Suppresion of autonomic postganglionic discharges by pentobarbital in dogs, with or without endotoxemia.

Initial effects of pentobarbital (8 mg/kg) on autonomic efferent and afferent discharge rates were studied in 26 dogs under morphine-chloralose anesthesia. Half of the dogs were given endotoxin E. coli (1 mg/kg) before pentobarbital. The postganglionic cervical vagal efferentation of all the dogs decreased as did the postganglionic cardiac sympathetic efferentation. The heart rate of the dogs given endotoxin decreased, while an increase in heart rate with abolition of respiratory arrhythmia, was observed in dogs without endotoxin. The aortic pressure of the former dogs dropped while it fell only slightly in the latter ones. The aortic arch baroreceptor activity decreased while the changes of left atrial B-type receptor activity were not significant. The changes of the left atrial and central venous pressures were slight but those of the pulmonary arterial pressure generally paralleled the changes in the aortic pressure. Pentobarbital, accordingly, seems to exert both sympatholytic and vagolytic effects. These explain the heart rate changes, as well as the impaired cardiac contractility it evokes. The obvious impairment of cardiovascular control mechanisms by pentobarbital should be seriously considered in investigations into the cardiovascular control.     

Suppression of autonomic postganglionic discharges by pentobarbital in dogs,with or without endotoxemia

Initial effects of pentobarbital (8 mg/kg) on autonomic efferent and afferent discharge rates were studied in 26 dogs under morphine-chloralose anesthesia. Half of the dogs were given endotoxin E. coli (1 mg/kg) before pentobarbital. The postganglionic cervical vagal efferentation of all the dogs decreased as did the postganglionic cardiac sympathetic efferentation. The heart rate of the dogs given endotoxin decreased, while an increase in heart rate with abolition of respiratory arrhythmia, was observed in dogs without endotoxin. The aortic pressure of the former dogs dropped while it fell only slightly in the latter ones. The aortic arch baroreceptor activity decreased while the changes of left atrial B-type receptor activity were not significant. The changes of the left atrial and central venous pressures were slight hut thosc of the pulmonary arterial pressure generally paralleled the changes in the aortic pressure. Pentobarbital, accordingly, seems to exert both sympatholytic and vagolytic effects. These explain the heart rate changes, as well as the impaired cardiac contractility it evokes. The obvious impairment of cardiovascular control mechanisms by pentobarbital should be seriously considered in investigations into the cardiovascular control.     

Influence of intravenous saline infusion on the aortic baroreceptor and left atrial B-type receptor activity in dogs

Influence of i.v. saline infusion on aortic arch pressure, left atrial mean pressure, heart rate, and the time-related characteristics of aortic arch baroreceptor and left atrial B-type receptor activities were studied in 20 beagle dogs. Saline infusion induced tachycardia in 10 dogs and bradycardia in 10. Aortic arch and left atrial pressures increased in both HR response groups. The average discharge rate of baroreceptors increased in both HR response groups, while the duration of baroreceptor burst, the number of baroreceptor action potentials/heart cycle and the average burst frequency did not increase significantly in the group that responded with tachycardia but increased significantly in the group that responded with bradycardia. The number of left atrial B-type action potentials/heart cycle, the average discharge rate and average burst frequency increased in both HR response groups. We conclude that the duration of baroreceptor burst, baroreceptor average burst frequency and the number of baroreceptor impulses/cardiac cycle are the important parameters eliciting baroreceptor reflex to i.v. saline infusion.     

Effect of acute intravenous volume loading on haemodynamics and aortic baroreceptor activity in dogs

This study evaluates the effect of acute intravenous volume loading on haemodynamics and aortic baroreceptor activity in order to determine the mechanistic factors responsible for divergent heart rate responses to volume loading. Eleven beagles were anaesthetized and instrumented for the recording of aortic pressure, diameter, flow and aortic baroreceptor activity. Isotonic saline, equal to 20% of the estimated blood volume, was infused intravenously within 60-90 s. The animals were divided into tachycardiac and bradycardic groups according to their heart rate response to volume loading. In the group developing the tachycardic response, aortic baroreceptor activity increased. Total peripheral resistance was reduced by 31% and variables representing aortic stretch, mean aortic pressure, diameter and tension remained unchanged. In contrast, in the group developing the bradycardiac response, aortic baroreceptor activity increased markedly. Also in this group peripheral resistance decreased, but only by 15%, which was significantly less than in the tachycardiac group. Factors determining aortic stretch, mean aortic pressure, diameter and tension also increased significantly. Earlier studies show that regardless of the resulting heart rate response, atrial receptor activity increases during volume loading. Thus, we conclude that during cardiac acceleration, marked peripheral vasodilation eliminates the stimulation of baroreceptors and therefore the tachycardic response caused by atrial receptors develops. In the case of cardiac slowing, vasodilation also takes place, but is not sufficient to prevent activation of baroreceptors. In consequence, increased baroreceptor activity overrides the tachycardic drive coming from the atrial receptors and a typical baroreceptor reflex becomes manifested.     

