The relative roles of external and internal CO(2) versus H(+) in eliciting the cardiorespiratory responses of Salmo salar and Squalus acanthias to hypercarbia.

Fish breathing hypercarbic water encounter externally elevated P(CO(2)) and proton levels ([H(+)]) and experience an associated internal respiratory acidosis, an elevation of blood P(CO(2)) and [H(+)]. The objective of the present study was to assess the potential relative contributions of CO(2) versus H(+) in promoting the cardiorespiratory responses of dogfish (Squalus acanthias) and Atlantic salmon (Salmo salar) to hypercarbia and to evaluate the relative contributions of externally versus internally oriented receptors in dogfish. In dogfish, the preferential stimulation of externally oriented branchial chemoreceptors using bolus injections (50 ml kg(-1)) of CO(2)-enriched (4 % CO(2)) sea water into the buccal cavity caused marked cardiorespiratory responses including bradycardia (-4.1+/-0.9 min(-1)), a reduction in cardiac output (-3.2+/-0.6 ml min(-1) kg(-1)), an increase in systemic vascular resistance (+0.3+/-0.2 mmHg ml min(-1) kg(-1)), arterial hypotension (-1.6+/-0.2 mmHg) and an increase in breathing amplitude (+0.3+/-0.09 mmHg) (means +/- S.E.M., N=9-11). Similar injections of CO(2)-free sea water acidified to the corresponding pH of the hypercarbic water (pH 6.3) did not significantly affect any of the measured cardiorespiratory variables (when compared with control injections). To preferentially stimulate putative internal CO(2)/H(+) chemoreceptors, hypercarbic saline (4 % CO(2)) was injected (2 ml kg(-1)) into the caudal vein. Apart from an increase in arterial blood pressure caused by volume loading, internally injected CO(2) was without effect on any measured variable. In salmon, injection of hypercarbic water into the buccal cavity caused a bradycardia (-13.9+/-3.8 min(-1)), a decrease in cardiac output (-5.3+/-1.2 ml min(-1) kg(-1)), an increase in systemic resistance (0.33+/-0.08 mmHg ml min(-1) kg(-1)) and increases in breathing frequency (9.7+/-2.2 min(-1)) and amplitude (1.2+/-0.2 mmHg) (means +/- S.E.M., N=8-12). Apart from a small increase in breathing amplitude (0.4+/-0.1 mmHg), these cardiorespiratory responses were not observed after injection of acidified water. These results demonstrate that, in dogfish and salmon, the external chemoreceptors linked to the initiation of cardiorespiratory responses during hypercarbia are predominantly stimulated by the increase in water P(CO(2)) rather than by the accompanying decrease in water pH. Furthermore, in dogfish, the cardiorespiratory responses to hypercarbia are probably exclusively derived from the stimulation of external CO(2) chemoreceptors, with no apparent contribution from internally oriented receptors.