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1 Neurobiology, Howard Florey Institute of Experimental Physiology and Medicine, Parkville, Victoria, Australia
2 Department of Physiology, University of Melbourne, Parkville, Victoria, Australia
3 Neurobiology, Howard Florey Institute of Experimental Physiology and Medicine, Parkville, Victoria, Australia; Department of Physiology, University of Melbourne, Parkville, Victoria, Australia
* To whom correspondence should be addressed. E-mail: m.mathai{at}hfi.unimelb.edu.au.
During mammalian pregnancy, body temperature decreases and there are changes in fluid and electrolyte balance. Angiotensin signalling mechanisms in the brain have been shown to influence thermoregulation and body fluid balance in the non-pregnant state. We hypothesised that brain angiotensin is also implicated in adjusting these physiological systems in the pregnant rat. We compared core temperature and fluid regulation in 3 groups of pregnant rats: untreated rats, rats receiving continuous infusion of an AT1antagonist candesartan (5µg/kg/d) into a lateral cerebral ventricle to block brain AT1receptors, and rats receiving vehicle (artificial cerebrospinal fluid, aCSF). Untreated and aCSF-treated rats showed a decrease in colonic temperature (-0.5°C and -0.8°C respectively) by day 20 of gestation. However, rats treated with candesartan had increased colonic temperature compared to baseline (+0.9°C) and their temperature was significantly higher on days 7 (P < 0.05), 17 (P < 0.05) and 20 (P < 0.001) compared to the other groups (aCSF and non-treated). Daily food and water intakes and body weight were not different between the 3 groups. Similarly, litter sizes and pup weights were equal in all groups. Finally, the expected decreases in plasma sodium and osmolality during pregnancy were equivalent in all groups. This study suggests that brain angiotensin mediates the progressive decrease in body temperature that occurs during pregnancy. However, the changes in fluid balance associated with pregnancy are not dependent on brain angiotensin.
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