Branchial CO(2) receptors and cardiorespiratory adjustments during hypercarbia in Pacific spiny dogfish (Squalus acanthias).

Adult Pacific spiny dogfish (Squalus acanthias) were exposed to acute (approximately 20 min) hypercarbia while we monitored arterial blood pressure, systemic vascular resistance (R(S)), cardiac output (V(b)) and frequency (fh) as well as ventilatory amplitude (V(AMP)) and frequency (f(V)). Separate series of experiments were conducted on control, atropinized (100 nmol kg(-1)) and branchially denervated fish to investigate putative CO(2)-chemoreceptive sites on the gills and their link to the autonomic nervous system and cardiorespiratory reflexes.In untreated fish, moderate hypercarbia (water CO(2 )partial pressure; Pw(CO2)=6.4+/-0.1 mmHg) (1 mmHg=0.133 kPa) elicited significant increases in V(AMP) (of approximately 92 %) and f(V) (of approximately 18 %) as well as decreases in fh (of approximately 64 %), V.(b) (approximately 29 %) and arterial blood pressure (of approximately 11 %); R(S) did not change significantly. Denervation of the branchial branches of cranial nerves IX and X to the pseudobranch and each gill arch eliminated all cardiorespiratory responses to hypercarbia. Prior administration of the muscarinic receptor antagonist atropine also abolished the hypercarbia-induced ventilatory responses and virtually eliminated all CO(2)-elicited cardiovascular adjustments. Although the atropinized dogfish displayed a hypercarbic bradycardia, the magnitude of the response was significantly attenuated (36+/-6 % decrease in fh in controls versus 9+/-2 % decrease in atropinized fish; means +/- s.e.m.).Thus, the results of the present study reveal the presence of gill CO(2) chemoreceptors in dogfish that are linked to numerous cardiorespiratory reflexes. In addition, because all cardiorespiratory responses to hypercarbia were abolished or attenuated by atropine, the CO(2) chemoreception process and/or one or more downstream elements probably involve cholinergic (muscarinic) neurotransmission.