Sympathetic and vagal interaction in the control of cardiac pacemaker rhythm in the guinea-pig heart: Importance of expressing heart rhythm using an appropriate metric.

There are many reports that, through pre- and post-junctional mechanisms, sympathetic and parasympathetic (vagal) nerves can interact in the control of heart rate. The predominant interaction is accentuated antagonism (AA), where the bradycardia produced by vagal stimulation (VNS) is amplified when heart rate has been increased by sympathetic stimulation (SNS) or beta-adrenergic agonists. The acetylcholine-activated potassium current (I), is the primary driver of vagal bradycardia.

Effects of tertiapin-Q and ZD7288 on changes in sinoatrial pacemaker rhythm during vagal stimulation.

Heart rate slowing produced by cardiac parasympathetic (vagal) stimulation is thought to be the result of modulation of the acetylcholine-activated K(+) current (IK,ACh) and the pacemaker current (If) in sinoatrial (SAN) pacemaker cells. However, the contribution of these and other ion currents to vagal slowing is controversial. Here, we examined the contributions of IK,ACh and If to vagal slowing in 15 isolated, vagal-innervated preparations of guinea-pig atria, using 300 nM tertiapin-Q (TQ) and 2 μM ZD7288 to obtain full and substantial block of these currents, respectively.

The muscarinic-activated potassium channel always participates in vagal slowing of the guinea-pig sinoatrial pacemaker.

Unlabelled: Controversy persists regarding participation of the muscarinic-activated potassium current (c(KACh)) in small and moderate vagal bradycardia. We investigated this by (i) critical examination of earlier experimental data for mechanisms proposed to operate in modest vagal bradycardia (modulation of I(f) and inhibition of a junctional Na(+) current) and (ii) experiments performed on isolated vagally-innervated guinea-pig atria. In 8 superperfused preparations, 10-s trains of vagal stimulation (1 to 20Hz) produced a bradycardia that ranged from 1 to 80%.

The relationship between aortic baroreceptor activity and arterial pressure is not monotonic.

Previous reports indicate that when aortic pressure (AP) falls below the threshold (P (th)) for baroreceptor sensitivity, activity in the aortic depressor nerve (ADN) may increase. To quantify and explain this anomalous behaviour, we analysed curves describing the relationship of baroreceptor fibre activity in rabbit left ADN to AP. Data were obtained in anaesthetised New Zealand White rabbits.

Tertiapin-Q removes a mechanosensitive component of muscarinic control of the sinoatrial pacemaker in the rat.

1. In an isolated right atrial preparation, an increase in right atrial pressure (RAP) produces an increase in atrial rate. This rate response is larger and occurs faster when there is background vagal or muscarinic stimulation.

Tongue pressure patterns during water swallowing.

Bolus propulsion during the normal oral phase of swallowing is thought to be characterised by the sequential elevation of the front, middle, and posterior regions of the dorsum of the tongue. However, the coordinated orchestration of lingual movement is still poorly understood. This study examined how pressures generated by the tongue against the hard palate differed between three points along the midline of the tongue.

Tertiapin-Q removes a large and rapidly acting component of vagal slowing of the guinea-pig cardiac pacemaker.

The participation of acetylcholine-activated potassium current (I(K,ACh)) and hyperpolarization-activated pacemaker current (I(f)) in vagal bradycardia were examined using vagally-innervated preparations of guinea-pig atria. Preparations were maintained in Krebs-Henseleit solution (36 degrees C). Before treatment, trains of vagal stimuli (10 s at 2, 5 and 10 Hz) produced graded bradycardias displaying rapid onset and offset.

The effects of tertiapin-Q on responses of the sinoatrial pacemaker of the guinea-pig heart to vagal nerve stimulation and muscarinic agonists.

Using Langendorff preparations of the guinea-pig heart, we have examined the participation of the acetylcholine (ACh)-activated potassium channel, IK,ACh, in the bradycardia produced by electrical stimulation of the vagus (parasympathetic) nerve and muscarinic agonists (ACh and bethanecol, bolus i.a.).

Are the carotid bodies of the guinea-pig functional?

We have previously observed that the guinea-pig appears to have a relatively poor ventilatory (V (E)) response to hypoxia, compared to other mammals. Therefore, in this study, we questioned the ability of the carotid bodies (primary peripheral chemoreceptors) in the guinea-pig to detect hypoxia. The ventilatory responses to poikilocapnic hypoxia (8% O(2)), poikilooxic hypercapnia (8% CO(2)), hyperoxia (100% O(2)) and cyanide (NaCN - 200 mug/kg, i.

The influence of heart rate on baroreceptor fibre activity in the carotid sinus and aortic depressor nerves of the rabbit.

The arterial baroreceptors and their afferent fibres provide the sensory arm of the reflex that regulates systemic arterial pressure. We have examined whether the relationship between mean baroreceptor discharge and mean arterial pressure is altered when heart rate changes. Experiments were performed on pentobarbitone-anaesthetized rabbits.

Do cardiac neurons play a role in the intrinsic control of heart rate in the rat?

Three experiments were performed to see whether cardiac neurons contribute to the intrinsic control of heart rate in right atria of adult rats. The intrinsic heart rate response (IRR) was examined by raising right atrial pressure from 2 to 8 mmHg for 3 min. In isolated preparations of the right atrium, the IRR was not significantly altered by the addition of either 1 microM atropine (n =6; control +19+/- 3 min(-1) ; atropine+18+/-3 min(-1); (mean /+/-S.

Respiratory sinus arrhythmia and the heart rate response to carotid baroreceptor activation after hard dynamic exercise in humans.

The aim of this study was to examine the influence of 20 min of hard exercise (HR>160 beats min(-1)) on the efficacy of the cardiac parasympathetic nervous control of heart rate in humans (20-31 years; of either sex). This intensity of exercise was chosen to produce strong activation of the cardiac sympathetic nerves. Using well-controlled stimulus parameters, the efficacy of cardiac parasympathetic control of heart rate was assessed by recording the heart rate response to carotid baroreceptor activation (CBR) and the amplitude of respiratory sinus arrhythmia (RSA).