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An Investigation of The History and Development of The Beta Blockers - Research Paper Example

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This research paper describes an investigation of the history and development of the Beta Blockers. This paper analyses this drug, their work, and composition, their usage in medical practice and bad consequences. …
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An Investigation of The History and Development of The Beta Blockers
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Beta blockers are a type of drug used for various indications but more often is used in the management of diseases like cardiac arrhythmias, for cardiac protection after a myocardial infarction or what is termed as mild heart attack and also for protection against diseases such as hypertension. As it can be noted, the drugs were formally meant to block norepinephrine and epinephrine (adrenaline) from binding to beta receptors on nerves. The drugs are primarily block beta 1 and beta 2 receptors which implies that they are meant to be located in the heart, eye, and kidneys in the case of beta 1 and in the lungs, blood vessels, liver and uterus in the case of the beta 2 receptors. The beta blockers reduce the heart rate, blood pressure by dilating blood vessels and may constrict air passages by stimulating the muscles that surround the air passages to contract by blocking the effect of norepinephrine and epinephrine. With this background, it is enough to note that here that its main use was in the cardiac room where there had to be new ways of dealing with the persistence cardiac arrests and prevent further death after heart attacks. Pharmacological development is being directed towards the improvement of selectivity either by alpha-receptor blockade or by other mechanisms. Development of therapeutic models has led to the use of beta-blockers in a wide variety of indications, principally in the cardiovascular system, but also elsewhere (Olivia 2001). Since the early 1960’s there has been continuing progress in the field of beta-blockade, both in terms of pharmacological development and in the wider appreciation of the clinical application, with continuing interesting developments. In the studies of Slogoff and Keats, continuation of chronic treatment with beta-blockers in patients undergoing cardiac surgery was associated with the less preoperative myocardial. In 1987 however, Pasternak et al presented a randomized trial that entailed the use of metoroprolol in abdominal aortic aneurysm repair to reduce the preoperative myocardial infarction in the treatment of the group (Neutel & Smith 1993, 184). Yeager et al on the contrary performed a retrospective study in patients undergoing vascular surgery to evaluate the risk factors of the preoperative infarcation. He found a 50% risk reduction in the patients taking the preoperative beta-blockers. It is through the cler and indicated symptoms that the scientists there after decided to add an oxymethylene bridge to the arylethanolamine structure of pronethalol thus greatly increasing the potency of the compound. This was meant to be a curative approach towards the blocking of norepinephrine using both the B1 and B2 adrenergic receptors (Neutel & Smith 1993, 184). This was after a break through in the research sector that saw a consensus arrived at given the fact that the research done by Mangano et al in 1996 brought clear knowledge on the way that non-cardiac surgery and those using the beta blockers responded upon receiving the atenolol. Patients reported a lower mortality overall and this meant that they were positively respondent to the drugs. The American college of physicians in 1997 took these results and presented a guideline to preoperative risks management given the risk the patients were at with coronary artery (Julian 2001, 215). This was the real need to move on to the next generation drugs that worked more efficiently given the fact hat the drugs had to be improved in order to help the people have strong membrane stabilizing activity at high concentrations. It was a development that enabled doctors to come up with ways in which they could sort out the issues of the patients in an effective way (Olivia, 2001). They were invented by Sir James Black in 1958 to upheaval the management of angina pectoris and were considered to be one of the most important contributions to clinical medicine and pharmacology of the 20th century (Olivia 2001). The research first started in Black’s Glasgow Veterinary school laboratory where he noticed that there was an increase in the cases of patients suffering from angina pectoris and also a rise in the number of people dying due to heart attacks. Taking conclusions from Dr. Claude, an American scientist, Black noticed that the scientist was working on a way in which he could increase the blood flow from non-cardiac sources and him he had to take a different approach to counter the