Cardiovascular responses to electrical stimulation of the recurrent laryngeal nerve in conscious toads (Bufo marinus)

Summary

Cardiovascular responses to electrical stimulation of the cut central end of the recurrent laryngeal nerve (rLN) were recorded in 19 conscious toads (Bufo marinus). Low intensity stimulation of the rLN (≧3.4±0.5 V, 1 ms, 10 Hz) elicited a slow 18–22% fall in heart rate and systolic and diastolic aortic arterial blood pressures (N=18), but had little or no effect upon ventilation (N=6). This low threshold depressor response (LTDR) was considered to represent the expression of the previously demonstrated pulmocutaneous baroreflex. Bilateral stimulation of the rLNs elicited greater LTDRs than did either left or right unilateral rLN stimulation. Blood pressure and heart rate responses to bilateral stimulation were 69–77% of the sum of responses to unilateral stimulation, and the mean summation was significant for the reduction in heart rate. Stimulus intensities of >4.7±0.7 V caused an immediate cessation of cardiac activity for up to 6.5±1.3 s (N=17) and a concomitant apnoea (N=6), which were followed by a lesser bradycardia and hypotension. This response was termed a high threshold depressor response (HTDR). During continued stimulation at intensities of >9.1±1.4 V, aortic blood pressure (Pa) and ventilation were rapidly restored, and aortic blood pressure continued to rise above control values (N=14). In some cases this high threshold pressor response (HTPR) was associated with an increase in heart rate. All responses to rLN stimulation were abolished by pithing (N=9) or by pentobarbital (40 mg/kg, i.p.,N=4), but LTDS and HTPRs could be elicited in urethanized (1.5–2.0 g/kg,N=4) toads.

During depressor responses, aortic arterial resistance fell by 18% in 18 of 20 trials in 5 toads, whereas pulmocutaneous arterial resistance increased by 76% in 12 of 15 trials in 4 toads. During the HTPR, aortic arterial resistance increased 40%, while pulmocutaneous arterial resistance remained unchanged. We suggest that depressor responses may actively redistribute blood flow from the pulmocutaneous to the aortic circulation, whereas the reverse should occur during HTPRs.