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Journal of Experimental Biology, Vol 201, Issue 22 3085-3095, Copyright © 1998 by Company of Biologists
JOURNAL ARTICLES |
AE Julio, CJ Montpetit and SF Perry
Department of Biology, University of Ottawa, Ottawa, Ontario, Canada K1N 6N5. sfperry@science.uottawa.ca.
The direct and modulating effects of acidosis on catecholamine secretion in rainbow trout (Oncorhynchus mykiss) were assessed in vivo using cannulated fish and in situ using a perfused cardinal vein preparation. In situ, acidosis (a reduction in perfusate pH from 7.9 to 7.4) did not elicit catecholamine release or modulate the secretion of catecholamines evoked by the non-specific cholinergic receptor agonist carbachol (3x10(-7) to 10(-5 )mol kg-1) or the muscarinic receptor agonist pilocarpine (10(-7 )mol kg-1). Acidosis, however, significantly increased the secretion rates of noradrenaline and adrenaline in response to nicotine (10(-8) to 10(-7 )mol kg-1). In vivo, intra-arterial injections of nicotine (300-600 nmol kg-1) into normocapnic or moderately hypercapnic fish (water PCO2=5 mmHg or 0.67 kPa) caused a dose-dependent elevation of circulating catecholamine levels. At the highest dose of nicotine, the rise in plasma catecholamine levels was significantly enhanced in the hypercapnic fish. Acute hypoxia in vivo caused an abrupt release of catecholamines when arterial haemoglobin O2-saturation was reduced to approximately 55-60 %; this catecholamine release threshold during hypoxia was unaltered in hypercapnic fish. However, the hypoxia-induced catecholamine release was significantly greater in hypercapnic fish than in normocapnic fish. The results of this study suggest that blood acid-base status, while not influencing catecholamine secretion directly or influencing the blood O2 content threshold for catecholamine release during hypoxia, may modulate the secretory process specifically in response to nicotinic receptor stimulation of chromaffin cells.
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