Role of angiotensin in sodium appetite of sodium-deplete sheep

Abstract

The role of the renin-angiotensin system (RAS) in the Na appetite of Na-deplete sheep was investigated. Intravenous infusion of the angiotensin-converting enzyme inhibitor, captopril, at 0.01 or 0.1 mg X kg-1 X h-1 did not cause any change in Na intake, although the higher dose caused a marked decrease in mean arterial blood pressure. Intravenous infusion of captopril at 1.0 mg X kg-1 X h-1 over 24 h decreased Na intake by 45-55% in the absence of any change in Na loss. The decrease in Na intake was restored to base-line level or above by concurrent intravenous infusion of angiotensin II (ANG II) at 3.8 or 24 micrograms/h over 24 h but not by intracerebroventricular (ICV) ANG II at 3.8 micrograms/h. In addition, ICV infusion of 0.7 M mannitol (1 ml/h over 3 h), which reduced cerebrospinal fluid (CSF) and brain extracellular fluid [Na], still increased Na intake when combined with intravenous captopril. Water intake was not altered during intravenous captopril or ANG II alone but was increased during ICV ANG II or 0.7 M mannitol (with or without iv captopril). In conclusion, these results suggest that the RAS is involved in the Na appetite of the Na-deplete sheep. Furthermore, it would appear that the brain area involved is one without a blood-brain barrier but with a CSF-brain barrier, such as one of the circumventricular organs. Also, it would appear that the effect of lowered cerebral Na and the effect of activation of the renin-angiotensin system on Na appetite are independent.

Functional correlates of activity in neurons projecting from the lamina terminalis to the ventrolateral periaqueductal gray

“…Circulating AngII acting centrally via the circumventricular organs is implicated in regulating thirst (Phillips et al, 1978;Buggy et al, 1979), evoking a pressor response Mangiapane & Simpson, 1980) and initiating a salt appetite (Bryant et al, 1980;Denton et al, 1984;Nicolaidis & Jeulin, 1984;Schulkin & Fluharty, 1985;Weisinger et al, 1987;Henry, 1988;Rowland et al, 1996;Thunhorst, 1996). To the extent that vlPAG is involved in one or more of these regulatory responses, our findings suggest that circulating AngII effects on the vlPAG are mediated by projections from the OVLT and SFO but not the MnPO.…”

Angiotensin-converting enzyme inhibition reverses diet-induced obesity, insulin resistance and inflammation in C57BL/6J mice

“…22,31 This could be because of increased bradykinin levels 44 or increased ANG-II synthesis in the brain. 45 As the fluid intake by the CAP-treated mice is elevated compared with that of the CON group, the reduction in food intake by the CAPtreated mice is not due to a general suppression of behaviour by CAP. Furthermore, ANG-II does not affect ghrelin-induced food intake, 46 although it causes a large increase in fluid intake.…”

“…Furthermore, ANG-II does not affect ghrelin-induced food intake, 46 although it causes a large increase in fluid intake. 45 Therefore, the decreased food intake by the CAPtreated mice is not due to increased fluid intake.…”

Richter and sodium appetite: From adrenalectomy to molecular biology

“…Subsequent studies further implicated the peptide in the arousal of salt appetite and provided potential sites of actions for this effect. For example, salt appetite resulting from the natriuretic-diuretic furosemide was attenuated by pharmacological reduction of circulating angiotensin II and was restored by intravenous administration of this peptide (Weisinger et al, 1997(Weisinger et al, , 1987.…”