Constancy and control of heart rate during an increase in temperature in the Antarctic fish Pagothenia borchgrevinki

The effect of an acute temperature increase on the control of the heart of the Antarctic teleost Pagothenia borchgrevinki was examined. Heart rate was thermally independent over the range −1.2°C to 3°C, although increasing the temperature from −1.2°C to 3°C elicited a decrease in ventral aortic pressure. Administration of the muscarinic receptor antagonist atropine and the β-adrenoreceptor antagonist sotalol abolished the thermal independence of heart rate, with heart rate increasing at Q₁₀=2. As temperature was increased from −1.2°C to 3°C, cholinergic tone on the heart also increased, from 44.6±4.2% to 70.0±8.4%. At the same time the adrenergic tone increased from 35.5±3.3% to 43.0±3.1%, but the effect on the heart was masked by the increase of cholinergic tone, leading to the thermal independence of heart rate.     

Thermal sensitivity of heart rate and insensitivity of blood pressure in the Antarctic nototheniid fish <Emphasis Type="Italic">Pagothenia borchgrevinki</Emphasis>

The Antarctic notothenioids are among the most stenothermal of fishes, well adapted to their stable, cold and icy environment. The current study set out to investigate the thermal sensitivity/insensitivity of heart rate and ventral aortic blood pressure of the Antarctic nototheniid fish Pagothenia borchgrevinki over a range of temperatures. The heart rate increased rapidly from –1 to 6°C (Q₁₀=2.0–3.3), but was relatively insensitive to temperature above the ~6°C lethal limit of the species (Q₁₀=1.2). The increase in heart rate from –1 to 6°C was the result of a 45% increase in excitatory adrenergic tone, masking a 37% increase in inhibitory cholinergic tone. Ventral aortic pressure was regulated well above the lethal limit, up to at least 10°C. With the return of the fish to environmental temperatures, the heart rate rapidly decreased back to control levels, while ventral aortic pressure increased and remained elevated for over an hour following a 6°C exposure.     

Autonomic nervous control of blood pressure and heart rate during hypoxia in the cod,Gadus morhua

Summary The autonomic nervous and possible adrenergic humoral control of blood pressure and heart rate during hypoxia was investigated in Atlantic cod. The oxygen tension in the water was reduced to 4.0–5.3 kPa (i.e.. P_wO₂=30–40 mmHg), and the fish responded with an immediate increase in ventral and dorsal aortic blood pressure (P _va P _da), as well as a slowly developing bradycardia. The plasma concentrations of circulating catecholamines increased during hypoxia with a peak in the plasma level of noradrenaline occurring before the peak for adrenaline. Bretylium was used as a chemical tool to differentiate between neuronal and humoral adrenergic control of blood pressure and heart rate (f _H) during hypoxia. The increase in P _va and P _da in response to hypoxia was strongly reduced in bretylium-treated cod, which suggests that adrenergic nerves are responsible for hypoxic hypertension. In addition, a small contribution by circulating catecholamines to the adrenergic tonus affecting P _va during hypoxia was suggested by the decrease in P _va induced by injection of the -adrenoceptor antagonist phentolamine. The cholinergic and the adrenergic tonus affecting heart rate were estimated by injections of atropine and the -adrenoceptor antagonist sotalol. The experiments demonstrate an increased cholicholinergic as well as adrenergic tonus on the heart during hypoxia.     

Chronic hypoxic incubation blunts thermally dependent cholinergic tone on the cardiovascular system in embryonic American alligator (Alligator mississippiensis)

