The regulation of arterial pressure in early vertebrate embryos and larvae with non-innervated hearts is poorly understood. We used nanoliter intravascular injections in anaesthetized Xenopus laevis larvae (stage 49–51) to assess their ability to maintain arterial pressure in the face of a volume load. Injections of saline and hetastarch (a volume expander) were made into the ventricle. Arterial pressure, end-diastolic ventricular volume, end-systolic ventricular volume and heart rate were measured. Injection of 800 nl caused a rapid rise in arterial pressure and stroke volume. There were no changes in heart rate, indicating the absence of an arterial baroreflex. Blood pressure in saline-injected animals recovered quickly (within 5 min), whereas hetastarch injections caused hypertension to be maintained for much longer, for over 40 min in the most extreme case. We surmise that Starling forces at the capillary play an important role in pressure regulation but are not adequate to explain the entire response. Finally, there was ample evidence for a Frank-Starling relationship in the ventricle.

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 (α)-adrenoreceptors of the systemic vasculature, this antagonist was used as a tool to assess the importance of (α)-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 (α)-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.

We present evidence to support the hypothesis that the arterial anastomosis and the cogteeth-like valves located in the sub-pulmonary conus in the right ventricle are important sites of cardiovascular regulation in the crocodile Crocodylus porosus. The influence of the arterial anastomosis on the development of the 'foramen spike' in the left aortic pressure trace, which occurs at the onset of diastole when the pressures in the right and left aortas become equal, and on gastrointestinal blood flow was examined in unanaesthetised C. porosus using blood vessel occluders. Measurements of blood flow in the arterial anastomosis showed that, during non-shunting conditions, there was a substantial systolic blood flow from the right aorta into the coeliac artery. The total coeliac artery blood flow was the sum of the anastomosis flow from the right aorta plus the left aortic flow originating from the right aorta via the foramen of Panizza during diastole. During mechanically induced pulmonary-to-systemic shunting, the anastomosis blood flow was reversed, with blood flowing from the left to the right aorta. The magnitude of the 'foramen spike' was directly related to the vascular resistance in the anastomosis. When vascular resistance in the anastomosis was high, such as during mechanical occlusion, there was an increase in the right aortic to left aortic pressure gradient during systole which resulted in an increase the foramen spike amplitude. Recordings of right intraventricular pressure in unanaesthetised C. porosus showed spontaneous changes in right intracardiac systolic pressure. The pressure recordings were biphasic, with the second contraction (isometric) being highly variable in size, indicating the control of pulmonary outflow resistance, possibly via the 'cogteeth valves' located in the sub-pulmonary conus in the right ventricle.

A variety of in vivo and in situ experiments were performed on the Atlantic hagfish (Myxine glutinosa) (i) to characterize the levels of circulating catecholamines during acute stresses, including hypoxia, anoxia or physical disturbance (air-exposure), and (ii) to evaluate the potential mechanisms of catecholamine release from the major sites of storage, the systemic heart and posterior cardinal vein (PCV). Adrenaline and noradrenaline were stored at roughly equivalent concentrations (approximately 20 microgram g-1) in cardiac tissue, whereas noradrenaline was the predominant catecholamine stored in the PCV (approximately 50 microgram g-1). The heart stored larger quantities of total catecholamines than did the PCV (approximately three times greater) owing to its larger mass and higher concentration of adrenaline. Exposure of chronically cannulated hagfish to acute hypoxia [mean water PO2 (PwO2)=1.4 kPa; 10.5 mmHg) for 30 min caused a significant decrease in arterial PO2 (from 11.5+/−1.3 kPa to 1.2+/−0.3 kPa) and arterial O2 content (from 3.9+/−0.3 ml 100 ml-1 to 0.9+/−0.2 ml 100 ml-1). The hypoxaemia was associated with a significant increase in plasma noradrenaline levels, whereas plasma adrenaline levels were unaffected. Exposure of uncannulated fish to anoxia (PwO2 approximately 0 kPa) or physical disturbance (15 min of air-exposure) also elicited pronounced increases in plasma noradrenaline levels (6–10 times) and, to a lesser extent, adrenaline levels (2–3 times). An in situ saline-perfused heart preparation was utilized in an attempt to elucidate the mechanism(s) underlying the stress-induced release of catecholamines from the chromaffin tissue of the heart and PCV. Non-specific cell membrane depolarization using 40 or 60 mmol l-1 K+ in the saline elicited a marked release of catecholamines, confirming the suitability of the preparation to assess specific physiological mechanisms of catecholamine release. Lower concentrations of K+ (15–20 mmol l-1) did not evoke catecholamine release, indicating that relatively minor elevation in plasma [K+], as might occur during hypoxia, is not a contributing factor. The cholinergic receptor agonist carbachol (10–5-10-4 mol kg-1) caused a significant release of catecholamines, yet the likelihood of a similar mechanism operating in vivo is doubtful because the hagfish heart is not thought to be innervated. Simulation of (i) internal hypoxaemia by perfusing with anoxic saline or (ii) physical disturbance by perfusing with relatively acidic saline (pH approximately 7.0) failed to elicit catecholamine release. Further, the elevation of perfusion (input) pressure to simulate a rise in venous blood pressure, as might occur during hypoxia or physical disturbance, was also without effect on release. The addition of pituitary extract (from Atlantic cod, Gadus morhua) to the inflowing saline caused a marked release of catecholamines from the chromaffin tissue.

