Periventricular lesions block natriuresis to hypertonic but not isotonic NaCl loads.

The renal excretion of Na and water after an intravenous load of hypertonic or isotonic saline was studied in conscious sheep in which periventricular tissue in the region of the lamina terminalis had been ablated. Hypertonic saline (3.4-4.2 mmol/l) was infused at 0.06 mmol.kg-1.min-1 for 40 min into the jugular vein. Plasma Na concentration increased 5 mmol/l, and in normal sheep a natriuresis and increase in glomerular filtration rate ensued during the next hour. Such a natriuretic effect did not occur in sheep with periventricular lesions. By contrast, intravenous infusion of isotonic saline (30 ml/kg body wt, i.e., 0.23 mmol.kg-1.min-1 for 20 min) caused similar increase in renal Na excretion in normal sheep and sheep with periventricular lesions. When the same intravenous load of NaCl (0.23 mmol.kg-1.min-1 for 20 min) was administered as hypertonic 20% NaCl, ablation of periventricular tissue greatly impaired the excretion of this Na load. We suggest that the periventricular tissue in the region of the lamina terminalis has a role in regulation of renal Na excretion in conditions where the plasma Na concentration increases. This tissue is also involved in osmoregulatory thirst and vasopressin secretion. We further propose that increased renal Na excretion in response to hypernatremia is another cerebrally mediated osmoregulatory response.