Environmental conditions play a major role in shaping reptilian embryonic development, but studies addressing the impact of interactions between chronic and acute environmental stressors on embryonic systems are lacking. In the present study, we investigated thermal dependence of cholinergic and adrenergic cardiovascular tone in embryonic American alligators (Alligator mississippiensis) and assessed possible phenotypic plasticity in a chronic hypoxic incubation treatment. We compared changes in heart rate (f _H) and mean arterial blood pressure (P _M) for chronically hypoxic and normoxic-incubated embryos after cholinergic and adrenergic blockade following three different acute temperature treatments: (1) 30 °C (control incubation temperature), (2) acute, progressive decrease 30–24 °C then held at 24 °C, and (3) acute, progressive increase 30–36 °C then held at 36 °C. f _H progressively fell in response to decreasing temperature and rose in response to increasing temperature. P _M did not significantly change with decreasing temperature, but was lowered significantly with increasing acute temperature in the normoxic group at 90 % of development only. Propranolol administration (β adrenergic antagonist) produced a significant f _H decrease at 24, 30, and 36 °C that was similar at all temperatures for all groups. For normoxic-incubated embryos at 90 % of development, atropine administration (cholinergic antagonist) significantly increased f _H in both 24 and 36 °C treatments, but not in the 30 °C control treatment. This atropine response at 24 and 36 °C demonstrated acute thermally dependent cholinergic tone on f _H late in development for normoxic-incubated, but not chronically hypoxic-incubated embryos. Collectively, data indicated that cardiovascular control mechanisms in embryonic alligators may be activated by thermal extremes, and the maturation of control mechanisms was delayed by chronic hypoxia.     

Drug induced changes in cardio-vascular parameters in the Atlantic cod,Gadus morhua

Summary Ventral (VAP) and dorsal (DAP) aortic blood pressure, heart rate (HR) and cardiac output ( ) were recorded simultaneously in unanaesthetized Atlantic cod, and the effects of vasoactive drugs on the cardio-vascular parameters studied. Mean resting values for the parameters were VAP=4,39 kPa, DAP=2,49 kPa, HR=41 beats/min, and = 29,1 ml/min×kg. Adrenaline constricted the systemic vasculature, dilated the branchial vasculature and caused a decrease of HR and due to a cholinergic reflex. After atropine pre-treatment this reflex was abolished, and the effect of adrenaline on blood pressure enhanced. A small decrease in persisted after atropine, presumably reflecting the effect of an increased end-systolic afterload.Phenylephrine produced a weak increase in systemic vascular resistance, while isoprenaline lowered both systemic and branchial vascular resistance. The effect of isoprenaline is probably mediated by beta adrenoceptors in both vascular beds, since propranolol antagonizes the effect.Acetylcholine in low doses produces a drop in without affecting HR, while higher doses also stop the heart. There is no significant change in either branchial and systemic vascular resistance after acetylcholine.Abbreviations VAP mean ventral aortic blood pressure - DAP mean dorsal aortic blood pressure - TBPD trans-branchial blood pressure drop - HR heart rate - SV stroke volume - cardiac output (ventral aortic blood flow) - VR _g branchial vascular resistance - VR _s systemic vascular resistance     

Effect of the dry-cold season dormancy on the tonic and phasic neural control of heart rate in the toad, Bufo paracnemis

This work examined basal heart rate and autonomic cardiac tone as well as sympathetic cardiac reactivity to hypotension induced by systemic nitroprusside injection in dormant toads (dry-cold season), Bufo paracnemis, comparing the values with those of toads collected during the active months (hot-rainy season). Autonomic tone was calculated according to the method of Lin and Horwath ('72), which allows its evaluation as a percentage of intrinsic heart rate. Specimens were maintained in an outdoors terrarium except for the week preceding surgery, when they were transferred to indoor nonclimatized tanks. The heart rate of dormant toads (27.8 +/- 2.7 beats/min) was lower than that of active toads at rest (38.6 +/- 2. 3). Cholinergic tone was higher than adrenergic tone both in active (26.2% and 7.8%, respectively) and aestivated (19.5% and 4.8%, respectively) animals. Thus, cholinergic tone and adrenergic tone were both lower in dormant animals. The reflex tachycardia elicited by nitroprusside-induced hypotension was lower in aestivated toads (9.3 +/- 0.9 beats/min) when compared to active toads (19.9 +/- 1.0), indicating a reduced sympathetic reactivity. Nitroprusside-induced hypotensions were not different in the two groups. We conclude that at rest Bufo paracnemis heart is under the influence of a double cholinergic and adrenergic tone, and that both influences, as well as the reflex adrenergic reactivity to the unloading produced by nitroprusside-induced hypotension, are reduced in aestivated toads.     

