Sinoatrial node

FIGURE 7.14 Time-course of G-protein-mediated activation of GIRK potassium channels in rabbit sinoatrial node cells, (a). Outward current evoked by a 33-msec, 50-nA iontophoretic pulse of acetylcholine (between arrows), (b). Response of the unclamped cell to an iontophoretic pulse of acetylcholine (ACh). (Record (a) is adapted with permission from Trautwein et al., in Drug Receptors and Their Effectors, Birdsall, N. J. M., Ed., Macmillan, New York, 1980, pp. 5-22 record (b) is adapted with permission from Noma, in Electrophysiology of Single Cardiac Cells, Noble, D. and Powell, T., Eds., Academic Press, San Diego, CA, 1987, pp. 223-246.)... 

Skeletal muscle is neurogenic and requires stimulation from the somatic nervous system to initiate contraction. Because no electrical communication takes place between these cells, each muscle fiber is innervated by a branch of an alpha motor neuron. Cardiac muscle, however, is myogenic, or self-excitatory this muscle spontaneously depolarizes to threshold and generates action potentials without external stimulation. The region of the heart with the fastest rate of inherent depolarization initiates the heart beat and determines the heart rhythm. In normal hearts, this "pacemaker region is the sinoatrial node. 

Cyclic nucleotide-modulated ion channels (Table 6-2) are not K+-selective. Nevertheless, their inward current of Na+ and Ca2+ ions is conducted through a channel that is similar in overall architecture to Shaker K+ channels. This protein family includes the CNG channels, which respond only to cyclic nucleotides, and the HCN channels, which are activated synergistically by hyperpolarization and cyclic nucleotide binding [38,40]. The CNG channels are involved in signaling of visual and olfactory information and serve as cyclic nucleotide-gated Ca2+ channels. In contrast, the HCN channels are required for normal rhythmic electrical discharges by the sinoatrial node in the heart and the pacemaker cells of the thalamus. 

Bolton Yes, but even in your own work you don t normally stretch the cell. With pacemaker cells which are driving the intestine the idea is that these things may be taking place spontaneously. (This is certainly true in the sinoatrial node Lipsius et al 2001.) Presumably you are not stretching there. 

Single-wall nanotubes (SWNTs), 12 232, 13 852, 26 737 Single-wall tanks, 24 296 Singular value decomposition, 6 28 S—I—N junctions, 23 821 Sinking solids, lifting and distribution of, 16 692-694 Sinoatrial node, 5 80... 

Ono, K. and Ito, H. (1995) Role of rapidly activating delayed rectifier K+ current in sinoatrial node pacemaker activity. The American Journal of Physiology, 269... 

Atropine generally increases heart rate, but it may briefly and mildly decrease it initially, due to Ml receptors on postganglionic parasympathetic neurons. Larger doses of atropine produce greater tachycardia, due to M2 receptors on the sinoatrial node pacemaker cells. There are no changes in blood pressure, but arrhythmias may occur. Scopolamine produces more bradycardia and decreases arterial pressure, whereas atropine has little effect on blood pressure (Vesalainen et al. 1997 Brown and Taylor 1996). 

Depolarisation of the membrane of the cardiomyocyte, resulting from the action potential, initiates contraction in cardiac as in skeletal muscle. This depolarisation arises in the sinoatrial node, a small group of cells in the right atrium, and then spreads through the heart causing, first, the muscles in the atria to contract and then the muscles in the ventricles to contract. 

Stimulation of the parasympathetic system releases acetylcholine at the neuromuscular junction in the sinoatrial node. The binding of acetylcholine to its receptor inhibits adenylate cyclase activity and hence decreases the cyclic AMP level. This reduces the heart rate and hence reduces cardiac output. This explains why jumping into very cold water can sometimes stop the heart for a short period of time intense stimulation of the vagus nerve (a parasympathetic nerve) markedly increases the level of... 

It opens a ion channel in the sinoatrial node, which slows the initiation of the electric signals that control the heartbeat (this is known as sinus bradycardia). 

The electrical impulse for contraction (propagated action potential p. 136) originates in pacemaker cells of the sinoatrial node and spreads through the atria, atrioventricular (AV) node, and adjoining parts of the His-Purkinje fiber system to the ventricles (A). Irregularities of heart rhythm can interfere dangerously with cardiac pumping func-tioa... 