Functional changes in baroreceptor afferent, central and efferent components of the baroreflex circuitry in type 1 diabetic mice (OVE26)

Baroreflex control of heart rate (HR) is impaired in diabetes mellitus. We hypothesized that diabetes mellitus induced functional changes of neural components at multiple sites within the baroreflex arc. Type 1 diabetic mice (OVE26) and FVB control mice were anesthetized. Baroreflex-mediated HR responses to sodium nitroprusside- (SNP) and phenylephrine- (PE) induced mean arterial blood pressure (MAP) changes were measured. Baroreceptor function was characterized by measuring the percent (%) change of baseline integrated aortic depressor nerve activity (Int ADNA) in response to SNP- and PE-induced MAP changes. The HR responses to electrical stimulation of the left aortic depressor nerve (ADN) and the right vagus nerve were assessed. Compared with FVB control mice, we found in OVE26 mice that (1) baroreflex-mediated bradycardia and tachycardia were significantly reduced. (2) The baroreceptor afferent function in response to MAP increase did not differ, as assessed by the parameters of the logistic function curve. But, the inhibition of Int ADNA in response to MAP decrease was significantly attenuated. (3) The maximum amplitude of bradycardic responses to right vagal efferent stimulation was augmented. (4) In contrast, the maximum amplitude of bradycardic responses to left ADN stimulation was decreased. Since Int ADNA was preserved in response to MAP increase and HR responses to vagal efferent stimulation were augmented, we conclude that a deficit of the central mediation of baroreflex HR contributes to the overall attenuation of baroreflex sensitivity in OVE26 mice. The successful conduction of physiological experiments on the ADN in OVE26 mice may provide a foundation for the understanding of cellular and molecular mechanisms of diabetes-induced cardiac neuropathy.     

Circulatory reflex responses during the initial stage of feline endotoxin shock.

Cardiovascular and autonomic nervous responses to an injection of E. coli endotoxin were followed for up to 15 min. in cats anesthetized with chloralose and given artificial respiration. Within 60 seconds, endotoxin induced a drop of aortic pressure, with simultaneous cardiac acceleration and slight central venous hypertension. There was an associated, almost complete cessation of the aortic arch baroreceptor afferentation. The cardiac sympathetic efferentation increased up to 1.4 times the control level at its maximum. The splenic sympathetic efferentation increased up to 10.6 times the control level at the end of the 15 min period, when the other parameters studied showed a trend to control level. The sympathetic autonomic system seems to be activated through cardiovascular receptors sensing hemodynamic changes touched off by endotoxin-induced release of vasoactive substances.     

Circulatory Reflex Responses during the Initial Stage of Feline Endotoxin Shock

Cardiovascular and autonomic nervous responses to an injection of E. coli endotoxin were followed for up to 15 min. in cats anesthetized with chloralose and given artificial respiration. Within 60 seconds, endotoxin induced a drop of aortic pressure, with simultaneous cardiac acceleration and slight central venous hypertension. There was an associated, almost complete cessation of the aortic arch baroreceptor afferentation. The cardiac sympathetic efferentation increased up to 1.4 times the control level at its maximum. The splenic sympathetic efferentation increased up to 10.6 times the control level at the end of the 15 min period, when the other parameters studied showed a trend to control level. The sympathetic autonomic system seems to be activated through cardiovascular receptors sensing hemodynamic changes touched off by endotoxin-induced release of vasoactive substances.     

Seventy years of the Bainbridge reflex

The discovery of the Bainbridge reflex 70 years ago, of a tachycardic response to a rise in central venous pressure, stimulated a lot of interest in this and other cardiovascular reflexes. The mechanoreceptors that elicit the reflex are located at the junction of the right atrium and caval veins or at the junctions of the pulmonary veins and the left atrium. The Bainbridge reflex is controversial, however, because its existence cannot always be demonstrated. Intravenous infusions, which usually elicit a reflex tachycardia, sometimes cause a bradycardic response. This paper reviews the history of the studies associated with the reflex. Results are reported, which demonstrate that the chronotropic response to i.v. infusions depends upon the resulting change in aortic diameter; bradycardia is evoked by infusions leading to a rise in aortic baroreceptor activity through increases in aortic diameter, volume or pressure; tachycardia follows whenever the infusion fails to trigger the baroreflex. The importance of the Bainbridge reflex as a counterbalance to the baroreceptor reflex is discussed.     