Autonomic control of heart rate is virtually independent of temperature but seems related to the neuroanatomy of the efferent vagal supply to the heart in the bullfrog, Lithobathes catesbeianus

Bullfrogs, Lithobathes catesbeianus, bearing a femoral artery cannula were held at 3 temperatures (10, 20 and 30 °C) for 24 h. Changes in heart rate were recorded before and after injection of cholinergic and adrenergic antagonists. Normal heart rate doubled for each temperature increment. Adrenergic tone on the heart varied around 20% at all 3 temperatures but cholinergic tone increased from −5% to 10% between 10 and 30 °C. In contrast, cholinergic tone increased from 75% at 5 °C to 329% at 25 °C in Xenopus laevis. Injection of the neural tracer True Blue into the cervical vagus of the bullfrog revealed a single location for vagal preganglionic neurons (VPN) in the dorsal vagal motor nucleus (DVN), while Xenopus had 30% of its VPN in a ventro-lateral group outside the DVN. Broader comparative studies have suggested that differences in the extent of vagal tone may relate to the location of VPN in the brainstem and this may be the case in these amphibians.     

Ontogeny of cholinergic and adrenergic cardiovascular regulation in the domestic chicken (Gallus gallus)

Adrenergic and cholinergic tone on the cardiovascular system of embryonic chickens was determined during days 12, 15, 19, 20, and 21 of development. Administration of the muscarinic antagonist atropine (1 mg/kg) resulted in no significant change in heart rate or arterial pressure at any developmental age. In addition, the general cardiovascular depressive effects of hypoxia were unaltered by pretreatment with atropine. In addition, the ganglionic blocking agent hexamethonium (25 mg/kg) did not induce changes in heart rate. The beta-adrenergic antagonist propranolol (3 mg/kg) induced a bradycardia of similar magnitude on all days studied, with a transient hypertensive action on days 19-20, indicating the existence of an important cardiac and vascular beta-adrenergic tone. Injections of the alpha-adrenergic antagonists prazosin or phentolamine (1 mg/kg) reduced arterial pressure significantly on all days of incubation studied. Collectively, the data indicate that embryonic chickens rely primarily on adrenergic control of cardiovascular function, with no contribution from the parasympathetic nervous system.     

Cholinergic and adrenergic influences on the heart of the African lungfish Protopterus annectens

Cardiac cholinergic and adrenergic tones were determined in minimally instrumented African lungfish Protopterus annectens. Mean ±S.E. routine heart rate (f_H) was 31·6 ± 1·4 beats min^?1, cholinergic tone was 34·6 ± 5·2% and adrenergic tone was 9·4 ± 2·3%, while the intrinsic f_H after blockade of both adrenergic and cholinergic control systems was 39·1 ± 1·3 beats min^?1. It is demonstrated that routine cholinergic tone has probably been underestimated in previous studies on lungfishes, suggesting that withdrawal of vagal tone may provide an important mechanism to increase f_H in this group of fishes during, for example, air breathing.     

Cardiac Arrest during Gamete Release in Chum Salmon Regulated by the Parasympathetic Nerve System

Cardiac arrest caused by startling stimuli, such as visual and vibration stimuli, has been reported in some animals and could be considered as an extraordinary case of bradycardia and defined as reversible missed heart beats. Variability of the heart rate is established as a balance between an autonomic system, namely cholinergic vagus inhibition, and excitatory adrenergic stimulation of neural and hormonal action in teleost. However, the cardiac arrest and its regulating nervous mechanism remain poorly understood. We show, by using electrocardiogram (ECG) data loggers, that cardiac arrest occurs in chum salmon (Oncorhynchus keta) at the moment of gamete release for 7.39±1.61 s in females and for 5.20±0.97 s in males. The increase in heart rate during spawning behavior relative to the background rate during the resting period suggests that cardiac arrest is a characteristic physiological phenomenon of the extraordinarily high heart rate during spawning behavior. The ECG morphological analysis showed a peaked and tall T-wave adjacent to the cardiac arrest, indicating an increase in potassium permeability in cardiac muscle cells, which would function to retard the cardiac action potential. Pharmacological studies showed that the cardiac arrest was abolished by injection of atropine, a muscarinic receptor antagonist, revealing that the cardiac arrest is a reflex response of the parasympathetic nerve system, although injection of sotalol, a β-adrenergic antagonist, did not affect the cardiac arrest. We conclude that cardiac arrest during gamete release in spawning release in spawning chum salmon is a physiological reflex response controlled by the parasympathetic nervous system. This cardiac arrest represents a response to the gaping behavior that occurs at the moment of gamete release.     

