Sympathetic and parasympathetic nerves: regulation of rhythm and contraction impulses
The increased permeability to calcium ions is at least one cause for the increase in myocardial contractility under sympathetic stimulation because calcium ions stimulate the contraction of myofibrils.
The heart is supplied with both sympathetic and parasympathetic nerves. The parasympathetic (vagal) nerves distribute mainly to the SA and AV nodes, to a lesser extent to the muscles of the two atria, and very little directly to the ventricular muscle. The sympathetic nerves, by contrast, are distributed to all parts of the heart, with strong representation to the ventricular muscle, as well as to all other areas.
Parasympathetic (vagal) stimulation slows the heart rate and conduction
Stimulation of the parasympathetic nerves to the heart (vagus nerve) causes the hormone acetylcholine to be released at the vagus nerve endings. This hormone has two main effects on the heart. First, it reduces the rate of sinus node rhythms, and second, it reduces the excitability of the AV fibres transitioning between the atrial muscle system and the AV node, thereby slowing the transmission of cardiac impulses to the heart. the seventh.
Weak to moderate excitability of the vagus nerve reduces the heart's pumping rate, often to nearly half of normal. Furthermore, intense stimulation of the vagus nerve can completely stop rhythmic stimulation of the sinus node or completely block the conduction of cardiac impulses from the atria into the ventricles through the AV node. In both cases, the rhythmic excitatory signals are no longer conducted into the ventricles. The ventricles may stop beating for 5 to 20 seconds, but then some small areas in the Purkinje fibres, usually in the septal portion of the AV bundle, develop a rhythm of their own and cause contraction. the ventricular rate at 15-40 beats per minute. This phenomenon is called loss.
Mechanism of action of the vagus nerve
The acetylcholine released at the vagus nerve terminals significantly increases the permeability of the fibrous membrane to potassium ions, allowing potassium to rapidly escape from the conductive fibres. This process causes an increase in the negative charge in the fibres, an effect called hyperpolarization, making these excitable tissues less irritated.
In the sinus node, the hyperpolarization causes the membrane resting potential of the sinus node fibres to be significantly more negative than normal, that is, -65 to -75 mV rather than the normal range of -55 to -60 mV. Therefore, the initial elevation of the sinus node membrane potential caused by the inward leakage of sodium and calcium requires more time to reach the threshold of the excitatory potential. This enormous requirement slows down the rate of the rhythm of the nodal fibres. If the vagus nerve stimulation is strong enough, it can stop all self-exciting rhythms of the sinus node.
In the AV node, an over polarization caused by vagus nerve stimulation makes it difficult for small atrial fibres to enter the node to generate sufficient electrical stimulation of the nodal fibres. Thus, the immobilization factor for the conduction of cardiac impulses through the transitional fibres into the AV nodal fibres is reduced. A moderate drop simply slows down the conduction of the impulse, but a large drop blocks conduction altogether.
Sympathetic stimulation increases heart rate and conduction
Sympathetic stimulation causes essentially opposite effects on the heart to those caused by vagal stimulation, specifically as follows: First, it increases the discharge rate of the sinus node. Second, it increases the conduction rate, as well as the level of excitability in all parts of the heart. Third, it significantly increases the contractile force of all myocardial systems, both atria and ventricles.
In short, sympathetic stimulation increases the overall activity of the heart. Maximal stimulation can nearly triple heart rate and can nearly double heart contractility.
Sympathetic mechanism of influence
Stimulation of the sympathetic nerves releases the hormone norepinephrine at sympathetic nerve endings.
Norepinephrine tends to stimulate β-1 adrenergic receptors, which indirectly affects heart rate. The exact mechanism by which β-1 adrenergic stimulation acts on myocardial fibres is somewhat unclear but is thought to be due to its increased permeability of fibroblast membranes to sodium and calcium ions. In the sinus node, increased sodium-calcium permeability induces a more positive resting potential and accelerates the upward migration of the diastolic membrane potential toward the threshold level for self-excitation, thereby promoting spontaneous stimulation and, therefore, increased heart rate.
In the AV node and AV bundles, increased sodium-calcium permeability facilitates action potentials to stimulate each successive segment of the conduction fibre bundles, thereby reducing the conduction time from the atria to the ventricles.
The increased permeability to calcium ions is at least one cause for the increase in myocardial contractility under sympathetic stimulation because calcium ions play a large role in stimulating contractility. contraction of the myofibrils (myofibril).