What question did this study set out to answer?

To evaluate whether aortic and carotid afferents mediate the renal vasodilation and renal sympathoinhibition provoked by acute hypernatremia.

Involvement of sinoaortic afferents in renal sympathoinhibition and vasodilation induced by acute hypernatremia

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To evaluate whether aortic and carotid afferents mediate the renal vasodilation and renal sympathoinhibition provoked by acute hypernatremia.
Urethane-anaesthetised male Wistar rats underwent either sinoaortic denervation or sham surgery (1.2 g/kg body weight, i.v.).
Mean arterial pressure (MAP), renal vascular conductance (RVC), and renal sympathetic nerve activity (RSNA) were measured during acute hypertonic saline infusion (3 mol/L NaCl, 1.8 mL/kg body weight, i.v.).
In sham rats, hypertonic saline elicited transient hypertension (12 ± 4 mmHg increase, peak at 10 min; P < 0.05), increased RVC (127 ± 9% at 20 min and 150 ± 13% at 60 min; P < 0.05), and decreased RSNA (-34 ± 10% at 10 min and -29 ± 5% at 60 min; P < 0.05).
In sinoaortic-denervated rats, hypertonic saline caused a sustained pressor response (30 ± 5 mmHg at 10 min and 17 ± 6 mmHg at 30 min; P < 0.05) and abolished both RVC elevation (85 ± 8% at 10 min) and RSNA suppression (-4 ± 3% at 10 min).

Population

Male Wistar rats, anaesthetised with intravenous urethane (1.2 g/kg bw)

Intervention

Sinoaortic denervation prior to hypertonic saline (HS) infusion (3 mol/L NaCl, 1.8 mL/kg bw, i.v.)

Comparator

Sham operation prior to hypertonic saline (HS) infusion

Outcome

Mean arterial pressure (MAP), renal vascular conductance (RVC), and renal sympathetic nerve activity (RSNA) up to 60 minutes post-infusionsurrogate

Aortic and carotid afferents are involved in the cardiovascular and renal sympathoinhibition responses induced by acute hypernatremia in rats.

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Aortic and carotid afferents mediate HS-induced renal sympathoinhibition in rats; leaves open translation to human volume regulation.

Silva et al. (2015) studied this question.

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