effect of adrenaline in the heart. With this, he came up with a way in which he could help in the production of drugs that could act as a block to the heart’s adrenaline-responsive- beta receptors which were commonly referred to as beta-blockers for simplicity. It is noted that the main aim of the blockers was to calm the body and help them quell the workload of the heart by blocking some of the actions taking place in the heart that in turn response to the stress levels in the body and also come up with ways in which we can be relieve cardiac stress by slowing the heart rate and reducing the force of heart muscles contracting. The diagram below explains the way they work in simpler way for easier understanding. How beta blockers work (Julian 2001, p.225) The first clinically successful beta blocker assumed the skeletal formula of propranolol. Structures of beta blocker (Julian, 2001, p.227) A common feature in the chemical structure of the major beta-blockers is that there is at least one aromatic ring structure attached to an alkyl chain possessing a secondary hydroxyl and amine functional group. Most of the beta-blockers available in the market today have one or more chiral centers in their structures, and in all cases, at least one of the chiral carbon atoms residing in the alkyl side chain is directly attached to a hydroxyl group. Except for timolol, which is marketed as S-enantiomer, each of the beta-blockers with one chiral center (e.g., propranolol, metoprolol, atenolol, esmolol, pindolol, and acebutolol) is marketed as a race mate consisting of two enantiomers. Additionally, labetalol, which has two chiral centres, is marketed as a race mate consisting of four isomers (DeQuattro & Jamerson, 1996, 22). As for nadolol, the drug has three chiral centres in its structure. However, the two ring hydroxyl groups are in the cis- orientation, allowing for only four isomers. The different types of health problems take different forms beta blockers that are in the market. They really deserve the knowledge of a trained physician given the fact that they have very adverse side effects when taken in the wrong quantity and with the wrong prescriptions. The data available regarding their pharmacologic action indicates that the interaction of these agents with beta-adrenoceptors is highly stereo-selective. The newer agent, carvedilol, is being marketed to treat hypertension and congestive heart failure. It is clear that this is anew version that counters the existing contraindication of the existing beta-blockers. Thus the continued improvement of the existing beta blockers is proving to be a real help in the prevention of adverse diseases in the population that we are leading right now (Neutel & smith, 1993). What they meant to achieve in the first instant was a drop in the number of heart cases and attacks that were being reported during that period. With the start of the study of the problems associated with the heart, there have been many queries on the way that they could be prevented. Many researches carried out in the consequent years have been found to agree to the value of beta-blockers in ischaemic heart disease. They have been found to also be the most effectual treatment for symptom relief in angina pectoris. It has also been demonstrated that beta-blockers improve prognosis post myocardial infarction and this has been through the demonstration in patients with poor left ventricular function. The antihypertensive feature of the beta blockers was the first non-predicted use to show their effect on human beings. This was achieved through the fact that the Beta1-selective agents were found to be more effective more than those that were non-selective agents. This showed just how they could achieve the best results through results from the tested patents. This is meant to be a way in which they could measure the viability of the drugs that were being provided by the people in the demonstration parade (Neutel & smith, 1993). Another thing that was achieved was that the Beta-blockers were shown to improve prognosis in younger patients while in the elderly, diuretics appear superior in primary prevention. Studies with some of the beta-blockers, that is bisoprolol, carvedilol and metoprolol, have revealed that the drugs carefully titrated even when added to a treatment regimen including ACE-inhibitors show a great deal of improvement in survival. Disadvantages were also noticed when it came to diabetes. While beta2- blockade should be avoided in patients on insulin, hypoglycaemic episodes are not rendered more of a problem by beta1- selective blockade. A recent study in diabetes type 2 has shown that tight control of blood pressure resulted in an improvement of various prognostic indicators, with results with atenolol treated patients throughout being at least as good as with the captopril treated subjects. By now, there have been very many developments that were made from the time these ideas were incepted into reality to date. It is clear that