Nervous system, autonomic 3-adrenergic

Adrenergic transmission is well known to be involved in the regulation of homeostatic control through its functions in the autonomic nervous system. Additionally, adrenergic projections in the brain have been identified with important roles in neurocognition. Adrenoreceptors are seven transmembrane G-protein-coupled receptors that mediate the physiological responses of epinephrine and norepinephrine. The first classification of these receptors resolved a (alpha)-adrenoreceptors (aARs) from P (beta)-adrenoreceptors (PARs) (Ahlquist, 1948). Since then, additional subtypes and variants have been described. 

Autonomic neuronal mechanisms also play an important role in regulating insulin release. In the sympathetic nervous system, o adrenergic agonists inhibit insulin release, whereas jS-adrenergic agonists stimulate the release of insulin. In Ihe parasympathetic nervous. system, cholinomimetic dmgs stimulate insulin release. 

A special feature of the iris is its autonomic innervation. Sympathetic activation widens the aperture of the iris whereas impulses from the parasympa thetic nervous system decrease the aperture size. Therefore adrenergic agonists and anticholinergic compounds both increase the aperture of the iris, i.e., cause mydriasis, and antiadrenergic and cholinergic agonists decrease it, i.e., cause miosis. The iris can thus be considered an excellent mirror reflecting the balance of the autonomic nervous system in the body. " ... 

Because cardiac muscle is myogenic, nervous stimulation is not necessary to elicit the heart beat. However, the heart rate is modulated by input from the autonomic nervous system. The sympathetic and parasympathetic systems innervate the SA node. Sympathetic stimulation causes an increase in heart rate or an increased number of beats/min. Norepinephrine, which stimulates ( -adrenergic receptors, increases the rate of pacemaker depolarization by increasing the permeability to Na+ and Ca++ ions. If the heart beat is generated more rapidly, then the result is more beats per minute. 

Adrenaline (epinephrine)-producing (adrenergic) and acetylcholine secreting (cholinergic) neurones of the autonomic nervous system have direct and complimentary effects on the tone of blood vessels. 

The autonomic nervous system is itself divided into two parts the sympathetic and parasympathetic nervous systems. The sympathetic nervous system serves several glands and involuntary muscles. The primary neurotransmitter of the sympathetic nervous system is norepinephrine, which acts through a and p adrenergic receptors. 

Class II— sympathoplegic drugs that reduce heart responsiveness to sympathetic autonomic nervous system excitation molecules that reduce adrenergic stimulation of the heart, usually P-adrenergic blocking agents... 

Ang II also interacts with the autonomic nervous system. It stimulates autonomic ganglia, increases the release of epinephrine and norepinephrine from the adrenal medulla, and—what is most important—facilitates sympathetic transmission by an action at adrenergic nerve terminals. The latter effect involves both increased release and reduced reuptake of norepinephrine. Ang II also has a less important direct positive inotropic action on the heart. 

We will proceed with this neurotransmitter system much as we did with the cholinergic system. Keep in mind that the main neurotransmitter here is norepinephrine and that adrenergic neurons are found in the sympathetic (fight or flight) portion ofthe autonomic, peripheral nervous system. 

A low level of tonic activity of the sympathetic nerves to vascular smooth muscle adrenergic receptors exists so that withdrawal of sympathetic vasomotor tone results in vasodilatation and reduced pressure. Conversely, enhancement of sympathetic vasomotor tone augments the level of vasoconstriction leading to elevated pressure. While the parasympathetic branch of the autonomic nervous system innervates some blood vessels, it does not generally play a role in regulating peripheral resistance. 

The authors reviewed the biphasic effect of marijuana on the autonomic nervous system. At low to moderate doses it causes increased sympathetic activity, producing a tachycardia and increase in cardiac output blood pressure therefore increases. At high doses it causes increased parasympathetic activity, leading to bradycardia and hypotension. They thought that this patient most probably had adrenergic atrial flutter. 

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