Central command: control of cardiac sympathetic and vagal efferent nerve activity and the arterial baroreflex during spontaneous motor behaviour in animals

Feedforward control by higher brain centres (termed central command) plays a role in the autonomic regulation of the cardiovascular system during exercise. Over the past 20 years, workers in our laboratory have used the precollicular-premammillary decerebrate animal model to identify the neural circuitry involved in the CNS control of cardiac autonomic outflow and arterial baroreflex function. Contrary to the traditional idea that vagal withdrawal at the onset of exercise causes the increase in heart rate, central command did not decrease cardiac vagal efferent nerve activity but did allow cardiac sympathetic efferent nerve activity to produce cardiac acceleration. In addition, central command-evoked inhibition of the aortic baroreceptor-heart rate reflex blunted the baroreflex-mediated bradycardia elicited by aortic nerve stimulation, further increasing the heart rate at the onset of exercise. Spontaneous motor activity and associated cardiovascular responses disappeared in animals decerebrated at the midcollicular level. These findings indicate that the brain region including the caudal diencephalon and extending to the rostral mesencephalon may play a role in generating central command. Bicuculline microinjected into the midbrain ventral tegmental area of decerebrate rats produced a long-lasting repetitive activation of renal sympathetic nerve activity that was synchronized with the motor nerve discharge. When lidocaine was microinjected into the ventral tegmental area, the spontaneous motor activity and associated cardiovascular responses ceased. From these findings, we conclude that cerebral cortical outputs trigger activation of neural circuits within the caudal brain, including the ventral tegmental area, which causes central command to augment cardiac sympathetic outflow at the onset of exercise in decerebrate animal models.     

The effects of haemorrhage in the unanaesthetized rabbit

1. The circulatory response following acute loss of 26% of the blood volume was examined in unanaesthetized rabbits. The groups of animals studied were normal rabbits; adrenalectomized rabbits; animals subjected to prolonged treatment with guanethidine in which peripheral adrenergic nerve transmission is blocked, but which can reflexly liberate adrenal medullary hormones; animals subjected to combined adrenalectomy and guanethidine treatment with no functional adrenergic effectors; in each case with or without administration of atropine. The responses of animals with section of the carotid sinus and aortic nerves were also examined.

2. The spontaneous rate of replacement of the blood volume after haemorrhage by reabsorption of extravascular fluid was the same in all the above preparations, the blood volume returning to normal 3-4 hr after bleeding.

3. The `passive' effects of haemorrhage were examined in animals without functioning autonomic effectors and include a large fall in right atrial pressure and cardiac output, arterial hypotension, no significant change in total peripheral resistance, and a bradycardia of gradual onset. Reflex autonomic effector activity in normal animals minimizes the fall in atrial pressure, cardiac output and arterial blood pressure, and produces a significant increase in total peripheral resistance and tachycardia. Increased sympathetic nerve activity and secretion of adrenal medullary hormones each play an important and complementary part in the normal circulatory response to haemorrhage of the rabbit. There is also reflex reduction in vagal efferent activity.

4. Reflexes from the carotid sinus and aortic arch limit the fall in arterial pressure for the first 4 hr after haemorrhage. These reflexes also account for the tachycardia normally observed after haemorrhage. The baroreceptor reflexes rather than the chemoreceptors appear to be dominant in these responses.

5. Twenty-four hours after haemorrhage the haemodynamic pattern is similar in all preparations irrespective of their autonomic effector status: blood volume, right atrial pressures and cardiac outputs are all elevated, and the arterial pressure has virtually recovered, consistent with the development of hypervolaemic anaemia at this time.