Resting and maximal heart rates in ectothermic vertebrates

Resting and maximal heart rates (HR) in ectothermic vertebrates are generally lower than those in endotherms and vary by more than an order of magnitude interspecifically. Variation of HR transcends phylogeny and is influenced by numerous factors including temperature, activity, gas exchange, intracardiac shunts, pH, posture, and reflexogenic regulation of blood pressure. The characteristic resting HR is rarely the intrinsic rate of the pacemaker, which is primarily modulated by cholinergic inhibition and adrenergic excitation in most species. Neuropeptides also appear to be involved in cardiac regulation, although their role is not well understood. The principal determinants of resting HR include temperature, metabolic rate and hemodynamic requirements. Maximal HRs generally do not exceed 120 b min-1, but notable exceptions include the heterothermic tuna and small reptiles having HRs in excess of 300 b min-1 at higher body temperatures. Temperature affects the intrinsic pacemaker rate as well as the relative influence of adrenergic and cholinergic modulation. It also influences the evolved capability to increase HR, with maximal cardiac responses matched to preferred body temperatures in some species. Additional factors either facilitate or limit the maximal level of HR, including: (1) characteristics of the pacemaker potential; (2) development of sarcoplasmic reticulum as a calcium store in excitation-contraction coupling; (3) low-resistance coupling of myocardial cells; (4) limitations of force development imposed by rate changes; (5) efficacy of sympathetic modulation; and (6) development of coronary circulation to enhance oxygen delivery to myocardium. In evolutionary terms, both hemodynamic and oxygen requirements appear to have been key selection pressures for rapid cardiac rates.     

Ambulatory blood pressure during once-daily randomised double-blind administration of atenolol,metoprolol, pindolol,and slow-release propranolol

Intra-arterial ambulatory blood pressure was measured over 24 hours, in 34 patients with newly diagnosed hypertension, both before and after double-blind randomisation to treatment with atenolol (n=9), metoprolol (n=9), pindolol (n=9), or propranolol in its slow-release form (n=7). The dosage of each drug was adjusted at monthly clinic visits until satisfactory control of blood pressure was achieved (140/90 mm Hg or less by cuff) or the maximum dose in the study protocol was reached. A second intra-arterial recording was made after these drugs had been taken once daily at 0800 for three to eight months (mean 5·0±SD 1·4) and was started four hours after the last dose.At the end of the 24-hour recordings blood pressure was significantly lower with all four drugs. The extent to which the drugs reduced blood pressure, however, differed over the 24 hours. Atenolol lowered mean arterial pressure significantly throughout all 24 recorded hours, metoprolol for 12 hours, pindolol for 15 hours, and slow-release propranolol for 22 hours. Neither metoprolol nor pindolol lowered blood pressure during sleep. A significant reduction in heart rate was observed over 20 hours with atenolol, 20 hours with metoprolol, 10 hours with pindolol, and 24 hours with slow-release propranolol. Atenolol, metoprolol, and slow-release propranolol continued to slow the heart rate 24 hours after the last tablet was taken; this effect on heart rate, however, was not sustained throughout the second morning in those patients taking atenolol. Pindolol, the only drug studied that has intrinsic sympathomimetic activity, increased heart rate and did not lower blood pressure during sleep.Atenolol and slow-release propranolol are effective as antihypertensive agents over 24 hours when taken once daily, whereas metoprolol and pindolol may need to be taken more frequently. At times of low sympathetic tone, however, such as during sleep, beta-blockers with intrinsic sympathomimetic activity may raise heart rate and attenuate the fall in blood pressure with treatment.     

Low and nonrhythmic heart rate of the mole rat (Spalax ehrenbergi): Control by the autonomic nervous system

Summary ECG of mole rats (Spalax ehrenbergi) was recorded by chronically implanted electrodes. The average heart rate of unrestrained, resting animals (mean body mass 191 g±35 S.D.) in normoxia and at room temperature is 152 beats/min±42 S.D. It is nonrhythmic and about one third of the rate expected for an animal of this mass. ECG revealed that each heart beat is normal. From atropine and propranolol administration, it was evident that the low heart rate results from : (a) low intrinsic heart rate (285 b/min±30 S.D.), (b) high parasympathetic tone (51%±12 S.D.) and (c) low sympathetic tone (3.6%±1.6 S.D.). Unilateral vagotomy showed that the degree of left or right vagus dominancy in the mole rat differs in each individual: it may even reach a complete left vagus control, in contrast to other mammals where right vagus dominancy is apparent.     

