Epinephrine smooth muscle effects

Epinephrine (adrenalin) 0.1 to 0.5 mg may be given by subcutaneous or intramuscular injection. Hypotension and shock may be treated with fluids and vasopressors. Bronchodilators are given to relax the smooth muscles of the bronchial tubes. Antihistamines may be given to block the effects of histamine. 

As discussed in the previous section, all the effects of the ANS in tissues and organs throughout the body, including smooth muscle contraction or relaxation alteration of myocardial activity and increased or decreased glandular secretion, are carried out by only three substances acetylcholine, norepinephrine, and epinephrine. Furthermore, each of these substances may stimulate activity in some tissues and inhibit activity in others. How can this... 

The major circulating hormones that influence vascular smooth muscle tone are the catecholamines epinephrine and norepinephrine. These hormones are released from the adrenal medulla in response to sympathetic nervous stimulation. In humans, 80% of catecholamine secretion is epinephrine and 20% is norepinephrine. Stimulation of cy-adrenergic receptors causes vasoconstriction. The selective a,-adrenergic receptor antagonist, prazosin, is effective in management of hypertension because it causes arterial and venous smooth muscle to relax. 

In particular, postsynaptic Oi-blockers act on the o-receptive regions located on the smooth muscle of blood vessels and counteract the pressor, vasoconstricting effect of epinephrine and norepinephrine. In addition, they exhibit a direct relaxant effect on smooth muscle, which leads to peripheral dilation of blood vessels, which in turn raises blood pressure. However, they also exhibit a cardiostimulatory effect, which is frequently a cause of tachycardia. 

The effect of a given adrenomimetic drug on a particular type of effector cell depends on the receptor selectivity of the drug, the response characteristics of the effector cells, and the predominant type of adrenoceptor found on the cells. For example, the smooth muscle cells of many blood vessels have only or predominantly a-adrenoceptors. The interaction of compounds with these adrenoceptors initiates a chain of events in the vascular smooth muscle cells that leads to activation of the contractile process. Thus, norepinephrine and epinephrine, which have high affinities for a-adrenoceptors, cause the vascular muscle to contract and the blood vessels to constrict. Since bronchial smooth muscle contains p2-adrenoceptors, the response in this tissue elicited by the action of p2-adrenoceptor agonists is relaxation of smooth muscle cells. Epinephrine and isoproterenol, which have high affinities for p2-adrenoceptors, cause relaxation of bronchial smooth muscle. Norepinephrine has a lower affinity for p2-adrenoceptors and has relatively weak bronchiolar relaxing properties. 

In any blood vessel, the final integrated response to either neuronally released norepinephrine or to circulating epinephrine probably depends on the relative participation of at least four populations of a-adreno-ceptors postjunctional i- and az-adrenoceptors mediate constriction of vascular smooth muscle, while prejunctional and endothelial az-adrenoceptors mediate vasodilation. An understanding of the vessel vascular response to adrenomimetic drugs also must include the effects of drugs on adventitial innervation, smooth muscle, and other vascular factors that may be present. 

The clinical uses of catecholamines are based on their actions on bronchial smooth muscle, blood vessels, and the heart. Epinephrine is also useful for the treatment of allergic reactions that are due to liberation of histamine in the body, because it produces certain physiological effects opposite to those produced by histamine. It is the primary treatment for anaphylactic shock and is... 

The bronchi have a rich parasympathetic innervation but there is no sympathetic innervation of bronchial smooth muscle and all sympathetic effects are due to circulating adrenaline (epinephrine and noradrenaline (norepinephrine) acting on (32 adrenoceptors. Stimulation of these receptors mediates bronchodilatation by relaxation of bronchial smooth muscle. Beta-adrenoceptor agonists also have limited antiinflammatory actions. They inhibit mediator release from mast cells and may stimulate... 

The effects of histamine released in the body can be reduced in several ways. Physiologic antagonists, especially epinephrine, have smooth muscle actions opposite to those of histamine, but they act at different receptors. This is important clinically because injection of epinephrine can be lifesaving in systemic anaphylaxis and in other conditions in which massive release of histamine—and other mediators— occurs. 