     

Baroreflex inhibition of cardiac sympathetic outflow is attenuated by angiotensin II in the nucleus of the solitary tract

Homeostatic regulation of arterial pressure is maintained by arterial baroreceptors. Activation of these receptors results in an inhibition of sympathetic activity to the heart. It is known that angiotensin II in the nucleus tractus solitarii attenuates the baroreceptor reflex-evoked vagal bradycardia. Here, we determined whether the cardiac sympathetic component of the baroreceptor reflex could be modulated by angiotensin II in the nucleus of the solitary tract. An in situ, arterially perfused working heart--brainstem preparation of rat was employed and the sympathetic inferior cardiac nerve recorded. Increases in perfusion pressure caused a reflex bradycardia and inhibition of inferior cardiac nerve activity. Microinjection of angiotensin II (500 fmol) in the nucleus of the solitary tract attenuated significantly both the reflex bradycardia and inhibition of inferior cardiac nerve activity (P<0.01). The latter was reversible and sensitive to losartan, an angiotensin II type 1 receptor antagonist. In contrast, the peripheral chemoreceptor reflex evoked an increase in inferior cardiac nerve activity that was not affected by angiotensin II applied exogenously in the nucleus of the solitary tract. We conclude that within the nucleus of the solitary tract angiotensin II exerts a powerful and specific inhibitory modulation of the baroreceptor reflex control of sympathetic nerve activity destined for the heart. We suggest that our data may have clinical implications relating to hypertension, a condition when angiotensin II activity is heightened in the brain and the efficacy of the baroreflex is reduced.     

Sympathetic transients caused by abrupt alterations of carotid baroreceptor activity in humans

We examined the role of carotid baroreceptors in the short-term modulation of sympathetic outflow to the muscle vascular bed and parasympathetic outflow to the heart in 10 healthy adults. Afferent carotid baroreceptor activity was modified with 30-mmHg neck suction or pressure applied during held expiration, and efferent sympathetic activity was measured with microelectrodes inserted percutaneously into peroneal nerve muscle fascicles. Sympathetic responses were conditioned importantly by directional changes of carotid transmural pressure: increased pressure (onset of neck suction or offset of neck pressure) inhibited (totally) sympathetic activity, and reduced pressure (offset of neck suction or onset of neck pressure) augmented sympathetic activity. Responses occurred after a latency of about 2 s and did not persist as long as changes of neck-chamber pressure. Cardiac intervals were prolonged by increased carotid transmural pressures and shortened by decreased carotid transmural pressures, but, in contrast to sympathetic responses, cardiac responses adapted only slightly during neck-chamber pressure changes. Our results suggest that in the human a common baroreceptor input is processed differently in central vagal and sympathetic networks. Muscle sympathetic responses to changing levels of afferent baroreceptor traffic are profound but transitory. They appear to be conditioned more by changes of arterial pressure than by its absolute levels.     

An experimental analysis of the tachycardia that follows vagal stimulation

1. Postvagal tachycardia, the transient increase in heart rate that follows the sinus bradycardia elicited by vagal stimulation, was investigated in thirty chloralosed cats. Maximum postvagal tachycardia was elicited by stimulation at frequencies of 20-60 Hz with train durations of 30-90 sec. A positive correlation was demonstrated between the magnitudes of postvagal tachycardia and of the preceding sinus bradycardia.2. Postvagal tachycardia was not affected by either spinal transection at C7 or by administration of propranolol (1.5 mg/kg I.V.), but was abolished by the administration of atropine (2.0 mg/kg I.V.).3. Postvagal tachycardia was observed to follow the vagal bradycardia induced reflexly either by administration of phenyldiguanide (100-300 mug I.V.) or by stimulation of the aortic depressor nerve.4. In the isolated atria-vagus preparations from six rabbits a positive correlation was demonstrated between the magnitude of postvagal tachycardia and of the preceding bradycardia elicited by vagal stimulation.5. Continuous intracellular recordings were obtained from four sinuatrial node pace-maker cells in the isolated atria-vagus preparation of the rabbit before, during and after vagal stimulation. During postvagal tachycardia the slope of the diastolic prepotential, the maximum diastolic potential, threshold potential and the overshoot were found to be increased; these changes are different from those found in pace-maker cells during adrenergic activation.6. These findings demonstrate that postvagal tachycardia is not mediated by sympathetic adrenergic mechanisms, but suggest that it is dependent upon the preceding vagal bradycardia and may be related to an increase in net sodium influx into pace-maker cells initiated by the hyperpolarization of the pace-maker cell membrane during and immediately after vagal stimulation.     

Left atrial receptors in arterial baroreflex control of heart rate

We have studied the influence of left atrial receptor stimulation on arterial baroreflex control of heart rate with a view to determine the role of cardiac efferent sympathetic and parasympathetic pathways in any interaction observed. Experiments were performed on anaesthetized, artificially ventilated, and thoracotomised cats and dogs. The sensitivity of baroreflex heart rate response was found to be higher in dogs as compared to cats. Both the sympathetic and parasympathetic effects contributed to the reflex chronotropic effects observed during changes in mean arterial blood pressure. The reflex tachycardia response during left atrial receptor stimulation was more pronounced in dogs than in cats. Stimulation of left atrial receptors caused slight inhibition of the baroreflex tachycardia response and potentiation of the bradycardia response.     

