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effects on heart

There is a small portion of crossover between the two sides of the vagus nerve, each side can innervate the other sides target tissues. The Vagus nerve slows the heart rate by releasing acetylcholine, which increases the SAN cells permeability to potassium. The increased intracellular potassium hyperpolarizes the membrane potential and slows the repolarisation of the pacemaker potential, making the time period between action potentials greater and the heart rate falls. There is very little parasympathetic negative inotropic innervation to the ventricles, but drugs such as propranolol which act as '-adrenoreceptor antagonists ('-blockers) do reduce the contractility of the myocardium.
             Sympathetic innervation of the heart serves to speed up the heart and increase the stroke volume. The sympathetic nerves begin in the spinal cord and then enter the myocardium and act on '-adrenrenergic receptors which when innervated release cAMP which causes the phosphorylation of Ca2+ voltage dependant gates via protein Kinase A. The Ca2+ gates remain open for longer and lead to a stronger force of contraction (positive inotropy).
             The sympathetic innervation of the heart increases the slope of the pacemaker potential, this produces a faster heart rate as the SAN pacemaker cells can reach the threshold for the action potentials faster. As in the parasympathetic pathways, the nerve fibres split off to the left and right sections of the heart, the left side fibres tend to have greater influence over myocardial contractility (inotropism) than heart rate (chronotropism) and visa versa for the right side fibres. .
             Sympathetic effects on the heart tend to decay away slowly as the norepinepherine that is released at the nerve terminals is re-up taken by the terminals and the rest is carried away in the blood stream, this process allows for another impulses to innervate the receptors very quickly and a summation effect to occur.


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