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.
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© 2010 Published by Elsevier Inc.