Cardiovascular centre is detected by baroreceptors in the aortic sinuses or carotid sinuses, the cardiovascular centre affects changes to the heart rate by sending a nerve impulse to the cardiac pacemaker (or SA node) via sympathetic fibres (to cause faster and stronger cardiac muscle contraction) and the vagus nerve (to cause slower and less strong cardiac muscle contraction). The cardiovascular centre also increases the stroke volume of the heart (that is, the amount of blood it pumps). These two changes help to regulate the cardiac output, so that a sufficient amount of blood reaches tissue. Hormones like epinephrine and norepinephrine can affect
Cardiac action potential membrane potential Ionic pumps as discussed above, like the sodium-calcium exchanger and the sodium-potassium pump restore ion concentrations back to balanced states pre-action potential. This means that the intracellular calcium is pumped out, which was responsible for cardiac myocyte contraction. Once this is lost the contraction stops and myocytic cells relax, which in turn relaxes the heart muscle. During this phase, the action potential fatefully commits to repolarisation. This begins with the closing of the L-type Cachannels, while the K channels (from phase 2) remain open. The main potassium channels involved in repolarization are the delayed rectifiers (I) and (I)