Involvement of the purinergic system in central cardiovascular modulation at the level of the nucleus ambiguus of anaesthetized rats

Anatomical studies have demonstrated the existence of purinergic P2 receptors in the nucleus ambiguus (NA), a site containing cardiac vagal motoneurons. However, very little is known about the functional role of these receptors in central cardiac vagal regulation. The aims of our study were to evaluate the following: (1) the blood pressure and heart rate responses following purinoceptor activation within the NA; (2) the role of purinoceptors and excitatory amino acid (EAA) receptors in mediating the cardiovascular responses evoked by ATP and L-glutamate stimulation of NA; and (3) the role of NA purinoceptors in mediating the cardiovascular responses of the Bezold-Jarisch reflex. In anaesthetized rats, microinjection of L-glutamate (5.0 nmol/50 nl) into the NA induced a marked and immediate onset bradycardia with minimal change in arterial pressure. Microinjection of ATP into the NA induced a dose-dependent (0.31-6.0 nmol/50 nl) bradycardia and pressor responses. It is noteworthy that the bradycardia occurred either before or simultaneously with a pressor response (when present), indicating that it was not a baroreceptor reflex mediated response due to the rise in arterial pressure. The pressor response was prevented by α(1)-adrenergic blockade with prazosin, whereas muscarinic blockade with methyl-atropine abolished the evoked bradycardia. Ipsilateral microinjection of PPADS (a P2 receptor antagonist; 500 pmol/100 nl) into the NA significantly attenuated the ATP-induced bradycardia but spared the pressor response. In contrast, PPADS in the NA had no effect on the L-glutamate-evoked bradycardic response. Ipsilateral injection of kynurenic acid (a non-selective EAA receptor antagonist; 10 nmol/50 nl) into the NA totally blocked the bradycardia induced by l-glutamate and partly attenuated the ATP induced bradycardia. Finally, both the depressor and the bradycardic responses of the Bezold-Jarisch reflex were attenuated significantly (P < 0.01 and P < 0.05, respectively) following bilateral microinjection of PPADS into the NA. These results identify ATP and purinergic P2 receptors within the ventrolateral medulla as excitatory to cardiovagal neurons. Additionally, our data show that P2 receptors within the ventrolateral medulla are integral to the cardiovascular responses of the Bezold-Jarisch reflex.     

Changes in renal sympathetic outflow during hypotensive haemorrhage in rats

The goal of this study was to investigate changes in renal sympathetic outflow during hypotensive haemorrhage. Normotensive Wistar-Kyoto rats were anaesthetized with chloralose (50 mg kg-1) and bled to an arterial blood pressure of 50 mmHg for 30 min. Changes in heart rate (HR) and renal nerve activity (RNA) were registered. The hypotensive haemorrhage induced a short-lasting sympathetic excitation that was followed within 5-10 min by a powerful sympathetic inhibition and bradycardia. The average maximal decrease in sympathetic activity was 65% and the maximal decrease in heart rate was 45 beats min-1. There was a close correlation between changes in heart rate and renal sympathetic activity. The marked depressor response was due at least in part to activation of vagal afferents because the depressor responses were acutely reversed by bilateral cervical vagotomy. As cardiac afferents are known to be activated by prostaglandins and bradykinins, and these agents are released by myocardial ischaemia, haemorrhage was repeated after use of indomethacin and aprotinin (a protein inhibitor decreasing bradykinin formation), and a marked sympathetic inhibition could still be elicited upon haemorrhage. We therefore suggest that the likely mechanism for activation of the vagal afferents is a squeezing of the myocardium when the heart has to contract around an almost empty chamber. In conclusion, this study demonstrated that hypotensive haemorrhage triggers profound inhibition of RNA in rats and that this sympathoinhibition is mediated primarily by mechanically sensitive cardiac vagal afferents.     

