RESUMO
Adult freshwater rainbow trout (Oncorhynchus mykiss) were exposed acutely (approximately 20 min) in a stepwise manner to increasing levels of environmental carbon dioxide ranging between 1.7 and 9.0 mmHg (0.23-1.2 kPa). Experiments were performed to examine, for the first time, the influence of hypercapnic acidosis on aspects of cardiovascular physiology including blood pressure, cardiac output and vascular resistance. Fish displayed dose (water CO(2) partial pressure) -dependent increases in ventral aortic (13-39 %) and dorsal aortic (17-54 %) blood pressures that reflected marked increases in systemic vascular resistance (16-78 %); branchial vascular resistance was unaffected by hypercapnia. At the highest level of hypercapnia (9.0 mmHg), central venous pressure was significantly elevated by 54 %. Although cardiac output remained constant, heart rate was significantly lowered by 4-7 beats min(-)(1) at the two highest levels of hypercapnia. To determine whether the cardiovascular responses to hypercapnia were being blunted by the stepwise increase in external P(CO2), a separate group of fish was exposed directly to a single step of hypercapnia (water P(CO2) 8.0 mmHg). The cardiovascular responses were similar to those exhibited by the more gradually exposed fish except that central venous pressure did not increase and the extent of the bradycardia was greater (13 beats min(-)(1)). After confirming the effectiveness of yohimbine in blocking the vasoconstrictory (&agr;)-adrenoreceptors of the systemic vasculature, this antagonist was used as a tool to assess the importance of (&agr;)-adrenoreceptor stimulation in promoting the cardiovascular responses during hypercapnia. Prior treatment of fish with yohimbine prevented the increased blood pressures and systemic vascular resistance during hypercapnia but did not influence the CO(2)-induced bradycardia. Plasma levels of catecholamines did not change during hypercapnia, and therefore the stimulation of the systemic (&agr;)-adrenoreceptors presumably reflected increased sympathetic nerve activity. To determine whether the cardiovascular changes elicited by hypercapnia were related to acidosis-induced hypoxaemia, fish were exposed to hypoxia in a stepwise manner (water P(O2) 65-151 mmHg). The cardiovascular responses to hypoxia were markedly different from those to hypercapnia and consisted of pronounced increases in systemic and branchial vascular resistance, but only at the most severe level of hypoxia; ventral and dorsal aortic pressures were unaffected. The differences between the responses to hypercapnia and hypoxia, coupled with the smaller reductions in blood oxygen content during hypercapnia, support the hypothesis that the cardiovascular responses to CO(2) are direct and are unrelated to hypoxaemia.
RESUMO
The stimulatory effects of angiotensin II (Ang II) on catecholamine release and the contributions of the renin-angiotensin system, humoral catecholamines and adrenergic nerves to blood pressure regulation were investigated in rainbow trout (Oncorhynchus mykiss) and American eel (Anguilla rostrata). In trout, bolus injections of homologous [Asn1,Val5]-Ang II (100 or 500 pmol kg-1) increased catecholamine secretion rates and plasma catecholamine concentrations from in situ posterior cardinal vein preparations and chronically cannulated fish, respectively. In contrast, in situ or in vivo injections of similar doses of Ang II in eel did not affect catecholamine release. &agr; -Adrenoceptor blockade (prazosin; 1 mg kg-1) reduced the pressor effect of exogenous Ang II (500 pmol kg-1) in both species. In eel, intravenous injection of the smooth muscle relaxant papaverine (10 mg kg-1) elicited a rapid decrease in dorsal aortic pressure (PDA; 58 %) followed by a gradual recovery back to the baseline value 85 min after the treatment. In trout, papaverine elicited a similar decrease in blood pressure (62 %); however, PDA recovered fully 20 min after treatment. Blockade of either &agr; -adrenoceptors with prazosin or adrenergic nerves with bretylium (10 mg kg-1) prior to papaverine treatment did not alter PDA recovery in eel. In trout, &agr; -adrenoceptor and adrenergic nerve blockade prior to the papaverine treatment prevented and attenuated PDA recovery, respectively. In both species, papaverine treatment elicited significant increases in plasma catecholamine and Ang II concentrations. However, the increases in plasma catecholamine concentrations were markedly greater in trout than in eel. Similarly, the papaverine-elicited increase in plasma Ang II levels occurred earlier and was greater in trout than in eel. Thus, while Ang II stimulates humoral catecholamine release in trout, there is no evidence for a similar interaction in eel. Moreover, during hypotensive stress, although the renin-angiotensin system is recruited in both species, an essential involvement of adrenergic nerves and humoral catecholamines in the restoration of blood pressure is only apparent in trout.
RESUMO
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.