Pacemaker cells

Segmentation contractions occur as a result of the basic electrical rhythm (BER) of pacemaker cells in the small intestine. This form of muscular activity is slight or absent between meals. The motility of the small intestine may be enhanced during a meal by ... 

Enteric Neuropathies. Different kinds of familial visceral neuropathies have been described the dominant type 1 [134], the recessive type 2 [135] and a recessive form with calcified basal ganglia [134], Furthermore, aganglionosis of the small bowel (Hirschsprung s disease) [136], hypergan-glionosis (neurofibromatosis) [137], neuronal intestinal dysplasia [138] and Parkinson s disease [139] are neuropathies to consider. The recognition of the pacemaker cells of the small bowel, the interstitial cells of Cajal, has prompted studies to detect abnormalities of these cells, another possible cause of pseudoobstruction [140],... 

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. 

Drugs may have antiarrhythmic activity by directly altering conduction in several ways. Drugs may depress the automatic properties of abnormal pacemaker cells by decreasing the slope of phase 4 depolarization and/or by elevating threshold potential. Drugs may alter the conduction characteristics of the pathways of a reentrant loop. 

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. 

McHale I would suggest that waves are more important in pacemaker cells than in smooth muscle cells. Our model for the way the urethra works is that the smooth muscle cells don t have waves but the pacemaker cells do. The oscillations of the pacemaker cells can then drive the smooth muscle cells. 

Myocardial infarction, 3 710-711 and blood coagulation, 4 81 Myocardial pacemaker cells, 5 81 Myocardium, 5 79—80 Myoglobin, properties of standard, 3 836t Myosin, role in heart excitation and contraction coupling, 5 81 Myrac aldehyde, 2 278 24 485 Myrascone, 24 571... 

General definitions relating to action potentials are given in Section 9. This section deals specifically with action potentials within the cardiac pacemaker cells and conducting system. 

You will be expected to have an understanding of action potentials in nerves, cardiac pacemaker cells and cardiac conduction pathways. 

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). 

Cardiac muscle is similar to skeletal muscle, but is not under conscious control. These mono-nucleate cells are much smaller, but still show a striated pattern. The cells are in electrical contact through communicating gap junctions. These are important for the orderly spread of excitation through the heart. Spontaneous electrical depolarization of the specialized pacemaker cells together with conducting fibres activate the bulk of the ventricular muscle in the chamber walls, in each case through direct electrical contacts. 

Li2S204 being the SEI component at the Li anode and the solid discharge product at the carbon cathode. The Li—SOCI2 and Li—SO2 systems have excellent operational characteristics in a temperature range from —40 to 60 °C (SOCI2) or 80 °C (SO2). Typical applications are military, security, transponder, and car electronics. Primary lithium cells have also various medical uses. The lithium—silver—vanadium oxide system finds application in heart defibrillators. The lithium—iodine system with a lithium iodide solid electrolyte is the preferred pacemaker cell. 

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... 

The initiation of an epileptic attack involves "pacemaker" cells these differ from other nerve cells in their unstable resting membrane potential, i.e a depolarizing membrane current persists after the action potential terminates. 

The rhythm of heart contractions depends on many parameters condition of pacemaker cells and the conduction system, myocardial blood flow, and other factors consequently, arrhythmia can originate for different reasons that are caused by disruptions in electrical impulse generation or conduction. They can be caused by heart disease, myocardial ischemia, electrolytic and acid-base changes, heart innervation problems, intoxication of the organism, and so on. 

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. 

Schibler U, Sassone-Corsi P 2002 A web of circadian pacemakers. Cell 111 919—922 Stirland JA, Hastings MH, Loudon AS, Maywood ES 1996 The tau (r) mutation in the Syrian hamster alters the photoperiodic responsiveness of the gonadal axis to melatonin signal frequency. Endocrinology 137 2183-2186... 

Automaticity can be defined as the ability of a cell to alter its resting membrane potential toward the excitation threshold without the influence of an external stimulus. The characteristic feature of cells with automaticity is a slow decrease in the membrane potential during diastole (phase 4) such that the membrane potential reaches threshold (Figure 16.2). During phase 4 in these pacemaker cells, the background potassium leak current decreases and an inward depolarizing current (h) is... 

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... 

The rate of pacemaker discharge within these specialized myocytes is influenced by the activity of both divisions of the autonomic nervous system. Increased sympathetic nerve activity to the heart, the release of catecholamines from the adrenal medulla, or the exogenous administration of adrenomimetic amines will cause an increase in the rate of pacemaker activity through stimulation of -adrenoceptors on the pacemaker cells (Figure 16.3). 

The parasympathetic nervous system, through the vagus nerve, inhibits the spontaneous rate of depolarization of pacemaker cells. The release of acetylcholine from cholinergic vagal fibers increases potassium conductance (gK+) in pacemaker cells, and this enhanced outward movement of K+ results in a more negative po-... 

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. 

Quinidine can depress the automaticity of ventricular pacemakers by depressing the slope of phase 4 depolarization. Depression of pacemakers in the His-Purkinje system is more pronounced than depression of sinoatrial node pacemaker cells. 

In pacemaker cells (whether normal or ectopic), spontaneous depolarization (the pacemaker potential) occurs during diastole (phase 4, Figure 14-1). This depolarization results from a gradual increase of depolarizing current through special hyperpolarization-activated ion channels (If, also called If,) in pacemaker cells. The effect of changing extracellular potassium is more complex in a pacemaker cell than it is in a nonpacemaker cell because the effect on permeability to potassium is much more important in a pacemaker (see Effects of Potassium). In a pacemaker—especially an ectopic one—the end result of an increase in extracellular potassium is usually to slow or stop the pacemaker. Conversely, hypokalemia often facilitates ectopic pacemakers. 

Latent pacemakers (cells that show slow phase 4 depolarization even under normal conditions, eg, some Purkinje fibers) are particularly prone to acceleration by the above mechanisms. However, all cardiac cells, including normally quiescent atrial and ventricular cells, may show repetitive pacemaker activity when depolarized under appropriate conditions, especially if hypokalemia is also present. 

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