Integration of autonomic and local mechanisms in regulating cardiovascular responses to heating and cooling in a reptile (Crocodylus porosus).
Reptiles change heart rate and blood flow patterns in response to heating and cooling, thereby decreasing the behavioural cost of thermoregulation. We tested the hypothesis that locally produced vasoactive substances, nitric oxide and prostaglandins, mediate the cardiovascular response of reptiles to heat. Heart rate and blood pressure were measured in eight crocodiles (Crocodylus porosus) during heating and cooling and while sequentially inhibiting nitric-oxide synthase and cyclooxygenase enzymes. Heart rate and blood pressure were significantly higher during heating than during cooling in all treatments. Power spectral density of heart rate and blood pressure increased significantly during heating and cooling compared to the preceding period of thermal equilibrium. Spectral density of heart rate in the high frequency band (0.19-0.70 Hz) was significantly greater during cooling in the saline treatment compared to when nitric-oxide synthase and cyclooxygenase enzymes were inhibited. Cross spectral analysis showed that changes in blood pressure preceded heart rate changes at low frequencies (< 0.1 Hz) only. We conclude that the autonomic nervous system controls heart rate independently from blood pressure at higher frequencies while blood pressure changes determine heart rate at lower frequencies. Nitric oxide and prostaglandins do not control the characteristic heart rate hysteresis response to heat in C. porosus, although nitric oxide was important in buffering blood pressure against changes in heart rate during cooling, and inhibition caused a compensatory decrease in parasympathetic stimulation of the heart.
Seebacher
Frank
F
Integrative Physiology, School of Biological Sciences A08, The University of Sydney, 2006 Sydney, NSW, Australia. fseebach@bio.usyd.edu.au
Franklin
Craig E
CE
D000489:Alligators and Crocodiles / Q000502:physiology*; D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001831:Body Temperature / Q000502:physiology; D002320:Cardiovascular Physiological Phenomena; D003080:Cold Temperature; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004008:Diclofenac / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006358:Hot Temperature; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology; D020030:Nitric Oxide Donors / Q000008:administration & dosage / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000008:administration & dosage / Q000494:pharmacology; D011453:Prostaglandins / Q000502:physiology
D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D020030:Nitric Oxide Donors; D011453:Prostaglandins; D004008:Diclofenac; D009599:Nitroprusside; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester