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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
Cardiorespiratory responses to hypercarbia in tambaqui Colossoma macropomum: chemoreceptor orientation and specificity
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 PCO2) 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 PCO2), 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 PCO2 (PwCO2) than to that in blood PCO2 (PaCO2). Similar responses to acute hypercarbia (15 min, final PwCO2 of 13.6 mmHg) were observed in acetazolamide-treated (30 mg kg-1) tambaqui. Acetazolamide treatment itself, however, increased PaCO2 (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 PCO2 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 PCO2, 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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