An acceleratory component of the parasympathetic control of heart rate

Iano, Thelma L.; Levy, Matthew N.; Lee, Moo H.

doi:10.1152/ajplegacy.1973.224.5.997

Cited by 21 publications

(6 citation statements)

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“…The authors' observations are in line with those of Fernandez de Molina & Perl (1965) and Corbett et al (1971), since they also failed to obtain convincing evidence for the reflex tachycardia in spinal dogs. Some acceleration of the heart rate, which occurred in two out of five non-vagotomized spinal dogs, could be vagally mediated (Weiss & Priola, 1972;Iano, Levy & Lee, 1973), since in vagotomized spinal dogs bradykinin applied to the heart failed to produce any changes in the heart rate, although regularly elicited reflex pressor effects. Since changes in metabolic state of the animal which may affect reflex tachycardia (Harry et al,197 1) were carefully controlled, and since cardioacceleratory responses to intravenous isoprenaline were not diminished but rather potentiated, inhibition of the reflex tachycardia observed in spinal dogs could not be attributed to a depression of cardiac responsiveness to sympathetic stimulation, but to an interruption of the reflex pathway to the cardiac pacemaker.…”

Section: Discussionmentioning

confidence: 92%

Sympathetic Cardiovascular Reflex Initiated by Bradykinin‐induced Stimulation of Cardiac Pain Receptors in the Dog

Staszewska-Barczak

Dusting

1977

Clin Exp Pharma Physio

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1. Bradykinin (0.02-5 microgram) applied to the epicardium of the left ventricle in the open-chest, anaesthetized dog, elicits dose-related reflex pressor effects and acceleration of the heart rate. 2. Bradykinin-induced reflex tachycardia was suppressed after the blockade of beta-adrenoceptors with propranolol, whereas reflex pressor responses were prevented by blocking the alpha-adrenoceptor sites with phenoxybenzamine. 3. Vagotomy and atropine treatment did not affect reflex hypertension and tachycardia to epicardial bradykinin. 4. After spinal section at C1, the pressor responses to epicardial bradykinin were significantly reduced, but still present in all but one experiment. A small acceleration of the heart occurred in two out of five spinal dogs with intact vagi and was absent in three vagotomized spinal dogs. 5. The results indicate the reflex activation of the sympathetic outflow to the heart and blood vessels, mediated mainly at a supraspinal level as a predominant mechanism for the cardiovascular response initiated by bradykinin-induced stimulation of cardiac pain receptors.

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Section: Discussionmentioning

confidence: 92%

Sympathetic Cardiovascular Reflex Initiated by Bradykinin‐induced Stimulation of Cardiac Pain Receptors in the Dog

Staszewska-Barczak

Dusting

1977

Clin Exp Pharma Physio

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“…Because the form of the sigmoidal equations used to describe brainstem neuronal groups was updated in the current model to express the gain more cleanly, parameter values for brainstem neuronal groups were updated to reproduce behavior from the prior model 3 . The remaining parameter values were selected to produce simulations that best matched experimental data associated with healthy conditions and electrophysiological behavior or were estimated from experimental data when more precise information from experiments relevant to vagal activity timing 30 and muscarinic receptor time delay 31 was available. Because we combined data from multiple sources and of different types, we have summarized key experimental details, including the model type used, number of replicates, and measured outputs for reference (Table 1).…”

Section: Methodsmentioning

confidence: 99%

“…The inclusion of principal neurons means that the timing of vagal stimulation relative to the phase of the cardiac cycle becomes important 21. Physiological evidence indicates that vagal nerve activity occurring near the beginning of the cardiac cycle causes larger decreases in heart rate compared with vagal nerve activity occurring near the end of the cardiac cycle 30,61. To model this phenomenon, experimental data from dogs on the percent change in heart rate as a function of the time of vagal activity since the start of the cardiac cycle were used to calculate the percent change of the calculated heart rate 30.…”

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confidence: 99%

Closed‐loop modeling of central and intrinsic cardiac nervous system circuits underlying cardiovascular control

et al. 2023

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The baroreflex is a multi-input, multi-output physiological control system that regulates blood pressure by modulating nerve activity between the brainstem and the heart. Existing computational models of the baroreflex do not explicitly incorporate the intrinsic cardiac nervous system (ICN), which mediates central control of heart function. We developed a computational model of closed-loop cardiovascular control by integrating a network representation of the ICN within central control reflex circuits. We examined central and local contributions to the control of heart rate, ventricular functions, and respiratory sinus arrhythmia (RSA). Our simulations match the experimentally observed relationship between RSA and lung tidal volume. Our simulations predicted the relative contributions of the sensory and the motor neuron pathways to the experimentally observed changes in the heart rate. Our closed-loop cardiovascular control model is primed for evaluating bioelectronic interventions to treat heart failure and renormalize cardiovascular physiology.

