Do the carotid body chemoreceptors mediate cardiovascular and sympathetic adjustments induced by sodium overload in rats?

Acute plasma hypernatremia induces several cardiovascular and sympathetic responses. It is conceivable that these responses contribute to rapid sodium excretion and restoration of normal conditions. Afferent pathways mediating these responses are not entirely understood. The present study analyses the effects of acute carotid chemoreceptor inactivation on cardiovascular and sympathetic responses induced by infusion of hypertonic saline (HS). All experiments were performed on anesthetized male Wistar rats instrumented for recording of arterial blood pressure (ABP), renal blood flow (RBF) and renal sympathetic nerve activity (RSNA). Animals were subjected to sham surgery or carotid chemoreceptor inactivation by bilateral ligation of the carotid body artery (CBA). In sham rats (n = 8), intravenous infusion of HS (3 M NaCl, 1.8 ml/kg b.wt.) elicited a transient increase (9 ± 2mmHg) in ABP, and long lasting (30 min) increases in RBF (138 ± 5%) and renal vascular conductance (RVC) (128 ± 5%) with concurrent decrease in RSNA (-19 ± 4%). In rats submitted to CBA ligation (n = 8), the pressor response to HS was higher (24 ± 2mmHg; p < 0.05). However, RBF and RVC responses to HS infusion were significantly reduced (113 ± 5% and 93 ± 4%, respectively) while RSNA was increased (13 ± 2%). When HS (3M NaCl, 200μl) was administrated into internal carotid artery (ICA), distinct sympathetic and cardiovascular responses were observed. In sham-group, HS infusion (3M NaCl, 200μl) into ICA promoted an increase in ABP (26 ± 8mmHg) and RSNA (29 ± 13%). In CBA rats, ABP (-3 ± 5.6mmHg) remained unaltered despite sympathoinhibition (-37.6 ± 5.4%). These results demonstrate that carotid body chemoreceptors play a role in the development of hemodynamic and sympathetic responses to acute HS infusion.