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Figure 1: The chemical structure of dichloroisoprenaline or dichloroisoproterenol (), abbreviated DCI — the first β-blocker to be developed. β adrenergic receptor antagonists (also called beta-blockers or β-blockers) were initially developed in the 1960s, for the treatment of angina pectoris but are now also used for hypertension, congestive heart failure and certain arrhythmias. [1]
Beta blockers vary in their lipophilicity (fat solubility) and in turn in their ability to cross the blood–brain barrier and exert effects in the central nervous system. [76] Beta blockers with greater blood–brain barrier permeability can have both neuropsychiatric therapeutic benefits and side effects, as well as adverse cognitive effects ...
The combination of beta blockers and antihypertensive drugs will work on different mechanism to lower blood pressure. [17] For example, the co-administration of beta-1 blocker atenolol and ACE inhibitor lisinopril could produce a 50% larger reduction in blood pressure than using either drug alone. [18]
Beta blockers work by blocking the effects of adrenaline, aka slowing your heart rate and reducing those physical signs and symptoms of nervousness and anxiety, he explained.
It was the first beta-blocker effectively used in the treatment of coronary artery disease and hypertension. [74] Newer, more cardio-selective beta blockers (such as bisoprolol, nebivolol, carvedilol, or metoprolol) are used preferentially in the treatment of hypertension. [74]
Bisoprolol, sold under the brand name Zebeta among others, is a beta blocker which is selective for the beta-1 receptor [7] and used for cardiovascular diseases, [7] including tachyarrhythmias, high blood pressure, angina, and heart failure. [7] [8] It is taken by mouth. [7]
Sir James Whyte Black (14 June 1924 – 22 March 2010 [2]) was a Scottish physician and pharmacologist.Together with Gertrude B. Elion and George H. Hitchings, he shared the Nobel Prize for Medicine in 1988 for pioneering strategies for rational drug-design, which, in his case, led to the development of propranolol and cimetidine.
The amount of methanol produced is similar to endogenous methanol production. Esmolol has a rapid distribution half-life of about two minutes and an elimination half-life of about nine minutes. [citation needed] Esmolol is classified as a beta blocker with low lipophilicity and hence lower potential for crossing the blood–brain barrier. [8]