Sinus rhythm: mechanisms and function

The normal cardiac rhythm originates in a specialized region of the heart, the sinus node that is part of the nodal tissue. The rhythmic, impulse initiation of sinus node pacemaker cells results from a spontaneous diastolic depolarization that is initiated immediately after repolarization of the preceding actions potential. This slow diastolic depolarisation is typical of automatic cells and essential to their function. Several currents are involved in this diastolic depolarisation: a hyperpolarization activated inward current, termed "pacemaker" I(f) current, two Ca2+ currents (a L type and a T type), a delayed K+ current and a Na/Ca exchange current. The frequency of the automatic discharge is the main determinant of heart rate. However the sinus node activity is regulated by adrenergic and cholinergic neurotransmitters. Acetylcholine provokes the hyperpolarization of pacemaker cells and decreases the speed of the spontaneous diastolic depolarisation, thus slowing the sinus rate. Catecholamines lead to sinus tachycardia by increasing the diastolic depolarisation speed. In normal conditions, the observed resting heart rate is lower than the intrinsic frequency of the sinus node due to a "predominance" of the vagal tone. Neural regulation of the heart rate aims at meeting the metabolic needs of the tissues through a varying blood flow. Differences between diurnal and nocturnal mean heart rates are accounted for by neural influences. During the night, the increased vagal tone results in decreased heart rate. The exercise-induced tachycardia results from the sympathetic stimulation. It allows more blood to reach skeletal muscles, and as a consequence an increased supply of oxygen and nutrients. Compared to the variety of clinical arrhythmias, sinus rhythm is the basis for optimal exercise capacity and quality of life.     

The modulatory effects of noradrenaline on vagal control of heart rate in the dogfish,Squalus acanthias

The possible interactions between inhibitory vagal control of the heart and circulating levels of catecholamines in dogfish (Squalus acanthias) were studied using an in situ preparation of the heart, which retained intact its innervation from centrally cut vagus nerves. The response to peripheral vagal stimulation typically consisted of an initial cardiac arrest, followed by an escape beat, leading to renewed beating at a mean heart rate lower than the prestimulation rate (partial recovery). Cessation of vagal stimulation led to a transient increase in heart rate, above the prestimulation rate. This whole response was completely abolished by 10(-4) M atropine (a muscarinic cholinergic antagonist). The degree of vagal inhibition was evaluated in terms of both the initial, maximal cardiac interval and the mean heart rate during partial recovery, both expressed as a percentage of the prestimulation heart rate. The mean prestimulation heart rate of this preparation (36+/-4 beats min(-1)) was not affected by noradrenaline but was significantly reduced by 10(-4) M nadolol (a beta-adrenergic receptor antagonist), suggesting the existence of a resting adrenergic tone arising from endogenous catecholamines. The degree of vagal inhibition of heart rate varied with the rate of stimulation and was increased by the presence of 10(-8) M noradrenaline (the normal in vivo level in routinely active fish), while 10(-7) M noradrenaline (the in vivo level measured in disturbed or deeply hypoxic fish) reduced the cardiac response to vagal stimulation. In the presence of 10(-7) M noradrenaline, 10(-4) M nadolol further reduced the vagal response, while 10(-4) M nadolol + 10(-4) M phentolamine had no effect, indicating a complex interaction between adrenoreceptors, possibly involving presynaptic modulation of vagal inhibition.     

Effects of autonomic blockade on acute thermal tolerance and cardioventilatory performance in rainbow trout,Oncorhynchus mykiss

