Sodium sensitivity of baroreceptors. Reflex effects on blood pressure and fluid volume in the cat.

The sodium sensitivity of the carotid sinus baroreceptor reflex was demonstrated in anesthetized cats. Decreases in carotid perfusate sodium concentration |Na ] o of 5% and 12.5% attenuated the depressor response to increased carotid sinus pressure. At constant sinus pressure, increases in systemic pressure and heart rate were produced when the carotid perfusate |Na]o was switched from 145 mM (control) to 138 or 127 miu, and this was accompanied by an increase in urine volume. The changes in |Na],, had no effect on the static pressure-volume relationship of the carotid sinus, indicating an action on the baroreceptors that already has been confirmed directly by studies of baroreceptor discharge. Chemoreceptor involvement, examined by recording chemoreceptor discharge, was negligible. The increase in urine volume was not dependent on intact renal sympathetic nerves, and renal denervation alone produced an increase in urine volume during control perfusion. At 87.5% carotid sinus |Na|(, the urine volume increased from 28 ± 2.0 (SEM) to 31 ± 3.0 /xl/min in innervated kidneys and decreased from 32 ± 3.1 to 27 ± 4.6 in denervated kidneys. Urine sodium excretion was higher in denervated kidneys (1.61 ± 0.21 /u.Eq/min compared to 1.40 ± 0.14 /iEq/min for innervated kidneys) and was unchanged in innervated kidneys (1.36 ± 0.18 /iEq/min) as carotid perfusate sodium was decreased. However, sodium excretion from denervated kidneys was increased (1.86 ± 0.3 /*Eq/min) as carotid perfusate sodium was lowered. Renal sympathetic discharge also was increased as carotid sinus sodium was reduced. Thus, reducing extracellular |Na],, by as little as 5% produces significant baroreceptor reflexes, including a rise in blood pressure, and diuresis with no change in total sodium excretion. These studies indicate a role of the sodium sensitivity of baroreceptors in the regulation of blood pressure, body fluid volume, and body sodium.