Chronotropism

Chronotropism refers to the effect of a substance or factor on the heart rate. Positive chronotropic agents increase heart rate, while negative chronotropic agents decrease it. This effect is primarily mediated by the autonomic nervous system and hormones.

The heart's natural pacemaker, the sinoatrial (SA) node, controls the heart rate. The SA node spontaneously generates electrical impulses that spread throughout the heart, causing it to contract. Sympathetic nervous system stimulation releases norepinephrine, which binds to beta-1 adrenergic receptors on the SA node cells. This increases the influx of sodium and calcium ions, leading to a faster rate of depolarization and thus an increased heart rate. Conversely, parasympathetic nervous system stimulation releases acetylcholine, which acts on muscarinic receptors on the SA node. This increases potassium efflux and decreases calcium influx, slowing the rate of depolarization and decreasing heart rate.

Hormones also play a role. Thyroid hormones can increase heart rate by upregulating beta-adrenergic receptors. Epinephrine, released by the adrenal medulla, has similar effects to norepinephrine. Certain medications, such as beta-blockers, are negative chronotropic agents that block the effects of norepinephrine and epinephrine, thereby slowing the heart rate. This property is utilized in treating conditions like supraventricular tachycardia and angina. Conversely, some drugs, like atropine, are positive chronotropic agents that block the vagal nerve's inhibitory effect on the heart. Understanding chronotropism is crucial in pharmacology and cardiology for managing cardiovascular function.