Muscle drugs causing relaxation

In addition to being used as antianginal and antiarrhythmic agents, calcium channel blockers are used to treat weak and moderate hypertension. These drugs prevent calcium ions from entering into the smooth muscle cells of peripheral vessels, and they cause relaxation of peripheral vessels, which leads to lowering of arterial blood pressure. In clinically used doses, calcium channel blockers relax smooth musculature of arteries and have little effect on veins. In doses that relax smooth musculature, calcium channel blockers have relatively little effect on cardiac contractility. 

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. 

Isoxsuprine is a vasodilator that also stimulates p-adrenergic receptors. It causes relaxation of vascular and uterine smooth muscles, and its vasodilating action is greater on the arteries supplying skeletal muscles than on those supplying skin. The drug also produces positive inotropic and chronotropic effects [39]. 

On the other hand, these compounds have a general depressant effect on the CNS that is, they cause a global decrease in CNS excitability that results in generalized sedation. It therefore seems possible that some of their muscle relaxant effects are caused by their sedative powers rather than a selective effect on specific neuronal reflex pathways.11,92 This observation is not to say that they are ineffective, because clinical research has shown that these drugs can be superior to a placebo in producing subjective muscle relaxation.8 20 80 97 However, the specific ability of these drugs to relax skeletal muscle remains doubtful, and it is generally believed that their muscle relaxant properties are secondary to a nonspecific CNS sedation. 

Only drugs causing skeletal muscle relaxation are used for clinical purposes... 

Bronchial smooth muscle contains B2 receptors that cause relaxation. Activation of these receptors results in bronchodilation (see Chapter 20 Drugs Used in Asthma and Table 9-3). The blood vessels of the upper respiratory tract mucosa contain receptors the decongestant action of adrenoceptor stimulants is clinically useful (see Clinical Pharmacology). 

Prazosin, oxazosin and terazosin (see p. 73) produce a competitive block of oci adrenoceptors. They decrease peripheral vascular resistance and lower arterial blood pressure by causing the relaxation of both arterial and venous smooth muscle. These drugs cause only minimal changes in cardiac output, renal blood flow, and glomerular filtration rate. Therefore, long-term tachycardia and increased renin release do not occur. Postural hypotension may occur in some individuals. Prazosin is used to treat mild to moderate hypertension and is prescribed in combination with propranolol or a diuretic for additive effects. Reflex tachycardia and first dose syncope are almost universal adverse effects. Concomitant use of a p-blocker may be necessary to blunt the short-term effect of reflex tachycardia. 

Erectile dysfunction Alprostadil injected into the corpus caver-nosum of the penis provides effective treatment of some forms of male impotence. The drug increases arterial inflow through vasodilation and decreases venous outflow by causing relaxation of the corporal smooth muscle that occludes draining venules. Possible side effects include pain at the site of injection and, rarely, prolonged erection. 

The piperidyl alkaloid propiverine is an anticholinergic drug that causes relaxation of the smooth muscle of the urinary bladder. Treatment of plasma samples with acetonitrile, in a ratio of 1 2 (plasma acetonitrile) resulted in precipitation of proteins. Subsequent centrifugation provided a clear aqueous acetonitrile super-... 

INSULIN MUSCLE RELAXANTS -BACLOFEN 1 hypoglycaemic effect of insulin Due to these drugs causing hyperglycaemia, the mechanism being uncertain at present t doses of insulin are often required for adequate glycaemic control... 

After infusion of the P2 adrenoceptor agonist terbutaline, a profound decrease in esophageal peristaltic amplitude was reported. Peristaltic velocity in the distal part of the esophagus was decreased by 2 adrenoceptor stimulation. Clenbuterol, which is used commonly in horses, caused relaxation of rat esophageal smooth muscle (de Boer et al 1993), but it is not known whether drugs such as clenbuterol or terbutaline will similarly affect the equine esophagus. 

Xanthines are a group of drugs that directly cause relaxation of bronchial smooth muscle and some central respiratory stimulation. They also have a slight diuretic effect. Xanthines are of principle use in the immediate phase reaction of asthma but also have some effect on the late phase reaction. They are used to treat severe acute asthma attacks and chronic asthma, in particular control of nocturnal asthma and early morning wheezing. Xanthines also have some use in chronic bronchitis. 

The drug exerts its action by causing relaxation of the hypertonic (i.e., in a state of greater than normal tension) muscles minimise the response to the sensory stimuli, and also causes a significant depression of the superficial reflexes. Its weak activity and transient effect are on account of the facile metabolism of the primary hydroxyl function. In has been observed that the carbamylation of the said moiety enhances its activity. Importantly, the /)ara-chlorination affords an appreciable increase in the prevailing lipid-water partition coefficient and helps in blocking the />ara-position from undergoing hydroxylation as far as possible. 

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