CNS‐induced natriuresis during dopamine receptor blockade. Further support for the existence of, at least, two separate natriuretic hormonal systems

Intracerebroventricular (ICV) stimulation with hypertonic sodium chloride solutions has previously shown indications to stimulate the release of a blood‐borne natriuretic factor. Sodium excretion in this situation increases in the order of 10–20 times. Acute isotonic volume expansion has shown to be a potent stimulus for endogenous release of the atrial natriuretic factor (ANF). It has also been demonstrated that the natriuretic response to both volume expansion and exogenously applied ANF can be attenuated by the dopamine receptor blocker haloperidol. The present study was performed to investigate if the natriuretic response to ICV stimulation also could be attenuated with haloperidol, thus indicating similar effector mechanisms as for ANF. A first group of anaesthetized animals was, therefore, pre‐treated with haloperidol (H) and then ICV stimulated (H‐ICV). A second group of animals was subjected to acute isotonic volume expansion (VE, 2% b.w.h.‐1) to evoke the documented ANF release. In a third group of animals pre‐treatment with haloperidol was followed by volume expansion (H‐VE). In the H‐ICV group there was a more than 30‐fold increase in sodium excretion, due to an increase both in urine flow rate (more than sixfold) and in the urinary concentration of sodium (more than fourfold). Potassium excretion increased more than eightfold, urine osmolality was unchanged, and blood pressure increased by 7%. In the VE group sodium excretion increased more than 18‐fold, consequent to large increases in urine flow rate (more than 23‐fold), while the urinary concentration of sodium tended to decrease. Potassium excretion increased more than threefold, urine osmolality decreased by 88%, and blood pressure was unchanged. In the H‐VE group the natriuretic response was only 42% of that in the VE group (sevenfold). Potassium excretion increased more than twofold, while urine osmolality and blood pressure was unaltered. In conclusion, dopamine receptor blockade achieved by haloperidol does not interfere with CNS‐induced natriuresis. However, the natriuretic response to acute isotonic volume expansion (partly ANF‐mediated) is severly attenuated by the haloperidol treatment. These findings are compatible with a suggestion of at least two separate natriuretic hormonal systems.