Cardiovascular responses of embryonic alligator (Alligator mississippiensis) exposed to 10% O2 and sodium cyanide (NaCN), a chemoreflex-inducing compound.

The possibly interactive effects of changes in atmospheric respiratory gases (hypoxia or hypercapnia) and pharmacological chemoreceptor stimulation have not been assessed previously. We present a series of experimental protocols investigating embryonic alligators' capacity to modulate a cardiovascular neural chemoreflex response to a known chemoreceptor stimulant, sodium cyanide (NaCN). We incubated alligator embryos in 21 % (normoxia) and 10 % O2 (hypoxia) beginning at 20 % of embryonic incubation, and at 70 % and 90 % of incubation we measured heart rate and blood pressure responses to NaCN. These NaCN responses also included examining the effects of NaCN after 1-h exposure to 10 % O2., ganglionic blockade with hexamethonium chloride and α-adrenergic blockade with phentolamine. Injections of NaCN into the chorioallantoic artery caused a rapid bradycardia followed by a secondary hypertension, which can be attributed to an autonomic nervous system mediated reflex loop. We compared the heart rate response to injections of 1 mg kg-1 NaCN before and after a 1-h 10 % O2 exposure, and it was clear that embryonic alligators lacked capacity to change the intensity of cardiovascular responses to this compound. Hexamethonium greatly lessened the rapid bradycardia, and at 90 % of incubation, the secondary hypertensive response to NaCN appeared due to α-adrenergic stimulation, as phentolamine lessened the response. Collectively, data indicate that while a cardiovascular chemoreflex can be induced by NaCN, the heart rate response lacks plasticity and is not modulated by hypoxic incubation in embryonic alligators.