This group consists of j3-adrenergic receptor blockers, the antiarrhythmic activity of which is associated with inhibition of adrenergic innervation action of the circulatory adrenaline on the heart. Because all 8-adrenoblockers reduce stimulatory sympathetic nerve impulses of catecholamines on the heart, reduce transmembrane sodium ion transport, and reduce the speed of conduction of excitation, sinoatrial node and contractibility of the myocardium is reduced, and automatism of sinus nodes is suppressed and atrial and ventricular tachyarrhythmia is inhibited. 

Conduction system abnormalities are common in chronic heart failure, occurring in 15-30% of the population with low left ventricular ejection fraction (LVEF) [1-3]. The prevalence in ischemic heart disease is roughly similar to that seen in other forms of dilated cardiomyopathy. Conduction system disease can occur both at the time of an acute myocardial infarction as well as slowly progressing in chronic ischemic heart disease. Intraventricular conduction delays are associated with a poor prognosis in heart failure, with up to a 70% increase in the risk of death, and are also more prevalent in patients with advanced symptoms [2,4]. In ischemic heart disease, all components of the conduction system are at risk of ischemic injury, from the sinoatrial node to the His-Pukinje system. These conduction system abnormalities have the potential to impair cardiac function by a number of mechanisms. Since conduction abnormalities impair cardiac function, it is logical that pacing therapies to correct or improve these conduction abnormalities may improve cardiac function. 

Additionally, the isolated heart can be used to measure chronotropic or inotropic effects. There are several additional ex vivo assays like the sinoatrial node preparation [76], left ventricular wedge preparation [77] available which address specific questions. All of the ex vivo studies mentioned above with the... 

Zhao, D. and Ren, L.M. (2003) Electrophysiological responses to imidazoline/alpha(2)-receptor agonists in rabbit sinoatrial node pacemaker cells. ActaPharmacolo caSinica,U, 1217-1223. 

Many visceral organs are innervated by both divisions of the autonomic nervous system. In most instances, when an organ receives dual innervation, the two systems work in opposition to one another. In some tissues and organs, the two innervations exert an opposing influence on the same effector cells (e.g., the sinoatrial node in the heart), while in other tissues opposing actions come about because different effector cells are activated (e.g., the circular and radial muscles in the iris). 

Transmembrane action potential of a sinoatrial node cell. In contrast to other cardiac cells, there is no phase 2 or plateau. The threshold potential (TP) is -40 mV. The maximum diastolic potential (MDP) is achieved as a result of a gradual decline in the potassium conductance (gK+). Spontaneous phase 4 or diastolic depolarization permits the cell to achieve the TR thereby initiating an action potential (g = transmembrane ion conductance). Stimulation of pacemaker cells within the sinoatrial node decreases the time required to achieve the TR whereas vagal stimulation and the release of acetylcholine decrease the slope of diastolic depolarization. Thus, the positive and negative chronotropic actions of sympathetic and parasympathetic nerve stimulation can be attributed to the effects of the respective neurotransmitters on ion conductance in pacemaker cells of the sinuatrial node. gNa+ = Na+ conductance. 

Myocytes within the sinoatrial node possess the most rapid intrinsic rate of automaticity therefore, the sinoatrial node serves as the normal pacemaker of the heart. Specialized cells within the atria, atrioventricular (A-V) node, and His-Purkinje system are capable of spontaneous depolarization, albeit at a slower rate. The more rapid rate of depolarization of the sinoatrial nodal cells normally suppresses all of the other cells with the potential for automaticity. The other cells will become pacemakers when their own intrinsic rate of depolarization becomes greater than that of the sinoatrial node or when the pacemaker cells within the sinoatrial node are depressed. When impulses fail to conduct across the A-V node to excite the ventricular myocardium (heart... 

Effects of norepinephrine and acetylcholine on spontaneous diastolic depolarization automaticity) in a pacemaker cell for the sinoatrial node. The pacemaker cell discharges spontaneously when the threshold potential (TP) is attained. The rate of spontaneous discharge is determined by the initial slope of the membrane potential and the time required to reach the threshold potential. 

The antiarrhythmic drugs in class I suppress both normal Purkinje fiber and His bundle automaticity in addition to abnormal automaticity resulting from myocardial damage. Suppression of abnormal automaticity permits the sinoatrial node again to assume the role of the dominant pacemaker. 

II Propranolol Metoprolol Nadolol Acebutolol Atenolol Pindolol Timolol Sotalol EsmoloF 3-Adrenoceptor antagonist, cardiac membrane stabilization, indirect effect on sinoatrial node to decrease rate of spontaneous diastolic depolarization. Indirect effect on A-V node to decrease conduction velocity and prolong ERR... 

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