Role of carotid body chemoreceptors in cardiovascular adjustments induced by hypernatremia in rats

Hypernatremia is known to induce renal vasodilation, but the afferent pathways that mediate these responses are not entirely understood. It is known that carotid chemoreceptors are sensitive to changes in plasma sodium concentration, but the physiological significance of this sensitivity is not clear. The present study examines the role of carotid chemoreceptors in cardiovascular responses to intravenous infusion of hypertonic saline (HS). Male Wistar rats (290–350 g) were anesthetized with urethane (1.2 g×kg⁻¹ b.w., i.v.), and instrumented for recording of arterial pressure, renal blood flow (RBF), and renal vascular conductance (RVC). The carotid chemoreceptors were inactivated by bilateral ligation of the carotid body artery (CBA). Sham surgery involved (visualization of these arteries). Thirty min later, HS (3 M NaCl, 1.8 ml×kg⁻¹ b.w., i.v.) was infused in 1 min. These infusions increase plasma osmolality by about 6%. In intact rats (n=8), blood pressure increased slightly (10 min after HS: 9±1.9 mmHg) and transiently (<20 min). HS increased RBF (by 38±4.9%, 10 min after HS) and RVC (by 28±5.1%, at 10 min after HS infusion), and these increases lasted for more than 60 min. In rats submitted to CBA ligation (n=8), the pressor response to HS was larger (24±2.2 mmHg, at 10 min after HS infusion) and prolonged (>60 min). However, increases in RBF and RVC induced by HS were significantly reduced after CBA ligation (RBF 13±5.0% above baseline, RVC 7±4.4% below baseline, 10 min after HS). These results demonstrate that integrity of carotid body afferent is essential for development of the renal vasodilation that follows acute changes in the composition of the extracellular fluid compartment.