Reflex control of renal sympathetic nerve activity during furosemide diuresis in rats.

To examine the relative role of cardiopulmonary and sinoaortic baroreceptor afferents in reflex changes in efferent renal sympathetic nerve activity (ERSNA) during furosemide diuresis, ERSNA was measured before and after administration of a maximal diuretic dose of furosemide (300 mg/kg iv) in four groups (n = 8 each) of pentobarbital sodium-anesthetized rats: animals with intact baroreflexes, sinoaortic denervation (SAD), bilateral vagotomy, or SAD plus bilateral vagotomy. In addition, measurements of left ventricular end-diastolic pressure (LVEDP), mean arterial pressure (MAP), heart rate, and afferent vagal nerve activity were performed. Furosemide administration produced an early increase in MAP (+40 mmHg) and ERSNA (+50%) that was maintained in rats with SAD plus vagotomy, suggesting that this effect is not of sinoaortic or cardiopulmonary baroreflex origin. The early pressor response was due to the vehicle, 2% ethanolamine, whereas the early renal sympathoexcitation was due to furosemide. Whereas MAP remained unchanged in rats with intact arterial baroreflexes, MAP gradually decreased along with a reduction in LVEDP during progressive diuresis-related volume depletion in animals with SAD. With progressive diuresis-related volume depletion and falling LVEDP, ERSNA increased in intact animals (delta ERSNA/delta LVEDP = 46.0 +/- 1.5%/mmHg). This late increase in ERSNA was inhibited by bilateral vagotomy or SAD, suggesting that vagal and sinoaortic baroreceptor afferents are both essential for expressing the reflex increase in ERSNA observed during furosemide-induced volume depletion. There were no significant differences among furosemide groups in urinary flow rate and sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)