Action of angiotensin converting enzyme inhibitors in rat brain: interaction with isoproterenol assessed by Fos immunocytochemistry

Rowland, Neil E.; Fregly, Melvin J.; Li, Bai-Han; Smith, Gloria C.

doi:10.1016/0006-8993(94)91568-7

Cited by 18 publications

(2 citation statements)

References 28 publications

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“…The distributions of Fos-ir-positive neurons in the SFO and OVLT of rats receiving Furo/Cap treatment are similar to those found in rats receiving intravenous infusions of exogenous ANG II in studies by McKinley and colleagues (17,19) and Rowland et al (26) and also during the generation of endogenous angiotensin in rats after intravenous (20) and subcutaneous (24) administration of isoproterenol. Therefore, the pattern of Fos-ir in SFO and OVLT during Furo/Cap treatment matches that produced by circulating ANG II.…”

Section: Discussionsupporting

confidence: 79%

Fos expression in rat brain during depletion-induced thirst and salt appetite

Thunhorst

Cicha

et al. 1998

American Journal of Physiology-Regulatory, Integrative and Comp

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The expression of Fos protein (Fos immunoreactivity, Fos-ir) was mapped in the brain of rats subjected to an angiotensin-dependent model of thirst and salt appetite. The physiological state associated with water and sodium ingestion was produced by the concurrent subcutaneous administration of the diuretic furosemide (10 mg/kg) and a low dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg; Furo/Cap treatment). The animals were killed 2 h posttreatment, and the brains were processed for Fos-ir to assess neural activation. Furo/Cap treatment significantly increased Fos-ir density above baseline levels both in structures of the lamina terminalis and hypothalamus known to mediate the actions of ANG II and in hindbrain regions associated with blood volume and pressure regulation. Furo/Cap treatment also typically increased Fos-ir density in these structures above levels observed after administration of furosemide or captopril separately. Fos-ir was reduced to a greater extent in forebrain than in hindbrain areas by a dose of captopril (100 mg/kg sc) known to block the actions of ACE in the brain. The present work provides further evidence that areas of lamina terminalis subserve angiotensin-dependent thirst and salt appetite.

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Section: Discussionsupporting

confidence: 79%

Fos expression in rat brain during depletion-induced thirst and salt appetite

Thunhorst

Cicha

et al. 1998

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Angiotensin II is a major influence in body fluid homeostasis and the β‐agonist Iso greatly elevates circulating levels of this peptide (Stocker et al 2000). Hypotension and consequent increases in circulating Ang II activate brain regions implicated in body fluid regulation (Oldfield & McKinley, 1994; Rowland et al 1994). Therefore, it is not surprising that Iso elicited robust Fos IR in the SON, PVN, SFO and OVLT in the present study.…”

Section: Discussionmentioning

confidence: 99%

Oestrogen and weight loss decrease isoproterenol‐induced Fos immunoreactivity and angiotensin type 1 mRNA in the subfornical organ of female rats

Krause

Curtis

Stincic

et al. 2006

The Journal of Physiology

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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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