Key result
Dietary salt loading in rats increases the bradycardic response to carotid chemoreceptor stimulation by ~260%.
Why the study?
Does dietary salt loading alter carotid chemoreceptor reflexes in Sprague Dawley rats?
Does dietary salt loading alter carotid chemoreceptor reflexes in Sprague Dawley rats?
A high-salt diet enhances the bradycardic response to carotid chemoreceptor stimulation in rats, potentially related to salt-induced hypokalaemia.
There is a strong association between salt intake and hypertension. Alterations in baroreceptor activity, which precede and contribute to the elevation in blood pressure, have also been shown to affect chemoreceptor reflex response. Dietary salt loading with 8% sodium chloride was carried out in Sprague Dawley rats aged 8 weeks for a period of 5-6 weeks. Blood pressure was thereafter recorded under anaesthesia from the common carotid artery with a Grass Polygraph 7D model, whereas serum Na and K concentrations were measured using a flame photometer. Salt loading resulted in elevated arterial blood pressure as well as hypokalaemia. Stimulation of the carotid chemoreceptor by injection of sodium dithionite resulted in elevated arterial blood pressure, decreased heart rate and hyperventilation in both control and salt-loaded rats. However, the bradycardic response as estimated by the difference in percentage reduction in heart rate was significantly higher in salt rats (36%) than in the control rats (10%). The results indicate that a high-salt diet results in enhanced bradycardic response to carotid chemoreceptor stimulation and that this observation may be related to the attendant hypokalaemia.
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Elias et al. (2004) studied Hypertension. Dietary salt loading vs. Control diet was evaluated on Bradycardic response (percentage reduction in heart rate) to carotid chemoreceptor stimulation. Dietary salt loading with 8% sodium chloride in rats resulted in a significantly higher bradycardic response to carotid chemoreceptor stimulation compared to controls (36% vs 10%).
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