In a muskrat model of simulated diving, initial dive bradycardia is not driven by facilitation of the baroreflex at the receptor level.
Nasal stimulation elicits bradycardia without baroreflex facilitation in muskrats; leaves open central mechanisms for further study in diving reflexes.
Nasal stimulation with water (simulated dive) in anesthetized muskrats (Ondatra zibethica) caused a significant increase in cardiac interval (209 ± 8 to 1370 ± 280 ms; mean ± SE) and decrease in mean arterial blood pressure (86 ± 8.6 mmHg to 75.7 ± 7.9 mmHg; 1 mmHg = 133.32 Pa). Baroreceptor activity, recorded from the peripheral end of a cut sinus nerve, stopped during the prolonged initial diastolic interval and in 3 of 10 fibres was absent for the first three heartbeats. Chemoreceptor activity did not change at the start of the nasal stimulation. As nasal stimulation continued, mean arterial blood pressure significantly increased (to 118.1 ± 9.5 mmHg), while cardiac interval decreased (to 740 ± 102 ms). This resulted in an increase in baroreceptor activity comparable with that seen during a similar increase in blood pressure in a pressor test. An increase in chemoreceptor activity also occurred during the latter part of nasal stimulation. Two types of efferent activity were recorded from the central end of a cut sinus nerve. One efferent responded to nasal stimulation with an immediate increase in neural activity, while activity of the other efferent halted. These responses would be expected to inhibit rather than foster baroreceptor activity in the intact nerve. The results suggest that there is no facilitation of the baroreflex engendered by changes at the receptor level that might contribute to the initiation of the dive bradycardia.
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Douse et al. (1988) studied this question.
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