the 100 ppm group. Renal renin concentration was normal in the 5 and 25 ppm groups, but was significantly increased in the 100 and 500 ppm groups. The ratio of plasma angiotensin II to PRA was normal in the 100 ppm group but significantly reduced in the 500 ppm group. We conclude that exposure of rats in utero and during lactation to doses of Pb which produce blood Pb concentrations similar to those generally present in human populations stimulates basal renin secretion in 1-month-old rats, but partially inhibits the response to renin-releasing stimuli. The highest dose reduces plasma angiotensin II at any given PRA. These results, taken with previous publications, emphasize that the effects of lead on plasma renin even within a single species are greatly affected by the timing of the exposure.