No, the parasympathetic n.s. will slow the heart down, the sympathetic n.s. will increase heart rate.
beta-one receptor
increase its rate and force of contraction
Preload refers to the degree of stretch of cardiac muscle cells before contraction. These muscles exhibit a length-tension relationship. When the cardiac muscle cells are at rest, they are shorter than their optimal length. The most important factor affecting the stretching of cardiac muscles is the venous return, that is, the amount of blood returning back to the heart. Slow heartbeat and exercise can increase the venous return. This will lead to the stretching of the ventricles and it will hence increase the contraction force.As reflected by the Frank-Starling Law, the stroke volume increases with the end diastolic volume. The greater filling volume will lead to the heart to stretch more and this will increase its force of contraction.
Mitral valve prolapse may decrease the stroke volume, if it is associated with significant backflow. It decreases the effeciency of the left ventricular contraction.
Potassium levels DECREASE heart rate, and maybe lead to severe cardiac arrest.and for sure, this is a mechanism of how potassium level in ECF can decrease heart rate:first, the potassium level increase in ECF making its efflux increase, due to activation of potassium channels in pacemaker cells, then the slope of pacemaker action potential will decrease, which means that the duration of one beat is prolonged, and this lead to decrease the numbers of beats in one minute, which by turn means that the heart rate is decreased.
Stretching a myocardial cell allows more Ca+2 into the cell and increases the force of contraction (the longer the muscle fiber when it begins to contract, the greater the force of contraction).
The catalyst decrease the needed activation energy.
Heart rate and ventricular wall tension
It is called concentric isotonic contraction.
extension and contraction in demand. extension mean increase in demand and contraction man decrease in demand
No, atenolol is a beta blocker that works by decreasing the heart rate and blood pressure, thereby reducing the myocardial oxygen demand.
Contraction of veins would increase venous return to the right atrium. It would increase the efficiency of the heart pumping.
Calcium slow channels play a crucial role in cardiac muscle contraction by allowing calcium ions to enter the cell. Activation of these channels leads to an increase in intracellular calcium levels, which ultimately shortens the contraction time of the heart by promoting cross-bridge formation between actin and myosin. In contrast, inhibition of calcium slow channels would lead to a lengthening of contraction time due to reduced calcium availability for muscle contraction.
Muscle fiber stretch affects myocardial contractility through the Frank-Starling mechanism, which states that an increase in the length of cardiac muscle fibers (due to increased venous return) enhances their contractile force. When myocardial fibers are stretched, the optimal overlap between actin and myosin filaments occurs, leading to more effective cross-bridge formation during contraction. This results in stronger heart contractions and improved stroke volume. However, excessive stretching can lead to decreased contractility and heart dysfunction.
The activation energy is lower and the reaction rate increase.
Its due to increase surge of catecholeamines cause by sympethetic nervous system....
Because the concentration is directly proportional to the rate of reaction (the rate will increase but k will remain the same), with an increase in concentration the activation energy will stay because the activation energy does not account for the concentration.