The effects of chloralose-urethane and sodium pentobarbitone anaesthesia on the local and autonomic components of the circulatory response to arterial hypoxia

1. The circulatory and respiratory responses to severe arterial hypoxia were studied in normal rabbits, ;de-efferented' rabbits without functioning autonomic effectors, and atropinized animals before anaesthesia and during chloralose-urethane and sodium pentobarbitone anaesthesia. Net systemic autonomic activity and autonomic activity to the heart was assessed from a comparison of the responses of the various preparations.2. In the normal spontaneously breathing animal each anaesthetic had a similar mode of action, and modified qualitatively the circulatory response present before anaesthesia. In the ;de-efferented' animal the circulatory response was determined by the local effects of hypoxia, and was altered only quantitatively during anaesthesia.3. In the normal unanaesthetized animal the reflex changes in autonomic activity during hypoxia consisted of a large increase in vagal efferent activity, a decrease in cardiac sympatho-adrenal activity, and an increase in total sympatho-adrenal constrictor activity.4 In hypoxia during anaesthesia the vagal efferent activity no longer increased, but the change in sympatho-adrenal activity to heart and systemic circulation was the same as before anaesthesia in the spontaneously breathing animal. During anaesthesia with controlled ventilation systemic sympatho-adrenal activity increased further, and bradycardia again developed. The bradycardia was now due exclusively to reduction in cardiac sympathetic activity and not to an increase in vagal efferent activity.     

Enhanced sympathetic mediation of chronotropic baroreflexes in old Sprague-Dawley rats

We compared reflex heart rate responses elicited during intravenous infusions of phenylephrine or sodium nitroprusside in conscious 4- and 24-month-old male Sprague-Dawley rats to determine whether baroreflex regulation changes with age. Underlying neural mechanisms were assessed by repeating baroreflex tests following cholinergic blockade with methylatropine or beta-adrenergic blockade with propranolol. Basal blood pressures always tended to be higher, while corresponding heart rates were lower, in old than in young rats. Reflex bradycardia (but not tachycardia) was initially weaker in 24-month-old rats as were reductions in both reflex bradycardia and tachycardia after cholinergic blockade. On the other hand, the reduction in reflex tachycardia following beta-adrenergic blockade in old rats was more pronounced and almost equal to that produced by combined cholinergic and beta-adrenergic blockade. From these results we conclude that with old age in male Sprague-Dawley rats, just as has been shown previously in Fischer 344 rats, predominant efferent pathways for regulating heart rate reflexes are also altered to become almost exclusively beta-adrenergic or sympathetic.     

Differential age-dependent attenuation of reflex tachycardia by verapamil in rats

To determine if verapamil alters baroreflex function differently depending on age, reflex heart rate responses to intravenous infusions of phenylephrine or sodium nitroprusside were compared in conscious 5- and 14-month-old rats before and after daily oral administration of verapamil (100 mg/kg) for 6 days. The effects of verapamil on parasympathetic and sympathetic mediation of heart rate were also assessed by repeating baroreflex tests after treatment with either propranolol or atropine. All reflex heart rate responses were initially smaller in 14- than in 5-month-old rats. Regardless of age, magnitude of reflex bradycardia or the effects on it of either cholinergic or beta-adrenergic blockade, were unaffected by verapamil. By contrast, reflex tachycardia which was attenuated in both age groups, was decreased further by subsequent cholinergic or beta-adrenergic blockade in 5-month-old rats, but only by cholinergic blockade in 14-month-old rats. These findings suggest that while verapamil did not affect autonomic mediation of reflex bradycardia, it reduced that of reflex tachycardia differently depending on age. Whereas it attenuated both sympathetic and parasympathetic mediation of reflex tachycardia in 5-month-old rats, it attenuated only sympathetic mediation in 14-month-old rats.     

Autonomic cardiovascular control during submergence and emergence in bullfrogs.

Unanesthetized bullfrogs were involuntarily submerged for 25 min in air-saturated water at 21 degrees C. Significant bradycardia was observed while systemic blood pressure was maintained or slightly elevated. Upon emergence, heart rates immediately returned to presubmergence levels or higher. Similar responses were observed in frogs allowed to make voluntary dives in an experimental tank. Heart rates of vagal-blocked (atropine) frogs did not change during submergence or emergence. beta-Adrenergic blockade (propranolol) had little effect on the magnitude of heart rate decrease during submergence or its increase upon emergence. After alpha-adrenergic blockade (phentolamine), frogs developed diving bradycardia while undergoing a fall in systemic blood pressure. It is concluded that, in bullfrogs, 1) bradycardia during submergence is entirely due to increased vagal activity, 2) the immediate cardiac rate increase upon emergence apparently results from a decrease in vagal tone; and 3) there appears to be no substantial reciprocal sympathetic influence on heart rate during alterations in vagal tone.