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Synbranchus marmoratus is a facultative air-breathing fish, which uses its buccal cavity as well as its gills for air-breathing. S. marmoratus shows a very pronounced tachycardia when it surfaces to air-breathe. An elevation of heart rate decreases cardiac filling time and therefore may cause a decline in stroke volume (Vs), but this can be compensated for by an increase in venous tone to maintain stroke volume. Thus, the study on S. marmoratus was undertaken to investigate how stroke volume and venous function are affected during air-breathing. To this end we measured cardiac output (a), heart rate (fH), central venous blood pressure (PCV), mean circulatory filling pressure (MCFP), and dorsal aortic blood pressures (PDA) in S. marmoratus. Measurements were performed in aerated water (PO2>130 mmHg), when the fish alternated between gill ventilation and prolonged periods of apnoeas, as well as during hypoxia (PO2⩽50 mmHg), when the fish changed from gill ventilation to air-breathing. Q increased significantly (luring gill ventilation compared to apnoea in aerated water through a significant increase in both fH and Vs. PCV and MCFP also increased significantly. During hypoxia, when the animals surface to ventilate air, we found a marked rise in fH, PCV, MCFP, Q and VS, whereas FDA decreased significantly. Simultaneous increases in PCV and MCFP in aerated, as well as in hypoxic water, suggests that the venous system plays an important regulatory role for cardiac filling and Vs in this species. In addition, we investigated adrenergic regulation of the venous system through bolus infusions of adrenergic agonists (adrenaline, phenylephrine and isoproterenol; 2 µg kg-1). Adrenaline and phenylephrine caused a marked rise in FCV and MCFP, whereas isoproterenol led to a marked decrease in FCV, and tended to decrease MCFP. Thus, it is evident that stimulation of both α- and β-adrenoreceptors affects venous tone in S. marmoratus. [ABSTRACT FROM AUTHOR]

The effects of adrenergic stimulation on mean circulatory filling pressure (MCFP), central venous pressure (PCV) and stroke volume (Vs), as well as the effects of altered MCFP through changes of blood volume were investigated in rattlesnakes (Crotalus durissus). MCFP is an estimate of the upstream pressure driving blood towards the heart and is determined by blood volume and the activity of the smooth muscle cells in the veins (venous tone). MCFP can be determined as the plateau in PCV during a total occlusion of blood flow from the heart. VS decreased significantly when MCFP was lowered by reducing blood volume in anaesthetised snakes, whereas increased MCFP through infusion of blood (up to 3 ml kg-1) only led to a small rise in Vs. Thus, it seems that end-diastolic volume is not affected by an elevated MCFP in rattlesnakes. To investigate adrenergic regulation on venous tone, adrenaline as well as phenylephrine and isoproterenol (α- and β-adrenergic agonists, respectively) were infused as bolus injections (2 and 10 μg kg-1). Adrenaline and phenylephrine caused large increases in MCFP and PCV, whereas isoproterenol decreased both parameters. This was also the case in fully recovered snakes. Therefore, adrenaline affects venous tone through both α- and β-adrenergic receptors, but the α-adrenergic receptor dominates at the dosages used in the present study. Injection of the nitric oxide donor SNP caused a significant decrease in PCV and MCFP. Thus, nitric oxide seems to affect venous tone. [ABSTRACT FROM AUTHOR]

The effects of endothelin-1 (ET-1) on systemic and pulmonary circulation were investigated in anaesthetised freshwater turtles (Trachemys scripta) instrumented with arterial catheters and blood flow probes. Bolus intra-arterial injections of ET-1 (0.4–400 pmol kg-1) caused a dose-dependent systemic vasodilatation that was associated with a decrease in systemic pressure (Psys) and a rise in systemic blood flow (Qsys), causing systemic conductance (Gsys) to increase. ET-1 had no significant effects on the pulmonary vasculature, heart rate (fH) or total stroke volume (VStot). This response differs markedly from mammals, where ET-1 causes an initial vasodilatation that is followed by a pronounced pressor response. In mammals, the initial dilatation is caused by stimulation of ETB-receptors, while the subsequent constriction is mediated by ETA-receptors. In the turtles, infusion of the ETB-receptor agonist BQ-3020 (150 pmol kg-1) elicited haemodynamic changes that were similar to those of ET-1, and the effects of ET-1 were not affected by the ETA-antagonist BQ-610 (0.15 μmol kg-1). Conversely, all effects of ET-1 were virtually abolished after specific ETB-receptor blockade with the ETB-antagonist BQ-788 (0.15 μmol kg-1). The subsequent treatment with the general ET-receptor antagonist tezosentan (15.4 μmol kg-1) did not produce effects that differed from the treatment with ETB-antagonist, and the blockade of ET-1 responses persisted. This present study indicates, therefore, that ETB-receptors are responsible for the majority of the cardiovascular responses to ET-1 in Trachemys. [ABSTRACT FROM AUTHOR]

The effects of endothelin-1 (ET-1) on systemic and pulmonary circulation were investigated in anaesthetised freshwater turtles (Trachemys scripta) instrumented with arterial catheters and blood flow probes. Bolus intra-arterial injections of ET-1 (0.4-400 pmol kg(-1)) caused a dose-dependent systemic vasodilatation that was associated with a decrease in systemic pressure (P(sys)) and a rise in systemic blood flow (Q(sys)), causing systemic conductance (G(sys)) to increase. ET-1 had no significant effects on the pulmonary vasculature, heart rate (fh) or total stroke volume (Vs(tot)). This response differs markedly from mammals, where ET-1 causes an initial vasodilatation that is followed by a pronounced pressor response. In mammals, the initial dilatation is caused by stimulation of ET(B)-receptors, while the subsequent constriction is mediated by ET(A)-receptors. In the turtles, infusion of the ET(B)-receptor agonist BQ-3020 (150 pmol kg(-1)) elicited haemodynamic changes that were similar to those of ET-1, and the effects of ET-1 were not affected by the ET(A)-antagonist BQ-610 (0.15 micromol kg(-1)). Conversely, all effects of ET-1 were virtually abolished after specific ET(B)-receptor blockade with the ET(B)-antagonist BQ-788 (0.15 micromol kg(-1)). The subsequent treatment with the general ET-receptor antagonist tezosentan (15.4 micromol kg(-1)) did not produce effects that differed from the treatment with ET(B)-antagonist, and the blockade of ET-1 responses persisted. This present study indicates, therefore, that ET(B)-receptors are responsible for the majority of the cardiovascular responses to ET-1 in Trachemys.