What is the difference between pacemaker potential and action potential

Also Visit CVpharmacology. Click here for information on Cardiovascular Physiology Concepts, 3rd edition, a textbook published by Wolters Kluwer Klabunde Cells within the sinoatrial SA node are the primary pacemaker site within the heart. These cells are characterized as having no true resting potential , but instead generate regular, spontaneous action potentials.

Unlike non-pacemaker action potentials in the heart, and most other cells that elicit action potentials e. This results in slower action potentials in terms of how rapidly they depolarize.

Schedule IV Schedule IV drugs, substances, or chemicals are defined as drugs with a low potential for abuse and low risk of dependence. Diazepam produced no change in baroreceptor sensitivity; however, there was a significant rise in heart rate and a significant fall in aortic systolic and left ventricular end-diastolic pressures. Cardiac index was unchanged, whereas stroke volume fell significantly.

Begin typing your search term above and press enter to search. Press ESC to cancel. Skip to content Home Philosophy What is the difference between pacemaker potential and action potential? Ben Davis November 11, What is the difference between pacemaker potential and action potential?

Why is there a plateau in cardiac action potential? Do pacemaker cells have a resting membrane potential? What determines action potential duration? How can you increase the frequency of an action potential? What happens during an action potential? Which drug shortens duration of action potential?

What is a class 3 antiarrhythmic? What happens to action potential if sodium channels are blocked? How do fast sodium channel blockers affect the heart? Is Benadryl a sodium channel blocker? Is Dilantin a sodium channel blocker? Is a sodium channel a blocker? Is keppra a sodium channel blocker? What drugs are sodium channel blockers? This is the process linking electrical excitation to contraction.

Calcium has an essential role in this process; a raised intracellular calcium concentration is the trigger that activates contraction. An understanding of calcium handling is essential to understanding the function of the heart. The intracellular calcium ion concentration in the cardiac myocyte at rest is 0.

During the plateau phase of the action potential, calcium ions flow down this steep concentration gradient and enter the myocyte. The influx of calcium triggers the release of further calcium from the sarcoplasmic reticulum via ryanodine receptors. This calcium-triggered calcium release is in contrast to skeletal muscle, where the action potential triggers calcium release directly.

Free intracellular calcium interacts with the C subunit of troponin. Cross bridge cycling occurs, leading to a shortening of the sarcomere and resultant muscular contraction. As intracellular calcium concentrations decrease during repolarization, calcium dissociates from troponin as intracellular calcium concentration decreases, resulting in relaxation.

Diastolic relaxation is an active ATP-dependent process. The strength of a contraction may be varied by increasing the amount of free intracellular calcium, by altering the sensitivity of the myofilaments to calcium, or both. The latter occurs during stretching of the myofilaments and is responsible for the Frank—Starling mechanism discussed later. Myofilament calcium sensitivity is reduced by acidosis.

High concentrations of phosphate and magnesium also impair cardiac function. Catecholamines activate beta-adrenergic receptors in the heart to produce a G-protein mediated increase in cAMP and enhanced activity of a cAMP-dependent protein kinase. This leads to the phosphorylation of calcium membrane channels, enhancing calcium entry into the cell. Phosphorylation of myosin also occurs, increasing the rate of cross bridge cycling. Catecholamines also increase the rate of re-uptake of calcium into the sarcoplasmic reticulum, thus aiding relaxation.

This increases during exercise. Oxygen extraction from blood in the coronary circulation is high; therefore, an increase in oxygen demand must be met by an increase in coronary blood flow.

The heart is very versatile in its use of metabolic substrates. Glucose and lactate are used in roughly equal proportions. The proportion of substrates utilized may vary depending on the nutritional state of the person. After a large meal containing glucose, more pyruvate and lactate are used. During periods of starvation, more fat is utilized. Insulin enhances glucose uptake into cardiac myocytes, and in untreated diabetes proportionally more fat is utilized.

This proportion increases during periods of hypoxaemia; however, lactic acidosis impairs myocardial function and can ultimately lead to myocardial cell death. The mechanics of cardiac myocyte contraction can be studied in the laboratory by examining the behaviour of an isolated muscle strip Fig.

The papillary muscle is convenient for this as its fibres run in roughly the same direction. The muscle is placed under an initial tension or preload. If the muscle strip is anchored at both ends and stimulated it undergoes isometric contraction.

The tension generated during isometric contraction increases with increasing initial length Fig. Alteration in initial fibre length is analogous to preload.

Increasing venous return to the heart results in an increased left ventricular end diastolic volume, thereby increasing fibre length. This produces an increase in the force of contraction and an increased stroke volume resulting in the familiar Starling curve. The conventional explanation for this is that at normal resting length, the overlap of actin and myosin is not optimal.

Increasing the initial length improves the degree of overlap and therefore increases the tension developed. It has become clear in recent years that this mechanism is unlikely to account for the shape of the Starling curve under physiological conditions. Several other possible mechanisms have been implicated. Lengthening the muscle increases the sensitivity of troponin to calcium length-dependent calcium sensitivity and can also lead to enhanced intracellular free calcium. Contractile properties of myocardial muscle.

Left: Simplified arrangement to study contraction of isolated cat papillary muscle. The weight labelled preload sets the resting length. If the preload is clamped in place contraction becomes isometric. Right: Three fundamental relations: a isometric contraction at increasing lengths, b and c isotonic contractions beginning from two different resting lengths 8 and 10 mm. Contractile force, velocity, and shortening are all increased by stretching the relaxed muscle.

If the muscle is able to shorten, but has to lift a weight, this is known as isotonic contraction. The weight moved by the muscle strip represents afterload. As afterload increases, both the amount and velocity of shortening decreases Fig. Conversely, reducing the afterload enhances shortening, a fact of considerable importance in the management of the failing heart.

If the preload is increased by stretching the muscle and the experiment repeated, both velocity and shortening are enhanced. In vivo , the initial phase of cardiac contraction, from the closure of the mitral and tricuspid valves to the opening of the aortic and pulmonary valves, is isotonic. Tension is developed, but the ventricle does not eject blood, as there is no muscle fibre shortening.

After the opening of the aortic and pulmonary valves, contraction becomes isotonic, tension is maintained, but blood is ejected and tonic shortening occurs. In vitro , perfusing papillary muscles with norepinephrine increases the strength and rapidity of the isometric contraction.