<<
>>

Parasympathetic Effects Are Opposite to Those of Sympathetic Activation but Are Generally Restricted to the Sinoatrial Node, Atrioventricular Node, and Atria

Parasympathetic nerves affect the heart by the release of acetyl­choline, which activates muscarinic cholinergic receptors on cardiac muscle cells. Qualitatively, all the effects of parasym­pathetic activation arc opposite to those of sympathetic activa­tion, because the effects of activating muscarinic cholinergic receptors are opposite to the effects Ofactivating β-adrenergic receptors.

Parasympathetic nerves have very powerful effects on the SA node pacemaker cells (see Figure 19-8) and on the AV node cells (see Table 19-2). In addition, parasympathetic nerves exert strong, antisympathetic influences on all the atrial cells. FIowever, parasympathetic nerves have relatively weak effects on the ventricular muscle cells, because very few ventricular cells receive direct parasympathetic innervation. By contrast, all ventricular muscle cells receive direct sym­pathetic innervation. In summary, the predominant para­sympathetic influences are exerted at the SA node (to decrease the rate),at the AV node (to slow conduction and lengthen the refractory period), and on all supraventricular cells (to lengthen the refractory period and make their contractions weaker and slower).

Parasympathetic neurons do exert a curious, indirect effect on ventricular muscle cells. In the ventricles, para­sympathetic neurons release their acetylcholine onto sym­pathetic neuron terminals. This acetylcholine activates muscarinic cholinergic receptors that are located on the sympathetic neuron terminals. The effect of this activation is to inhibit the release of norepinephrine from the terminals, which weakens the effects of sympathetic activation on ventricular cells.

Parasympathetic effects on the heart can be mimicked by the administration of a muscarinic cholinergic agonist (e.g., acetylcholine or muscarine) and blocked by the admin­istration of a muscarinic cholinergic antagonist (e.g., atropine). Some therapeutic applications are mentioned later.

<< | >>
Source: Cunningham J.G., Klein B.G.. Textbook of Veterinary Physiology. Elsevier Health Sciences,2007. — 720 đ.. 2007

More on the topic Parasympathetic Effects Are Opposite to Those of Sympathetic Activation but Are Generally Restricted to the Sinoatrial Node, Atrioventricular Node, and Atria: