Blockers 3-Blocking

One source of calcium ions, which cause contraction of smooth muscle in arterial walls, is inflow through ion-specific channels. So, the calcium blockers block the channels, limiting inflow of calcium and keeping muscle cells in relaxed states for a longer time. 

Nelson We have seen Ca2+ channel blockers block the voltage dependence of the frequency of the STOCs. 

Beta-adrenoceptor blockers block the sympathetic system antagonising the effect on the lungs, resulting in bronchoconstriction. Non-steroidal anti-inflammatory drugs inhibit prostaglandin synthesis, which may lead to bronchoconstriction. 

Amlodipine is a calcium channel blocker used to treat hypertension and angina pectoris. Calcium channel blockers block the passage of calcium, an essential factor in muscle contraction, into the heart and smooth muscles. Such blockage interferes with the contraction of these muscles, which in turn dilates the veins that supply blood to them. This reduces blood pressure. 

In overdose, 3 blockers block both and 32 adrenoceptors selectivity, if any, is lost at high dosage. The most toxic blocker is propranolol. As little as two to three times the therapeutic dose can cause serious toxicity. This may be because propranolol has additional properties At high doses it may cause sodium channel blocking effects similar to those seen with quinidine-like drugs, and it is lipophilic, allowing it to enter the CNS (see Chapter 10). 

Beta-blockers block norepinephrine and epinephrine from binding to beta-adrenoceptors and a calcium channel blocker inhibits the flow of calcium ions into muscles. Both slow down and relax the heart. 

ACE inhibitors prevent the conversion of angiotensin I to angiotensin II. Angiotensin II receptor blockers block the effects of angiotensin II on the vasculature and various other tissues... 

Pathophysiology Angiotensin-receptor blockers block the action of angiotensin II at the receptor level, and hence, block the effects of angiotensin II produced in addition by the chymase pathway. Current angiotensin II receptor blockers block the angiotensin II type I receptors (associated with hypertrophy and... 

P-Scorpion toxins] Scorpion venom V-Na+ CH blockers (block... 

Histamine2 blockers Histamine2 blockers block the H2 receptors of the parietal cells in the stomach, reducing gastric acid secretion and concentration. Side effects are headaches, dizziness, constipation, pruritus, skin rash, gynecomastia, decreased libido, and impotence. 

Betaxolol, timolol Beta blockers Block actions of NE at ciliary epithelium 4- aqueous humor formation... 

Diphenhydramine (Benadryl) Hi receptor blocker Blocks the actions of histamine on Hi receptor... 

Doxazosin a-Adrenergic blocker, Blocks ai-adrenergic receptor,... 

Toxin potent sodium channel blocker blocks action potential propagation in nerve, heart, and skeletal muscle. From puffer fish, California newt. Tox paresthesias, paralysis. Saxitoxin (paralytic shellfish poison) is similar. 

Beta blockers Nonspecific beta blockers (block both Pj and P receptors) have been used as first-step antihypertensive agents. Because these agents block P receptors as well as Pj receptors, bronchospasm may occur. Newer agents are P,-specific and are not contraindicated in asthmatic patients. 

Ganglionic blockers block impulse transmission at the sympathetic ganglia. Neurotransmission within the sympathetic and parasympathetic ganglia ... 

Histamine blockers block receptors on the parietal cells. 

Other agents are also used for the treatment of manic-depressive disorders based on preliminary clinical results (177). The antiepileptic carbamazepine [298-46-4] has been reported in some clinical studies to be therapeutically beneficial in mild-to-moderate manic depression. Carbamazepine treatment is used especially in bipolar patients intolerant to lithium or nonresponders. A majority of Hthium-resistant, rapidly cycling manic-depressive patients were reported in one study to improve on carbamazepine (178). Carbamazepine blocks noradrenaline reuptake and inhibits noradrenaline exocytosis. The main adverse events are those found commonly with antiepileptics, ie, vigilance problems, nystagmus, ataxia, and anemia, in addition to nausea, diarrhea, or constipation. Carbamazepine can be used in combination with lithium. Several clinical studies report that the calcium channel blocker verapamil [52-53-9] registered for angina pectoris and supraventricular arrhythmias, may also be effective in the treatment of acute mania. Its use as a mood stabilizer may be unrelated to its calcium-blocking properties. Verapamil also decreases the activity of several neurotransmitters. Severe manic depression is often treated with antipsychotics or benzodiazepine anxiolytics. 

Some P-adrenoceptor blockers have intrinsic sympathomimetic activity (ISA) or partial agonist activity (PAA). They activate P-adrenoceptors before blocking them. Theoretically, patients taking P-adrenoceptor blockers with ISA should not have cold extremities because the dmg produces minimal decreases in peripheral blood flow (smaller increases in resistance). In addition, these agents should produce minimal depression of heart rate and cardiac output, either at rest or during exercise (36). 

Propranolol. Propranolol hydrochloride, considered the prototype of the P-adrenoceptor blocking agents, has been in use since 1964. It is a nonselective, highly Hpid-soluble P-adrenoceptor blocker having no ISA. It is a mixture of (+) and (—) enantiomers, and the (—) enantiomer is the active moiety. The local anesthetic effects of propranolol are equipotent to those of Hdocaine [137-58-6] C 4H22N20, (see Anesthetics). Therapeutic effects include termination of catecholamine-induced arrhythmias, conversion of SA nodal tachycardias (including flutter and fibrillation) and AV nodal tachyarrhythmias to normal sinus rhythm, digitahs-induced arrhythmias, and ventricular arrhythmias (1,2). The dmg also has cardioprotective properties (37,39). 

Bopindolol is a long-acting, nonselective P-adrenoceptor blocker. It has mild membrane stabilizing activity and ISA. In vivo, the compound is hydrolyzed to its active metabohte. Because of this prodmg feature the onset of action is slower than other available P-adrenoceptor blockers. Preliminary pharmacokinetic studies indicate that the compound is weU absorbed, is 70% bioavailable, and peak plasma levels are achieved in about 2 h. Whereas its elimination half-life is 4—8 h, P-adrenoceptor blocking action (- 40%) is stiU apparent after 48 h. The dmg is being studied in hypertension, angina, and arrhythmias (43). 

The electrophysiological effects of amiodarone may be a composite of several properties. In addition to prolonging action potential duration and refractory period in ad tissues of the heart, the compound is an effective sodium channel blocker (49), calcium channel blocker (50), and a weak noncompetitive -adrenoceptor blocking agent (51). Amiodarone slows the sinus rate, markedly prolongs the QT interval, and slightly prolongs the QRS duration (1,2). 

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