Oestrogen and weight loss decrease isoproterenol-induced Fos immunoreactivity and angiotensin type 1 mRNA in the subfornical organ of female rats
Studies from our laboratory and others show that oestrogen reduces angiotensin II (Ang II)-induced water intake by ovariectomized rats. Elimination of endogenous oestrogen by ovariectomy causes weight gain that can be reversed or prevented by oestrogen replacement. Changes in body weight modify card...
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Veröffentlicht in: | The Journal of physiology 2006-05, Vol.573 (1), p.251-262 |
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Sprache: | eng |
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Zusammenfassung: | Studies from our laboratory and others show that oestrogen reduces angiotensin II (Ang II)-induced water intake by ovariectomized
rats. Elimination of endogenous oestrogen by ovariectomy causes weight gain that can be reversed or prevented by oestrogen
replacement. Changes in body weight modify cardiovascular responses to Ang II but whether such changes have similar effects
on central and behavioural responses to Ang II is unknown. The goal of this study was to evaluate the contributions of oestrogen
and weight loss to isoproterenol (isoprenaline; Iso)-induced Fos immunoreactivity (IR) and to angiotensin type 1 (AT1) receptor
mRNA in forebrain regions implicated in the control of fluid balance. Isoproterenol significantly increased Fos IR in the
hypothalamic paraventricular and supraoptic nuclei, the subfornical organ (SFO), and the organum vasculosum of the lamina
terminalis, but had no effect on AT1 mRNA expression. However, both Iso-induced Fos IR and the AT1 mRNA were attenuated in
the SFO of the oestrogen and weight loss groups compared with that of the control group. Consequently, we examined the effect
of weight loss on Iso-induced water intake and plasma renin activity (PRA) and found that weight loss decreased water intake
after Iso, but had no effect on PRA. Thus, we propose that weight loss decreases Ang II-elicited water intake in the female
rat by down-regulating the expression of the AT1 receptor. |
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ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1113/jphysiol.2006.106740 |