The influence of temperature and anaemia on the adrenergic and cholinergic mechanisms controlling heart rate in the rainbow trout

1979 ◽  
Vol 57 (12) ◽  
pp. 2440-2447 ◽  
Author(s):  
Chris M. Wood ◽  
Patricia Pieprzak ◽  
J. N. Trott

The capacity for cardioacceleration by adrenergic and cholinergic mechanisms was studied in resting rainbow trout, Salmo gairdneri, at 5, 12, and 20 °C. The trout were fitted with chronic dorsal aortic catheters for heart rate and blood pressure measurements. At all three temperatures, muscarinic cholinergic blockade with atropine caused substantial tachycardia, thereby indicating the presence of cholinergic vagal tone in resting animals. The relative effect of atropine was significantly greater at 5 °C (+53% of resting heart rate) than at 12 and 20 °C (≈ +30%). Maximal adrenergic stimulation (via adrenaline) after atropine caused a small further cardioacceleration at all temperatures. The adrenaline effect increased significantly from +8% (of resting heart rate) at 5 °C to +15% at 20 °C. The findings provide qualified support for the hypothesis that a reduction in vagal cholinergic activity is relatively more important in tachycardia at low temperature, and that adrenergic stimulation is relatively more important at high temperature, although the cardioacceleratory capacity of the cholinergic mechanism remains dominant throughout. The increase in heart rate accompanying experimental anaemia (haematocrit ≤ 6%) at all three temperatures was almost entirely due to a removal of vagal cholinergic tone; the contribution of adrenergic mechanisms, if any, was small.

1975 ◽  
Vol 53 (11) ◽  
pp. 1569-1577 ◽  
Author(s):  
Chris M. Wood

The adrenergic and cholinergic mechanisms regulating branchial vascular resistance in the trout have been studied using a whole gill preparation perfused at constant flow under approximately normal afferent and efferent levels of blood pressure. The receptors have been pharmacologically characterized by agonist potency comparisons within individual preparations and by the use of specific antagonists. The predominant response to adrenergic stimulation is vasodilation mediated by β-receptors, but a more rapid vasoconstriction mediated by α-receptors may also occur. The β-adrenoreceptors appear to be of the β1, variety, as in the homologous coronary vasculature of mammals. The cholinergic receptors of the gills are purely muscarinic in nature and mediate vasoconstriction. The possible functions of the mechanisms are discussed.


1996 ◽  
Vol 199 (7) ◽  
pp. 1563-1568 ◽  
Author(s):  
P E Signore ◽  
D R Jones

Neural control of the cardiac responses to exercise in air (running) and under water (diving) was studied in the muskrat (Ondatra zibethicus) by means of acute pharmacological blockade with the muscarinic blocker atropine and the beta-adrenergic blocker nadolol. Saline injection was used as a control. Controls running on a treadmill showed a marked increase in heart rate with exercise. Atropine-treated animals had a higher resting heart rate than controls, but heart rate still increased with running. Nadolol-treated animals had a lower resting heart rate than controls and displayed a less pronounced increase in heart rate with running than controls. Animals treated with a combination of atropine and nadolol had a resting heart rate similar to that of controls but their heart rate was unaffected by running. Thus, exercise tachycardia in muskrats is due to activation of the sympathetic system and also to a reduction in parasympathetic tone. Heart rate decreased markedly during voluntary submergence in controls but rose as muskrats swam submerged against increasing water flows. Nevertheless, diving bradycardia was still present. Free-diving bradycardia and the relative increase in heart rate with underwater exercise were abolished by atropine and unaffected by nadolol. Hence, unlike the cardiac response to exercise in air, the cardiac response to underwater exercise is due only to a reduction in parasympathetic tone. Injection of the beta-adrenergic agonist isoproterenol markedly increased heart rate in air but had little effect during voluntary and forced dives, indicating a marked decrease in the sensitivity of cardiac cells to adrenergic stimulation during submergence. These results strongly suggest that accentuated antagonism between the two branches of the autonomic nervous system occurs during diving so that parasympathetic influences on the heart predominate and inhibit any chronotropic response to adrenergic stimulation.


