Key result
Colon-derived secretin stimulates salt appetite through a gut-to-brain neural circuit.
Why the study?
The relative contributions of peripheral versus central angiotensin II to sodium appetite expression in adrenal-intact rats were unclear.
p-value: p=<0.0001
Activation of the renin-angiotensin system has been shown to arouse both water and sodium intake in the rat. The following experiments examine the contributions of the peripheral and central renin-angiotensin systems to the expression of sodium appetite in the adrenal-intact rat. Firstly, we find that, unlike intracerebroventricular angiotensin II, intravenous administration of the hormone at dipsogenic doses does not arouse sodium intake in the sodium replete rat when given alone or in combination with systemic mineralocorticoid pretreatment. Secondly, in the sodium depleted rat, we find that interference with central, but not peripheral, angiotensin II action suppresses sodium appetite. Together, these data confirm recent evidence which demonstrates that it is angiotensin II of cerebral origin, not angiotensin II of renal origin, that is necessary for the expression of sodium appetite.
No takes yet. Share an insight, caveat, or question.
Sakai et al. (1990) studied Sodium deficiency. Colon-specific secretin (SCT) manipulation and NTS-SCTR+ neural circuit modulation vs. Control (sodium-satisfied mice or vehicle/sham) was evaluated on 1-hour cumulative 3% saline intake (p=<0.0001).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: