General Principles and Intrinsic Cardiac Nervous Regulation
Heart function is never strictly monotonous: it plastically adapts to changing environmental conditions. The baseline level of control consists of myogenic autoregulation mechanisms (such as Starling's law). Powerful neural and humoral influences are superimposed on this foundation.
A special role is played by the intrinsic cardiac nervous system, which helps the myocardium cope with changes in preload (venous pressure — VP). The response depends on the volume of incoming blood:
- With a moderate increase in venous return: atrial stretching occurs, which activates intracardiac reflex arcs and adrenergic nerve fibers. Norepinephrine (NE) is released. This produces a stimulating sympathomimetic effect — contraction force increases, and the heart successfully pumps the increased volume of blood, normalizing pressure.
- With an excessive increase in venous return: there is a risk of overstretching. To save the organ from energy depletion, cholinergic fibers are activated. They provide a "braking" action — limiting the excessive rise in contraction force.
Classification of Regulatory Influences
Sympathetic and parasympathetic reflexes can exert both stimulating (positive, +) and inhibitory (negative, -) effects on various aspects of cardiac activity. Traditionally, five main effects are distinguished:
- Chronotropic — influence on the frequency of impulse generation by the pacemaker.
- Inotropic — alteration of the amplitude and force of contractions of the working myocardium.
- Bathmotropic — shift in the excitability threshold of muscle cells.
- Dromotropic — acceleration or deceleration of electrical signal conduction.
- Tonotropic — alteration of the degree of tension (tone) of the heart muscle during the resting phase.
Influence of the Sympathetic Nervous System
Sympathetic nerve fibers innervate the entire heart, including the atria, ventricles, and conduction system. Their activation is aimed at the maximal mobilization of the organ's resources.
Key mechanisms of sympathetic action:
- Slow diastolic depolarization (SDD) is accelerated in the cells of the sinoatrial node (SAN — the primary pacemaker).
- The overall excitability of both typical working and atypical cardiomyocytes increases.
- The influx of $Ca^{2+}$ ions into muscle cells increases.
As a result, sympathetic stimulation causes a complex of positive effects: heart rate increases (positive chronotropic effect), excitability rises (positive bathmotropic), and impulse conduction velocity increases (positive dromotropic). In addition, the duration of action potentials (APs) in ventricular cardiomyocytes increases.
Extracardiac Regulation and Protection Against Overload
If venous pressure rises excessively, intrinsic cardiac mechanisms become insufficient. Inhibitory mechanisms of extracardiac regulation are engaged, with the vagus nerve (n. vagus) playing the leading role.
Its fibers release the neurotransmitter acetylcholine (ACh), which blocks the stimulating effects of norepinephrine and targets critical zones:
- Sinoatrial node (SAN): impulse generation slows down, heart rate drops (negative chronotropic effect).
- Atrioventricular node (AVN): the speed of excitation transmission from the atria to the ventricles decreases (negative dromotropic effect).
- Working myocardium: the force of contraction decreases (negative inotropic effect).
Such generalized inhibition of heart function is necessary to prevent myocardial damage and preserve its resources under conditions of critical volume overload.