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“…According to Spear and Moore (1973), propranolol had no effect on the dip in the triphasic curve, but in the experiments of Iano et al (1973), the blocking agent accentuated the trough in the curve and increased the ratio of acceleration to inhibition of heart rate. In our experiments, epinephrine abolished the dip in the inhibitory curve, and propranolol restored it.…”

Section: The Po8tinhibitory Reboundmentioning

confidence: 94%

Phasic effects of vagal stimulation on pacemaker activity of the isolated sinus node of the young cat.

Jalife

Moe

1979

Circulation Research

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SUMMARYWe studied the functional interactions between the sinoatrial (SA) nodal pacemaker and the vagus nerve in isolated right atrium-vagus nerve preparations of the kitten. Brief trains of stimuli applied to the vagus nerve scanning the spontaneous pacemaker cycle induce a brief hyperpolarization of the membrane of cells in the pacemaker region. Aa a result of this hyperpolarization, there occur phasic changes in pacemaker cycle length that depend on the timing, amplitude, and duration of the hyperpolarization and, also, on the relationship between the duration of the hyperpolarization and the pacemaker cycle length. If the duration of the hyperpolarization is long relative to the duration of the spontaneous cycle, the next discharge can be delayed but not accelerated, no matter when during the cycle vagal stimuli are applied. If the duration of the hyperpolarization is briefer than the spontaneous cycle and the vagal input is presented early in the cycle, a postinhibitory rebound accelerates the next discharge. These effects of the vagal burst on the pacemaker cycle can be described by an inhibitory curve consisting of several components: a latent period of about 200 msec, a phase of major prolongation of the first and sometimes the second pacemaker cycle, a phase of relative or actual acceleration, and a final phase of lesser deceleration lasting several seconds. These effects can be approximated closely in a sucrose gap preparation of the sinus node by brief hyperpolarizing current pulses spanning the spontaneous pacemaker cycle in the test compartment. Ore Re* 45: 595-607, 1979 THE EFFECTS of parasympathetic discharges on the sinoatrial (SA) node are characterized by a brief latency and brief duration; accordingly, the magnitude of the cardiac response to brief bursts of vagal stimuli bears a phasic relationship to the timing of the nerve impulses in the cardiac cycle (Brown and Eccles, 1934;Stade and Weiss, 1956;Levy et al., 1970;Dong and Reitz, 1970;Eckberg, 1976). Particularly at slow heart rates, discrete bursts of discharges in efferent cardiac vagal fibers may be related to the arterial pressure pulses, resulting in complex frequency-dependent interactions between the cardiac pacemaker and the vagal activity (Jewett, 1964;Katona et al., 1970;Iriuchijima and Kumada, 1963).Recent studies (Levy et al., 1969;Reid, 1969; have demonstrated that periodically repeated vagal stimuli can entrain the SA nodal pacemaker so that its cycle length assumes a fixed ratio to that of the stimulus interval. Spontaneous pacemaker activity in isolated strands of Purkinje tissue mounted in a sucrose-gap preparation also can be entrained by the electrotonic effects of depolarizing and hyperpolarizing current pulses (Jalife and Moe, 1976). Hyperpolarizing pulses induced early in the pacemaker cycle accelerate, and pulses of similar magnitude initiated late in the cycle delay the subsequent discharge. Because vagal stimuli have been shown to cause hyperpolarization in cells of the SA node and of the atrium, we have undert...

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An acceleratory component of the parasympathetic control of heart rate

Cited by 21 publications

References 0 publications

Sympathetic Cardiovascular Reflex Initiated by Bradykinin‐induced Stimulation of Cardiac Pain Receptors in the Dog

Sympathetic Cardiovascular Reflex Initiated by Bradykinin‐induced Stimulation of Cardiac Pain Receptors in the Dog

Closed‐loop modeling of central and intrinsic cardiac nervous system circuits underlying cardiovascular control

Phasic effects of vagal stimulation on pacemaker activity of the isolated sinus node of the young cat.

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