Жүрекшелердің оң жағындағы кардиостимулятор түйіні

Group of cells located in the wall of the right atrium of the heart

The sinoatrial node (also known as the sinuatrial node, SA node or sinus node) is an oval shaped region of special cardiac muscle in the upper back wall of the right atrium made up of cells known as pacemaker cells. The sinus node is approximately 15 mm long, 3 mm wide, and 1 mm thick, located directly below and to the side of the superior vena cava. These cells can produce an electrical impulse known as a cardiac action potential that travels through the electrical conduction system of the heart, causing it to contract. In a healthy heart, the SA node continuously produces action potentials, setting the rhythm of the heart (sinus rhythm), and so is known as the heart's natural pacemaker. The rate of action potentials produced (and therefore the heart rate) is influenced by the nerves that supply it.

The sinoatrial node is an oval shaped structure that is approximately 15 mm long, 3 mm wide, and 1 mm thick, located directly below and to the side of the superior vena cava. The size can vary but is usually between 10 30 mm long, 5–7 mm wide, and 1–2 mm deep.

The SA node is located in the wall (epicardium) of the right atrium, laterally to the entrance of the superior vena cava in a region called the sinus venarum (hence sino + atrial). It is positioned roughly between a groove called the crista terminalis located on the internal surface of the heart and the corresponding sulcus terminalis, on the external surface. The connective tissue, along with the paranodal cells, insulate the SA node from the rest of the atrium, preventing the electrical activity of the atrial cells from affecting the SA node cells. Unlike the atrial cells, SA node cells contain fewer mitochondria and myofibers, as well as a smaller sarcoplasmic reticulum. This means that the SA node cells are less equipped to contract compared to the atrial and ventricular cells. Action potentials pass from one cardiac cell to the next through pores known as gap junctions. These gap junctions are made of proteins called connexins. There are fewer gap junctions within the SA node and they are smaller in size. This is again important in insulating the SA node from the surrounding atrial cells.

There are no large veins that drain blood away from the SA node. Instead, smaller venules drain the blood directly into the right atrium.

Heart rate depends on the rate at which the sinoatrial node produces action potentials. At rest, heart rate is between 60 and 100 beats per minute. This is a result of the activity of two sets of nerves, one acting to slow down action potential production (these are parasympathetic nerves) and the other acting to speed up action potential production (sympathetic nerves). Modulation of heart rate by ANS is carried by two types of channel: Kir and HCN (members of the CNG gated channels). The sympathetic nerves begin in the thoracic region of the spinal cord (in particular T1 T4). These nerves release a neurotransmitter called noradrenaline (NA). This binds to a receptor on the SA node membrane, called a beta 1adrenoceptor. Binding of NA to this receptor activates a G protein (in particular a Gs Protein, S for stimulatory) which initiates a series of reactions (known as the cAMP pathway) that results in the production of a molecule called cyclic adenosinemonophosphate (cAMP). This cAMP binds to the HCN channel (see above). Binding of cAMP to the HCN increases the flow of Na+ and K+ into the cell, speeding up the pacemaker potential, so producing action potentials at a quicker rate and increasing heart rate. An increase in heart rate is known as positive chronotropy. The parasympathetic nerves supplying the SA node (in particular the Vagus nerves) originate in the brain. These nerves release a neurotransmitter called acetylcholine (ACh). ACh binds to a receptor called an M2 muscarinic receptor, located on the SA node membrane. Activation of this M2 receptor then activates a protein called a G protein (in particular Gi protein, i for inhibitory). Activation of this G protein blocks the cAMP pathway, reducing its effects, therefore inhibiting sympathetic activity and slowing action potential production. The G protein also activates a potassium channel GIRK 1 and GIRK 4, which allows K+ to flow out of the cell, making the membrane potential more negative and slowing the pacemaker potential, therefore decreasing the rate of action potential production and therefore decreasing heart rate. A decrease in heart rate is known as negative chronotropy. The first cell to produce the action potential in the SA node isn't always the same; this is known as pacemaker shift. In certain species of animals—for example, in dogs—a superior shift (i. e., the cell that produces the fastest action potential in the SA node is higher than previously) usually produces an increased heart rate whereas an inferior shift (i. e. the cell producing the fastest action potential within the SA node is further down than previously) produces a decreased heart rate. Blockage of the arterial blood supply to the SA node (most commonly due to a myocardial infarction or progressive coronary artery disease) can therefore cause ischemia and cell death in the SA node. This can disrupt the electrical pacemaker function of the SA node, and can result in sinus node dysfunction. If the SA node does not function or the impulse generated in the SA node is blocked before it travels down the electrical conduction system, a group of cells further down the heart will become its pacemaker.

The sinoatrial node was first discovered by a young medical student, Martin Flack, in the heart of a mole, whilst his mentor, Sir Arthur Keith, was on a bicycle ride with his wife. They made the discovery in a makeshift laboratory set up in a farmhouse in Kent, England, called Mann's Place. Their discovery was published in 1907.