1975 ◽  
Vol 228 (2) ◽  
pp. 337-344 ◽  
Author(s):  
B Nuwayhid ◽  
Brinkman CR ◽  
C Su ◽  
JA Bevan ◽  
NS Assali

Development of parasympathetic and sympathetic reflexes controlling heart rate, vascular pressures, and blood flows was investigated in fetal lambs weighing 300-5,800 g (65-165 days' gestation). Cardiovascular responses to veratridine injections, atrial stretching, bilateral cervical vagotomy, and cholinergic blockade with atropine were used to test parasympathetic activities. Responses to propranolol and phenoxybenzamine were used to test beta- and alpha-adrenergic activities. Autonomic ganglionic blockade and stimulation provided additional information on both cholinergic and adrenergic systems. Fetal responses to various tests were compared to those of the mother. Results show: a) little parasympathetic tone on resting heart rate and other circulatory functions exists prior to fetal maturity; b) despite the feeble resting tone, the parasympathetic system is capable of exerting significant control when stimulated in both premature and mature fetuses, the capability increases as fetus approaches term; c) alpha- and beta-adrenergic tone in control of resting heart rate and peripheral circulation exists in early fetal life and increases as the fetus reaches maturity, and both adrenergic receptors respond strongly to stimuli in immature, premature, and mature fetuses; d) in immature fetuses, veratridine does not elicit a vagally mediated reflex; instead, it produces a centrally mediated alpha- and beta-adrenergic stimulation; e) the fetal cardiovascular response to any given test is dampened by the existence of the various vascular shunts, the umbilicoplacental circulation and, possibly, by incomplete maturation of vasomotor tone.


1989 ◽  
Vol 2 (3) ◽  
pp. 247-254 ◽  
Author(s):  
Craig W. Hawryshyn ◽  
Margaret G. Arnold ◽  
Duane J. Chaisson ◽  
Patricia C. Martin

AbstractThe present study examines the changes in ultraviolet (UV) photosensitivity that occur during the growth of rainbow trout (Salmo gairdneri). A comparison of the ocular media transmission of small (n = 3) and large (n = 3) trout eyes did not reveal large changes in the transmission of UV radiation through the eye. We used the heart-rate conditioning technique to measure spectral sensitivity in immobilized trout. Four trout, each weighing less than 30 g, exhibited a UV-sensitivity peak at 360 nm while four additional trout weighing more than 60 g each exhibited no evidence of UV sensitivity. Spectral-sensitivity measurements of two trout weighing 44 g and 60 g revealed UV sensitivity, but when measured one month later (after a 25% increase in body weight) both fish exhibited no UV-sensitivity peak. At this time their sensitivity appeared to conform to the known blue-sensitive cone mechanism.


1992 ◽  
Vol 167 (1) ◽  
pp. 179-201 ◽  
Author(s):  
M. Axelsson ◽  
W. Davison ◽  
M. E. Forster ◽  
A. P. Farrell

The aim of this study was to investigate cardiac performance and cardiovascular control in two red-blooded nototheniid species of antarctic fishes, Pagothenia bernacchii (a benthic fish) and P. borchgrevinki (a cryopelagic fish), and to make comparisons with existing information on haemoglobin-free antarctic teleosts. In quiescent P. bernacchii at 0 degrees C ventral aortic pressure (PVA) was 3.09 kPa and cardiac output (Q) was 17.6 ml min-1 kg-1, with a heart rate (fH) of 10.5 beats min-1 and stroke volume of 1.56 ml kg-1. Following atropine treatment, Q was maintained but heart rate increased and stroke volume decreased. Resting heart rate resulted from an inhibitory cholinergic tone of 80.4% and an excitatory adrenergic tone of 27.5%. The intrinsic heart rate was 21.7 beats min-1 at 0 degrees C. In quiescent P. borchgrevinki at 0 degrees C, PVA was 3.6 kPa, Q was 29.6 ml min-1 kg-1 and stroke volume was 2.16 ml kg-1. The resting heart rate in P. borchgrevinki of 11.3 beats min-1 resulted from an inhibitory cholinergic tone of 54.5% and an excitatory adrenergic tone of 3.2%. The intrinsic heart rate was 23.3 beats min-1. P. bernacchii maintained Q during a progressive decrease in water oxygen tension from 20 to 6.7 kPa, but fH was increased significantly. Thus, although there is cholinergic control of the heart, no hypoxic bradycardia was observed. Recovery from hypoxia was associated with increases in Q and fH; stroke volume returned to control values. PVA declined in recovery as total vascular resistance decreased. Hypoxic exposure following atropine treatment resulted in progressive increases in PVA, Q and stroke volume; fH decreased during the recovery period. Hypoxic exposure in P. borchgrevinki produced similar cardiovascular responses to those observed in P. bernacchii. During an acute increase in water temperature from 0 to 5 degrees C, P. bernacchii regulated Q and total vascular resistance. Stroke volume decreased as fH increased. The intrinsic heart rate had a Q10 of 1.96 over this temperature range. P. bernacchii maintained chronotropic inhibition up to a temperature of 2.5-3.0 degrees C. However, by 5 degrees C this chronotropic inhibition of the heart rate was lost. Infusion of adrenaline into the ventral aorta of P. bernacchii resulted in significant increases in Q, fH, PVA and total vascular resistance. Infusion of adrenaline after atropine treatment caused similar cardiovascular changes without the change in fH. P. borchgrevinki could sustain swimming in a water tunnel at approximately 1 body length per second for 6–10 min.(ABSTRACT TRUNCATED AT 400 WORDS)


Author(s):  
Lucas A. Zena ◽  
Andreas Ekström ◽  
Albin Gräns ◽  
Catharina Olsson ◽  
Michael Axelsson ◽  
...  

