Abstract
Ventriculo-cisternal perfusion of low-sodium artificial CSF causes large decrements in sodium excretion and increases in plasma renin activity (1). This report presents findings on the possible roles of the renal nerves and plasma antidiuretic hormone (ADH) in mediating the antinatriuresis.
Ventriculo-cisternal perfusion was performed in seven dogs, anesthetized with pentobarbital iv. Surgical preparations in these animals included: placement of stainless steel cannulas in lateral ventricle and cisterna magna; laparatomy; and cannulation of the ureter (s); cannulation of both brachial veins; and cannulation of the femoral artery. Changes in plasma ADH concentration and plasma renin activity were examined in three of these animals. In the remaining four animals, the right kidney was denervated by peeling the adventitia from the renal vessels, and cutting all visible nerves accompanying the renal artery, renal vein, and ureter. 4 To verify the extent of denervation, the fall in renal blood flow (RBF) (monitored with a square wave electromagnetic flowmeter), in response to a timed tracheal occlusion, was measured before and after this surgery. The left kidney was removed from one of the denervated animals (dog 34). Three other animals were used for evaluation of the denervation technique, but were not subjected to ventriculo-cisternal perfusion.
Clearance techniques, ventriculo-cisternal perfusion methods, blood pressure measurement, and analytical methods for sodium, potassium, creatinine, PAH, and plasma renin activity have been described earlier (1). Plasma ADH activity was measured by the method of Share and Levy (2) as modified by Bonjour and Malvin (3).
Protocol. After surgical preparation, the control solution (artificial dog CSF) (1) and the low-sodium solution (identical to control minus 25 mEq/liter of NaCl) were perfused (0.8 ml/min) from lateral ventricle to cisterna magna for alternating 50-min periods. The first control period was extended to 70-80 min to allow an initial equilibration.
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