ADRENAL MEDULLA HORMONES. Adrenaline (epinephrine) and its immediate biological precursor noradrenaline (norepinephrine, levartei-nol) are the principal hormones of the adult adrenal medulla. See Fig.l. Some of the physiological effects produced by adrenaline arc contraction of the dilator muscle of the pupil of the eye (mydriasis), relaxation of the smooth muscle of the bronchi constriction of most small blood vessels dilation of some blood vessels, notably those in skeletal muscle increase in heart rate and force of ventricular conlraction relaxation of the smooth muscle of the intestinal tract and either contraction or relaxation, or both, of uterine smooth muscle. Electrical stimulation of appropriate sympathetic (adrenergic) nerves can produce all the aforementioned effects with exception of vasodilation in skeletal muscle. 

Presumably, vasoactive substances act upon smooth muscle cells by intimate association with them, and are destroyed in the process of stimulation or depression. Epinephrine, when injected intravenously, can be recovered in much larger amounts from arterial than from venous blood minute doses given intraarterially may affect only the local circulation. If amines formed from the incomplete catabolism of amino acids are active in hypertension, one must postulate their formation by ischemic organs in direct venous connection with the heart (kidneys, brain, liver, adrenals, etc.) or in direct arterial connection with the arteriolar bed (heart and lungs). If the former, they must not be destroyed in large amounts by the lungs. Furthermore, arterial blood could be expected to contain larger quantities than venous. Absorption from or formation in the intestinal tract or spleen of amines would not produce vascular effects, as these substances probably would be metabolized by the liver. 

Since Clenbuterol dilates blood vessels in skeletal muscle but relaxes smooth muscle blood vessels, the physical reactions are quite similar to the body s own epinephrine and can effect heart rate. It also reduces the level of the amino acid taurine in the heart which stabilizes cardiac rhythms, or the electrical activity in the heart. Increased intake for taurine during use was noted as wise. 

At first, ephedrine was assumed to have a mechanism of action similar to that of epinephrine, acting through the same receptive mechanism. Later, as it was found that not all the effects of epinephrine could be duplicated by ephedrine, it was conjectured that some of its effects were due to direct excitation of smooth muscle. 

In general, ephedrine produces the same effects on smooth muscle as epinephrine. Inhibition of the intact gastrointestinal musculature and contraction of the splenic capsule and of pilomotor muscles are produced. Ephedrine has the same myometrial and urinary bladder actions as does epinephrine. 

Vascular smooth muscle tone is regulated by adrenoceptors consequently, catecholamines are important in controlling peripheral vascular resistance and venous capacitance. Alpha receptors increase arterial resistance, whereas 2 receptors promote smooth muscle relaxation. There are major differences in receptor types in the various vascular beds (Table 9-4). The skin vessels have predominantly receptors and constrict in the presence of epinephrine and norepinephrine, as do the splanchnic vessels. Vessels in skeletal muscle may constrict or dilate depending on whether ffor 13 receptors are activated. Consequently, the overall effects of a sympathomimetic drug on blood vessels depend on the relative activities of that drug at and 8receptors and the anatomic sites of the vessels affected. In addition, Di receptors promote vasodilation of renal, splanchnic, coronary, cerebral, and perhaps other resistance vessels. Activation of the Di receptors in the renal vasculature may play a major role in the natriuresis induced by pharmacologic administration of dopamine. 

These mediators can produce a number of effects including bronchiolar constriction, capillary dilatation, or urticaria (i.e., hives). In severe episodes of type I reactions a life-threatening anaphylaxis can develop in humans due to extreme bronchoconstriction and precipitate hypotension. Epinephrine is the principal drug used in the acute management of these critical effects since it achieves (1) an elevated blood pressure via activation of alpha receptors in peripheral resistance blood vessels and (2) relaxation of bronchiolar smooth muscle via activation of (32 receptors in the lung. Relief from the dermatological problem (i.e., hives) is also achieved via vasoconstriction of capillaries in the skin that reduce permeability, and, hence, fluid accumulation. Penicillin is a classic example of a drug that can cause a type I reaction. 

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