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First published online March 14, 2005
Journal of Experimental Biology 208, 1095-1107 (2005)
Published by The Company of Biologists 2005
doi: 10.1242/jeb.01480

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Cardiorespiratory responses to hypercarbia in tambaqui Colossoma macropomum: chemoreceptor orientation and specificity

K. M. Gilmour^1,2,*, W. K. Milsom^1,3, F. T. Rantin¹, S. G. Reid^1,4 and S. F. Perry^1,2

¹ Department of Physiological Sciences, Federal University of São Carlos, Via Washington Luiz km 235, São Carlos, SP, 13565-905, Brazil
² Department of Biology, University of Ottawa, 150 Louis Pasteur, Ottawa, ON, K1N 6N5 Canada
³ Department of Zoology, University of British Columbia, Vancouver, BC, V6T 1Z4 Canada
⁴ Department of Life Sciences, University of Toronto at Scarborough, Toronto, ON, M1C 1A4 Canada

^* Author for correspondence (e-mail: Katie.Gilmour{at}science.uottawa.ca)

Accepted 3 January 2005

Experiments were carried out to test the hypothesis that ventilatory and cardiovascular responses to hypercarbia (elevated water P_CO2) in the tambaqui Colossoma macropomum are stimulated by externally oriented receptors that are sensitive to water CO₂ tension as opposed to water pH. Cardiorespiratory responses to acute hypercarbia were evaluated in both the absence and presence of internal hypercarbia (elevated blood P_CO2), achieved by treating fish with the carbonic anhydrase inhibitor acetazolamide. Exposure to acute hypercarbia (15 min at each level, final water CO₂ tensions of 7.2, 15.5 and 26.3 mmHg) elicited significant increases in ventilation frequency (at 26.3 mmHg, a 42% increase over the normocarbic value) and amplitude (128%), together with a fall in heart rate (35%) and an increase in cardiac stroke volume (62%). Rapid washout of CO₂ from the water reversed these effects, and the timing of the changes in cardiorespiratory variables corresponded more closely to the fall in water P_CO2 (Pw_CO2) than to that in blood P_CO2 (Pa_CO2). Similar responses to acute hypercarbia (15 min, final Pw_CO2 of 13.6 mmHg) were observed in acetazolamide-treated (30 mg kg^-1) tambaqui. Acetazolamide treatment itself, however, increased Pa_CO2 (from 4.81±0.58 to 13.83±0.91 mmHg, mean ± S.E.M.; N=8) in the absence of significant change in ventilation, heart rate or cardiac stroke volume. The lack of response to changes in blood P_CO2 and/or pH were confirmed by comparing responses to the bolus injection of hypercarbic saline (5% or 10% CO₂; 2 ml kg^-1) into the caudal vein with those to the injection of CO₂-enriched water (1%, 3%, 5% or 10% CO₂; 50 ml kg^-1) into the buccal cavity. Whereas injections of hypercarbic saline were ineffective in eliciting cardiorespiratory responses, changes in ventilation and cardiovascular parameters accompanied injection of CO₂-laden water into the mouth. Similar injections of CO₂-free water acidified to the corresponding pH of the hypercarbic water (pH 6.3, 5.6, 5.3 or 4.9, respectively) generally did not stimulate cardiorespiratory responses. These results are in agreement with the hypothesis that in tambaqui, externally oriented chemoreceptors that are predominantly activated by increases in water P_CO2, rather than by accompanying decreases in water pH, are linked to the initiation of cardiorespiratory responses to hypercarbia.

Key words: tambaqui, Colossoma macropomum, hypercarbia, blood pressure, ventilation, blood flow, acetazolamide, CO₂, pH

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