Why nerves to coronary vessels?

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The Human Cardiovascular System: Facts and Concepts

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Spasm of the coronary arteries: Causes and consequences (the scientist's viewpoint)

Both β1- and α1-adrenoceptors are present on canine coronary arteries, and they are accessible to norepinephrine released from the sympathetic nerves. Under normal conditions, these arteries relax because of the predominance of the β1-adrenoceptors, whereas constriction prevails in the presence of β1-adrenoceptor antagonists. The coronary arteries also have cholinergic nerves. When activated, these nerves release acetylcholine, which acts on muscarinic receptors on the sympathetic nerve terminals to reduce the output of norepinephrine and thereby lessen the relaxation mediated by β1-adrenoceptors. Thus, muscarinic agonists can precipitate coronary artery spasm. If the smooth muscle cells of the coronary arteries become hypoxic, their responsivneness to β-adrenergic stimulation is lost and constrictor responses are exaggerated. Cardiac glycosides prevent the predominance of the β-adrenergic effects of norepinephrine. Therefore, after treatment with ouabain, release of norepinephrine from the sympathetic nerves leads not to relaxation but to further contraction of coronary arteries. The endothelium of the coronary arteries inhibits platelet aggregation by the formation and release of prostacyclin, and it reacts to platelet products by causing relaxation of the underlying smooth muscle. In addition, if any thrombin is formed, it also causes endothelium-mediated relaxation. If the endothelium is damaged, these protective mechanisms are lost. Patients with coronary artery spasm usually have morphologic changes in the artery at the site of the spasm. Platelets can aggregate at this site and release vasoactive substances, which - aided by formation of thrombin - cause contraction. Thus, the blood supply to the myocardium is reduced; the ensuing hypoxia augments the constriction. Acute myocardial ischemia caused by coronary vasospasm may precipitate acute cardiac rhythm disturbances and sudden death by ventricular tachycardia or fibrillation.link_to_subscribed_fulltex

Thermosensitivity and veins.

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Adrenergic pharmacology of human and canine peripheral veins

A comparison has been made of the factors concerned with the response of canine and human saphenous veins to adrenergic stimulation. Both vessels have prejunctional muscarinic and β-adrenergic receptors. When activated by appropriate agonists these receptors decrease and increase the output, respectively, of norepinephrine from the nerve endings. Both vessels have postjunctional α1 and α2 adrenoceptors and postjunctional β adrenoceptors. Activation of the former two receptors leads to contraction of the smooth muscle, and of the latter to relaxation. There are, however, qualitative differences. In the human veins the responsiveness of the prejunctional β adrenoceptors exceeds that of the postjunctional, whereas the reverse is true in the dog. As a consequence, in the human vein β-adrenergic agonists augment, and in the canine veins they depress, the contractile response to sympathetic nerve stimulation.link_to_subscribed_fulltex

Effect of anoxia on reactions of isolated cutaneous veins to vasoactive agents

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Activity and thermosensitivity of canine cutaneous veins after inhibition of monoamine oxidase and catechol-O-methyl transferase.

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Role of the venous system in circulatory control

The sytemic venous system is a dynamic component of the cardiovascular system, and it has a key role in the maintenance of the appropriate filling of the chambers of the heart and hence of the stroke volume. Studies in man and animals have characterized the different mechanisms that control the three major components - the splanchnic, muscle, and cutaneous vascular beds - and have provided information on the changes caused by disease and by chemical agents. Concerning man, much of the information has of necessity been derived from the behavior of the limb veins, the control of which is different from that of the splanchnic capacitance vessels. Studies of the behavior of the splanchnic capacitance vessels are needed before the action of drugs that affect the cardiovascular system of man is fully understood.link_to_subscribed_fulltex

Effect of cooling on beta-receptor mechanisms in isolated cutaneous veins of the dog

Alpha-adrenergic activation of cutaneous veins by nerve stimulation or norepinephrine has been shown to be facilitated by a decrease in temperature. In the present study, the effects of cooling on beta-adrenergic mechanisms in the cutaneous veins were investigated by recording changes in isometric tension in helical strips of saphenous veins. At 37°, low doses of isoproterenol had negligible relaxing effects on the preparations but reduced their reactivity to electric stimulation; in higher doses, isoproterenol caused contraction of the saphenous vein strips. Cooling the bath to 29° slightly decreased the basal tension of the preparations and markedly augmented the contracting effect of higher doses of isoproterenol. The depressing action of that drug on the reactivity to electric stimulation was markedly accentuated by cooling. In the presence of alpha-adrenolytic drugs, the relaxing action of norepinephrine was also facilitated by a decrease in temperature. Thus, in the cutaneous vein of the dog, both the venodilator (beta-adrenergic) and the venoconstrictor (alpha-adrenergic) actions of catecholamines are facilitated by a decrease in temperature. © 1970.link_to_subscribed_fulltex

Local modulation of adrenergic neurotransmission in blood vessels

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