the people in the research area are doing what they can to see that the best drugs with minimal side effects have been brought forth to the market given the fact that they are supposed to come up with environmental friendly as well as user friendly. It is important to note that the wider use of the beta blockers has been found to be very effective in saving thousands of lives at reasonable prices. According to research done by Julian (2001, 210), providing of beta blockers would save almost seven times more years of life by the year 2020. The study further projected another 4000 lives saved from coronary diseases and 3500 heart attacks averted over 20 years at a reasonable cost simply by providing beta-blockers to those affected by the hart problems among the current heart attack survivors. This just tells one of the major achievements that have been realized over the years given the fact that the people in the health sector are continually experiencing new disease that are of concern to both the patient and the clinician. It is likely that these developments will go on in the near future to come up with the best services that will offer more resistance and better improvement when it comes to being of help to the patients. We can not limit the development of new curative and preventive drugs given the fact that technology and skills are being advanced as days go by. The pharmacology of the beta-blockers is one that is more profound and requires keen study for one to conclusively come up with the desired way of knowing which one fits the prescribed symptoms. The Beta blockers react by blocking the action of endogenous epinephrine and norepinephrine on beta-adrenergic receptors. There are three known types of beta receptor, designated beta1, beta2 and beta3. Beta1-Adrenergic receptors are located mainly in the heart. Beta2-Adrenergic receptors are on the other hand located mainly in the lungs, gastrointestinal tract, vascular smooth muscle, and skeletal muscle. Beta3-receptors are located in fat cells. The beta receptors work in various ways. The beta1 receptors are stimulated by epinephrine to help induce a positive chronotropic and inotropic effect on the heart and in turn increase the cardiac conduction velocity and automaticity. Stimulation of the beta2 receptors induces tremor in skeletal muscle, induces smooth muscle relaxation and increases glycogenolysis in the liver and skeletal muscle. Stimulation of the beta3 receptors induces lipolysis. Beta blockers are meant to inhibit these normal epinephrine-mediated sympathetic actions, though it has been found out that they have very minimal effect on resting subjects. This implies that they reduce the effect of physical exertion on the heart rate and thus forces contractions, dilation of blood vessels, opening of bronchi and breakdown of glycogen. Since they appear to cause vasoconstriction, it is unexpected that non-selective beta blockers have an antihypertensive effect. Antianginal effects result from decrease in the cardiac workload and oxygen demand. The antiarrhythmic effects of beta blockers arise from the nervous system where sympathetic notions are blocked and these results into the depression of sinus node function and atrioventricular node conduction. Sotalol, another type of beta blocker, has additional antiarrhythmic properties and prolongs action potential duration through potassium channel blockade. Some beta blockers like oxprenolol and pindolol are found to exhibit intrinsic sympathomimetic activity (ISA) which has the capability of exerting low level agonist activity at the beta-adrenergic receptor while simultaneously acting as a receptor site antagonist (Frishman 1994, 1465). Despite the fact that beta blockers have been found to effectively reduce the chances of death among the people with heart problems, it is clear that they still have doubts on the adverse side effects of the drugs and are therefore afraid of the repercussions of taking these medications. However, lately, researches have shown that there is a gap in the information availed to the people in with these conditions. A research done in 1996 by Epstein and Bakris (1970)showed that there had been very little increase in the number of cases reported in the clinics with depression as the 35000 patients in 15 clinical tries portrayed no signs of increase in depression. It is important to note that the there were few cases of minimal increase in fatigue after the medication was given to them. This is one sector that the scientists are working on to ensure that true information is disseminated to all the people without having to create fear among those undergoing the medication (Weir 1998). Effects of beta blockers are also very diverse. We can look at it in terms of the way that the scientist are working to se that they have dealt with these adverse effects and come up with counteractive measures of handling the shortcomings. For example, effects of the central nervous system have been found to be caused common