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

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Abstract
The Na sensitivity of the carotid sinus baroreceptor reflex was demonstrated in anesthetized cats. Decreases in carotid perfusate Na concentration [Na+]0 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+]0 was switched from 145 mM (control) to 138 or 127 mM. and this was accompanied by an increase in urine volume. The changes in [Na+]0 had no effect on the static pressure-volume relationship of the carotid sinus, indicating an action on the baroreceptors that already was 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+]0 the urine volume increased from 28 .+-. 2.0 (SEM [standard error of the mean]) to 31 .+-. 3.0 .mu.l/min in innervated kidneys and decreased from 32 .+-. 3.1 to 27 .+-. 4.6 in denervated kidneys. Urine Na excretion was higher in denervated kidneys (1.61 .+-. 0.21 .mu.eq/min compared to 1.40 .+-. 0.14 .mu.eq/min for innervated kidneys) and was unchanged in innervated kidneys (1.36 .+-. 0.18 .mu.eq/min) as carotid perfusate Na was decreased. Na excretion from denervated kidneys was increased (1.86 .+-. 0.3 .mu.eq/min) as carotid perfusate Na was lowered. Renal sympathetic discharge also was increased as carotid sinus Na was reduced. Thus, reducing extracellular [Na+]0 by as little as 5% produces significant baroreceptor reflexes, including a rise in blood pressure, and diuresis with no change in total Na excretion. A role of the Na sensitivity of baroreceptors in the regulation of blood pressure, body fluid volume and body Na is indicated.