The effects of serotonin (5-hydroxytryptamine; 5-HT) on catecholamine release from chromaffin tissue were investigated in the rainbow trout (Oncorhynchus mykiss) in vivo and in situ. Intra-arterial injections of serotonin in vivo caused dose-dependent (50–250 nmol kg-1) increases in both plasma noradrenaline and adrenaline levels. Pre-treatment of fish with the serotonergic receptor antagonist methysergide did not abolish these increases. An in situ saline-perfused head kidney preparation was developed and validated to study the potential direct effect of serotonin on catecholamine release. The chromaffin cells in the preparation showed a dose-dependent release of catecholamines in response to bolus injections of the cholinergic receptor agonist carbachol (10–7-10-4 mol kg-1). The carbachol-induced release of noradrenaline, but not of adrenaline, was reduced significantly when the nicotinic receptor antagonist hexamethonium (10–4 mol l-1) was present in the perfusion fluid. The removal of calcium from the perfusion fluid prevented the usual release of catecholamines evoked by carbachol. Bolus injections of serotonin (250 nmol kg-1) into the inflowing perfusion fluid resulted in significantly increased levels of adrenaline and noradrenaline in the outflowing perfusate. Addition of hexamethonium to the perfusion fluid did not abolish this serotonin-induced release of catecholamines. The serotonin-induced release of adrenaline, however, was abolished totally by the addition of methysergide. Serotonin is present in high concentrations (44.61+/−5.96 microgram g-1 tissue) in the anterior region of the posterior cardinal vein within the head kidney. Carbachol (10–5 mol kg-1) did not elicit release of the stored serotonin from the perfused head kidney preparation. We conclude that the chromaffin cells in the perfused trout head kidney preparation display characteristics similar to those of other vertebrates and that this preparation is a useful tool for studying the control of catecholamine release in fish. The results demonstrate that serotonin has a direct impact on the chromaffin cells by interacting with methysergide-sensitive receptors to initiate the release of adrenaline. The potential physiological role of serotonin on catecholamine release in trout is discussed.

The effects of serotonin (5-hydroxytryptamine; 5-HT) on continuously recorded dorsal and ventral aortic blood pressures, (Pda, Pva), arterial oxygen tension (PaO2), arterial carbon dioxide tension (PaCO2), extracellular pH (pHa), buccal pressure (Pbuccal) and plasma catecholamine levels were investigated in rainbow trout, Oncorhynchus mykiss. Intra-arterial injections of serotonin (50–250 nmol kg-1) caused a rapid decrease in Pda and an increase in Pva, suggesting vasoconstriction of the branchial vasculature. The blood pressure changes were accompanied by a reduction in PaO2 (approximately 3–8 kPa depending on the dose injected), an increase in PaCO2 (approximately 0.03–0.07 kPa) and a decrease in pHa (approximately 0.02–0.12 pH units). These changes, indicative of impaired gas transfer, occurred despite obvious hyperventilation based on measurements of buccal pressure. After pre- treatment with the serotonergic receptor antagonist methysergide, injections of 100 nmol kg-1 serotonin caused an increase in PaO2, a reduction in PaCO2 and an increase in pHa. Methysergide treatment did not affect the usual serotonin-induced hyperventilation or the reduction in Pda but did abolish the rise in Pva; indeed, Pva was lowered significantly by serotonin after methysergide treatment. This reduction in Pva was eliminated by pre-treatment of fish with the combination of methysergide and sotalol (beta-adrenoceptor antagonist), suggesting an adrenergic component to the overall blood pressure response. Analysis of plasma catecholamines after injection of serotonin revealed that high doses (50, 100, 250 nmol kg-1) caused significant increases in concentrations of both noradrenaline and adrenaline. We conclude that the cardio-respiratory effects of exogenous serotonin injections are complex and arise from several integrated responses, including the direct action of serotonin on receptors within the branchial and systemic vasculatures, indirect action on ganglionic receptors, and the stimulation of catecholamine release from adrenergic nerves and/or chromaffin cells.

Cardiac output, ventral and dorsal aortic blood pressure, heart rate, and coeliac and mesenteric artery blood flow were recorded simultaneously in the Atlantic cod, Gadus morhua L., at rest, during exercise, during hypoxia and after feeding. In the resting unfed animals, coeliac artery blood flow was 4.1 +/− 0.8 ml min-1 kg-1 and mesenteric artery blood flow was 3.5 +/− 1.1 ml min-1 kg-1 (mean +/− S.E.M., N = 10); together, these flows represent approximately 40% of the cardiac output. Exercise or exposure to hypoxia resulted in increased visceral vascular resistance, leading to reductions in the coeliac and mesenteric artery blood flows. Coeliac and mesenteric blood flows were increased 24 h after feeding and the coeliac and systemic vascular resistances decreased in comparison with the prefeeding values. Phentolamine did not affect the gastrointestinal artery blood flow, but produced a significant decrease in the mesenteric and systemic vascular resistance. Treatment with bretylium and phentolamine revealed differences between the coeliac and the mesenteric vasculature regarding the control mechanisms during hypoxia and during exercise and feeding. During hypoxia, an adrenergic control of the gastrointestinal vasculature with both nervous and humoral components was found, whereas during exercise and after feeding an additional non-adrenergic mechanism controlling gut blood flow was demonstrated.