Predicted future increases in global temperature may impose challenges for ectothermic animals like fish, but the physiological mechanisms determining the critical thermal maximum (CT_max) are not well understood. One hypothesis suggests that impaired cardiac performance, limited by oxygen supply, is an important underlying mechanism. Since vagal bradycardia is suggested to improve cardiac oxygenation and adrenergic stimulation may improve cardiac contractility and protect cardiac function at high temperatures, we predicted that pharmacological blockade of cardiac autonomic control would lower CT_max. Rainbow trout was instrumented with a flow probe and a ventilation catheter for cardioventilatory recordings and exposed to an acute thermal challenge until CT_max following selective pharmacological blockade of muscarinic or β-adrenergic receptors.Contrary to our prediction, CT_max (~26 °C) was unchanged between treatments. While β-adrenergic blockade reduced heart rate it did not impair cardiac stroke volume across temperatures suggesting that compensatory increases in cardiac filling pressure may serve to maintain cardiac output. While warming resulted in significant tachycardia and increased cardiac output, a high cholinergic tone on the heart was observed at temperatures approaching CT_max. This may represent a mechanism to maintain scope for heart rate and possibly to improve myocardial contractility and oxygen supply at high temperatures. This is the first study evaluating the importance of autonomic cardiac control on thermal tolerance in fish. While no effects on CT_max were observed, this study raises important questions about the underlying mechanisms determining thermal tolerance limits in ectothermic animals.     

Thermal bradycardia during radiofrequency irradiation

The present study was performed to determine if any heart rate or blood pressure changes occur during intermittent exposure to radiofrequency radiation (RFR), and to determine if parasympathetic blockade due to atropine has any effect on these changes or on thermal responses. Anesthetized rats were exposed to 2.8 GHz pulsed RFR at an average power level of 60 mW/cm2 (average specific absorption rate, 14 W/kg). During an initial exposure period to raise colonic temperature to 39.5 degrees C, heart rate decreased significantly. This thermal bradycardia is similar to that reported by other investigators during environmental heat exposure. Intermittent exposure to radiation, which was designed to result in 1 degree C colonic temperature changes, did not significantly affect heart rate or mean arterial blood pressure, before or after atropine administration. The time courses of these 1 degree C temperature changes were not altered significantly by atropine. Following administration of atropine, the thermal bradycardia during the initial heating period was still evident. Thus, factors other than vagal activity are responsible for the phenomenon. It is possible that the bradycardia is a consequence of a general reduction in metabolism, which occurs also during environmental heat exposure.     

Cardiac output and peripheral resistance of swim-trained rats under urethan anesthesia.

Several circulatory variables were determined in control and swim-trained white rats under urethan anesthesia. Trained animals exhibited significantly lower heart rate and cardiac index and significantly higher peripheral resistance than control animals. Blood pressure, systolic index and left ventricular work output were not statistically different in the two groups. These results suggest an alteration of resting cardiovascular regulation in trained animals. Beta adrenergic mechanisms are suppressed by increased parasympathetic tone, and the resting circulatory balance is maintained mainly by increased alfa adrenergic mechanisms.     

Heat production as a criterion of adrenergic regulation of metabolic processes of the myocardium

Bolus injection of adrenaline in coronary perfusion blood flow caused different-directed changes in coronary venous blood temperature. Directivity and myocardium heat production changes are determined by peculiarities of interactions between adrenergic and cholinergic mechanisms of cardiodynamics and myocardial metabolism regulation. Cholinergic blockade by atropine++ increases heat production and limits negative ino- and chronotropic components of cardiac adrenergic reactions. That increase is completely eliminated by subsequent obsidan blockade of beta-adrenoreceptors.     

Autonomic control of the heart in the Asian swamp eel (Monopterus albus)

The Asian swamp eel (Monopterus albus) is an air-breathing teleost with very reduced gills that uses the buccal cavity for air-breathing. Here we characterise the cardiovascular changes associated with the intermittent breathing pattern in M. albus and we study the autonomic control of the heart during water- and air-breathing. The shift from water- to air-breathing was associated with a rise in heart rate from 27.7 ± 1.6 to 41.4 ± 2.6 min(-1) and an increase in cardiac output from 23.1 ± 3.0 to 58.7 ± 6.5 mLmin(-1)kg(-1), while mean systemic blood pressure did not change (39.0 ± 3.5 and 46.4 ± 1.3 cmH(2)O). The autonomic control of the heart during water- and air-breathing was revealed by infusion of the β-adrenergic antagonist propranolol and muscarinic antagonist atropine (3 mgkg(-1)) in eels instrumented with an arterial catheter. Inhibition of the sympathetic and parasympathetic innervations of the heart revealed a strong vagal tone on the heart of water-breathing eels and that the tachycardia during air-breathing is primarily mediated by withdrawal of cholinergic tone.