Coronary arteriosclerosis is a common feature of both wild and farmed salmonid fishes and may be linked to stress-induced cardiac pathologies. Yet, the plasticity and capacity for long-term myocardial restructuring and recovery following a restriction in coronary blood supply is unknown. Here, we analyzed the consequences of acute (3 days) and chronic (from 33 to 62 days) coronary occlusion (i.e., coronary artery ligation) on cardiac morphological characteristics and in vivo function in juvenile rainbow trout, Oncorhynchus mykiss. Acute coronary occlusion resulted in elevated resting heart rate and decreased inter-beat variability, which are both markers of autonomic dysfunction following acute myocardial ischemia, along with severely reduced heart rate scope (maximum – resting heart rate) relative to sham-operated trout. We also observed a loss of myocardial interstitial collagen and compact myocardium. Following long-term coronary- ligation, resting heart rate and heart rate scope normalized relative to sham-operated trout. Moreover, a distinct fibrous collagen layer separating the compact myocardium into two layers had formed. This may contribute to maintain ventricular integrity across the cardiac cycle, or alternatively, demark a region of the compact myocardium that continues to receive oxygen from the luminal venous blood. Taken together, we demonstrate that rainbow trout may cope with the aversive effects caused by coronary artery obstruction through plastic ventricular remodeling, which, at least in part, restores cardiac performance and myocardium oxygenation.


2013 ◽  
Vol 142 (2) ◽  
pp. 113-126 ◽  
Author(s):  
Pietro Mesirca ◽  
Laurine Marger ◽  
Futoshi Toyoda ◽  
Riccardo Rizzetto ◽  
Matthieu Audoubert ◽  
...  

Parasympathetic regulation of sinoatrial node (SAN) pacemaker activity modulates multiple ion channels to temper heart rate. The functional role of the G-protein–activated K+ current (IKACh) in the control of SAN pacemaking and heart rate is not completely understood. We have investigated the functional consequences of loss of IKACh in cholinergic regulation of pacemaker activity of SAN cells and in heart rate control under physiological situations mimicking the fight or flight response. We used knockout mice with loss of function of the Girk4 (Kir3.4) gene (Girk4−/− mice), which codes for an integral subunit of the cardiac IKACh channel. SAN pacemaker cells from Girk4−/− mice completely lacked IKACh. Loss of IKACh strongly reduced cholinergic regulation of pacemaker activity of SAN cells and isolated intact hearts. Telemetric recordings of electrocardiograms of freely moving mice showed that heart rate measured over a 24-h recording period was moderately increased (10%) in Girk4−/− animals. Although the relative extent of heart rate regulation of Girk4−/− mice was similar to that of wild-type animals, recovery of resting heart rate after stress, physical exercise, or pharmacological β-adrenergic stimulation of SAN pacemaking was significantly delayed in Girk4−/− animals. We conclude that IKACh plays a critical role in the kinetics of heart rate recovery to resting levels after sympathetic stimulation or after direct β-adrenergic stimulation of pacemaker activity. Our study thus uncovers a novel role for IKACh in SAN physiology and heart rate regulation.


1978 ◽  
Vol 56 (8) ◽  
pp. 1678-1683 ◽  
Author(s):  
D. G. Smith

Mean dorsal aortic blood pressure (Pda) and heart rate were measured in free-swimming rainbow trout (Salmo gairdneri). The fish were swum in a water tunnel at 0.5 body lengths/s (control) and were exercised at 45-min intervals by a 5-min period of rapid swimming at 2 body lengths/s.Control Pda was 4.0 ± 0.11 kPa and control heart rate was 56 ± 2.1 beats/min. During rapid swimming Pda and heart rate increased by 15 and 13% respectively. α-Receptor blockade with phentolamine (2 mg/kg) or adrenergic transmitter release blockade with bretylium (10 mg/kg) prevented the exercise hypertension and converted it to a decrease of 5% (phentolamine) or 18% (bretylium). Exercise tachycardia was reduced slightly by each compound. Phentolamine decreased the control Pda by 5%. Acute bretylium treatment increased Pda by 39% but Pda in fish treated chronically with bretylium was 30% below control and decreased by a further 6% during rapid swimming. The acute effects of these and other antihypertensive compounds are discussed. It is concluded that systemic blood pressure in trout is controlled by tonically active adrenergic nerves acting on systemic vessels via α-adrenoreceptors. These nerves produce a selective increase in peripheral resistance during rapid swimming.


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