Neural Control of Atrial Natriuretic Peptide Actions on Fluid Intake and Excretion

Abstract

Conclusions

In conclusion, it is now clear that Ang II and ANP in the brain play important and opposite roles in the control of water and salt intake, Ang II promoting the intake of both and ANP inhibiting intake of both, perhaps by inhibiting the secretion within the brain of Ang II. In fact, there is probably a reciprocal relationship between the activity of these two neuronal systems. Again, on the output side, the two are related since ANP release is stimulated in situations of volume expansion to increase renal sodium and potassium loss, and at the same time, ANP not only blocks the release of renin from the kidney, thereby decreasing Ang II stimulation of aldosterone release but also directly inhibits aldosterone secretion. Decreased aldosterone secretion results in increased natriuresis. ANP neurons in the hypothalamus inhibit the release of corti-cotrophin-releasing factor and VP, thereby ACTH release which also reduces aldosterone secretion.

Therefore, both of these peptides play a key role in the maintenance of body fluid homeostasis in the body. ANP acts slowly via natriuresis to reduce effective circulating blood volume. The rapid release of ANP following BVE would first produce vasodilatation by activating particular guanylate cyclase, leading to the production of cyclic GMP, which would relax vascular smooth muscle. These combined actions would result in a rapid reduction in the effective circulating blood volume. The longer-term effects would be mediated not only by diuresis and natriuresis but also by decreased intake of salt and water.