agents that are of greater lipid solubility. This is because they have the ability to cross the blood-brain barrier into the nervous system. It is clear that the adverse effects in the central nervous system have been fond to be less in common agents that are of greater aqueous solubility. This is one way in which the scientists have come up with counteractive measures to combat the said effects. They are inclusive of hallucinations, insomnia and depression. It is through these effects that the scientists decided to look for options that would effectively serve the people with these complications and cause fewer effects that would go contrary to their body reactions. Adverse effects associated to the beta2 adrenergic receptor like the vasoconstriction of the peripherals alteration of the glucose and lipid metabolism, are less common when one uses the beta1 selective which is often termed as the cardio-selective receptor agents. The scientists however found out that the receptor selectivity diminished at higher doses. It is clear that scientists are doing what they can to come up with ways in which they can come up with alternative ways to handle these effects. However some of the effects have not yet been countered and are still being researched. Like the causes associated with either the withdrawal or drugs used in hypertension. A recent study by Virginia (2005, 320), Beta-blocker therapy was found to increase the absolute annual risk of hypotension in 11 per 1,000 patients, dizziness in 57 per 1,000 patients, and bradycardia in 38 per 1,000 patients. The relative risk for these adverse effects was 1.41 for hypotension, 1.37 for dizziness, and 3.62 for bradycardia. It was established that there were no significant increases in the absolute risk for fatigue. Beta-blocker therapy had positive aspects that included a reduction in all-cause mortality in 34 per 1,000 patients, a reduction in heart failure hospitalizations in 40 per 1,000 patients, and a reduction in worsening of heart failure in 52 per 1,000 patients. In conclusion, we can say that the higher the dosage, the higher the rate at which the people will be affected by these cardiac problems. It can also be noted that the drugs have been found to assist a whole lot of other people who were affected by other incurative or adverse diseases that either culminated to death or hospital admissions. The important indications, in terms of the numbers treated, are: Ischaemic heart disease, as a symptomatic treatment for angina pectoris and in secondary prevention after myocardial infarction, hypertension as a first line drug according to current guidelines. More recently beta-blockers have become accepted, after careful dose escalation, in the treatment of heart failure. Beta-blockers also have a useful place in glaucoma, migraine and a wide variety of other indications. They have a useful place as a prophylactic in migraine and useful applications in a variety of other conditions, although they account for relatively few prescriptions when compared to the main indications discussed above, cardiac arrhythmias, congenital obstruction of the outflow tract, phaeochromocytoma, etc. Diabetes had been regarded as a relative contra-indication, but recent evidence indicates this should no longer be the case. Similarly beta-blockers should not necessarily be withheld, when otherwise indicated, in patients with co-existent less severe peripheral vascular disease, chronic obstructive pulmonary disease without an important reversible component, although clearly a beta1-selective agent should be used. References: Epstein M, Bakris G. 1996, use of fixed-dose combination therapy: Newer approaches to antihypertensive therapy. Arch Intern Med; 156: 1969–78. Frishman WH 1994, A multifactorial trial design to assess combination therapy in hypertension. Arch Intern Med; 154: 1461–8. Frishman WH 1995, First-line therapy option with low-dose hydrochlorothiazide and low-dose bisoprolol fumarate in patients with stage I and stage II systemic hypertension. J Clin Pharmacol; 35: 182–8. Jamerson K, DeQuattro V. 1996, The impact of race on response to antihypertensive therapy. Am J Med: 101 (Suppl 3A): 22s–32s. Julian W. 2001, A Vital New Program to Prevent, Treat, and Reduce High Blood Pressure: Reversing Hypertension, new York: Grand Central Publishing, p.200-27 Neutel JM and Smith DHG 1993, Application of ambulatory blood pressure monitoring in differentiating between antihypertensive agents. Am J Med, 94: 181–7. Olivia V. 2001, Cardiology secrets, London: Elsevier Health Sciences, 127-39 Prisant LM 1995, Low dose drug combination therapy: an alternative first-line approach to hypertension treatment. Am Heart Journal 130: 359–66. Virginia P. 2005, Pharmacotherapeutics for advanced practice, Manchester: Lippincott Williams & Wilkins, p.300-45 Weir MR. 1998, The rationale for combination versus single-entity therapy in hypertension. Am J Hypertens; 11: 1635–95. Read More
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