Xem 1-20 trên 39 kết quả Receptor pharmacology
  • For about four decades now, a course in receptor pharmacology has been given at University College London for undergraduate students in their final year of study for the Bachelor of Science degree in pharmacology. More recently, the course has also been taken by students reading for the Bachelor of Science degree in medicinal chemistry. The students following the course have relied for their reading upon a variety of sources, including original papers, reviews, and various textbooks, but no single text brought together the material included in the course.

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  • The last decade or so has seen remarkable advances in our knowledge of cough. This applies especially to its basic mechanisms: the types of airway sensors, the pharmacological receptors on their membranes, the brainstem organization of the ‘cough centre’, and the involvement of the cerebral cortex in the sensations and the voluntary control of cough. With the exception of the last of these, nearly all the studies have been on experimental animals rather than humans, for obvious reasons.

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  • Less than 20 years ago the field of cannabis and the cannabinoids was still considered a minor, somewhat quaint, area of research. A few groups were active in the field, but it was already being viewed as stagnating. The chemistry of cannabis was well known, Δ9-tetrahydrocannabinol (Δ9-THC), identified in 1964, being the only major psychoactive constituent and cannabidiol, which is not psychoactive, possibly contributing to some of the effects. These cannabinoids and several synthetic analogs had been thoroughly investigated for their pharmacological effects.

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  • How drugs act and interact, how they enter the body, what happens to them inside the body, how they are eliminated from it; the effects of genetics, age, and disease on drug action — these topics are important for, although they will generally not be in the front of the conscious mind of the prescriber, an understanding of them will enhance rational decision taking. Knowledge of the requirements for success and the explanations for failure and for adverse events will enable the doctor to maximise the benefits and minimise the risks of drug therapy. Pharmacodynamics.

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  • Nicotine is no longer possible, even in the face of an intensive and synchronized release of ACh (C). Although nicotine mimics the action of ACh at the receptors, it cannot duplicate the time course of intrasynaptic agonist concentration required for appropriate high-frequency ganglionic activation. The concentration of nicotine in the synaptic cleft can neither build up as rapidly as that of ACh released from nerve terminals nor can nicotine be eliminated from the synaptic cleft as quickly as ACh.

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  • Adverse Drug Effects premature breakdown of red blood cells (hemolysis) in subjects with a glucose6-phosphate dehydrogenase deficiency. The discipline of pharmacogenetics deals with the importance of the genotype for reactions to drugs. The above forms of hypersensitivity must be distinguished from allergies involving the immune system (p. 72). Lack of selectivity (C). Despite appropriate dosing and normal sensitivity, undesired effects can occur because the drug does not specifically act on the targeted (diseased) tissue or organ.

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  • Drug-Receptor Interaction partial charges. When a hydrogen atom bearing a partial positive charge bridges two atoms bearing a partial negative charge, a hydrogen bond is created. A van der Waals’ bond (B) is formed between apolar molecular groups that have come into close proximity. Spontaneous transient distortion of electron clouds (momentary faint dipole, !!) may induce an opposite dipole in the neighboring molecule. The van der Waals’ bond, therefore, is a form of electrostatic attraction, albeit of very low strength (inversely proportional to the seventh power of the distance).

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  • Chronic consumption For benefits of chronic alcohol consumption, see page 187. Central nervous system. The development of dependence on alcohol appears to involve alterations in central nervous system neurotransmission. The acute effect of alcohol is to block NMDA receptors for which the normal agonist is glutamate, the main excitatory transmitter in the brain. Chronic exposure increases the number of NMDA receptors and also 'L type' calcium channels, while the action of the (inhibitory) GABA neurotransmitter is reduced.

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  • The reality is more complex since the receptor binding profile of clozapine and the newer atypical antipsychotic agents suggests that D2-receptor blockade is not essential for antipsychotic effect. The atypical drugs act on numerous receptors and modulate several interacting transmitter systems. Clozapine is a highly effective antipsychotic. It has little affinity for the D2-receptor compared with classical drugs but binds more avidly to other dopamine subtypes (e.g. D1, D3 and D4). It blocks muscarinic acetylcholine receptors, as do certain classical agents (e.g.

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  • Overdose, including self-poisoning, causes bradycardia, heart block, hypotension and low output cardiac failure that can proceed to cardiogenic shock; death is more likely with agents having membrane stabilising action (see Table 23.1). Bronchoconstriction can be severe, even fatal, in patients subject to any bronchospastic disease; loss of consciousness may occur with lipid-soluble agents that penetrate the central nervous system. Receptor blockade will outlast the persistence of the drug in the plasma. Rational treatment includes: • Atropine (1-2 mg i.v.

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  • Drugs Acting on Motor Systems spinal disorders. Benzodiazepines enhance the effectiveness of the inhibitory transmitter GABA (p. 226) at GABAA receptors. Baclofen stimulates GABAB receptors. !2-Adrenoceptor agonists such as clonidine and tizanidine probably act presynaptically to inhibit release of excitatory amino acid transmitters. The convulsant toxins, tetanus toxin (cause of wound tetanus) and strychnine diminish the efficacy of interneuronal synaptic inhibition mediated by the amino acid glycine (A).

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  • Acetylcholine is a widespread chemotransmitter in the body, mediating a broad range of physiological effects.There are two distinct classes of receptor for acetylcholine defined on the basis of their preferential activation by the alkaloids, nicotine (from tobacco) and muscarine (from a fungus, Amanita muscaria). Cholinergic drugs (acetylcholine agonists) mimic acetylcholine at all sites although the balance of nicotinic and muscarinic effects is variable.

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  • Pharmacokinetic Interactions Causing Decreased Drug Effects Gastrointestinal absorption can be reduced if a drug interaction results in drug binding in the gut, as with aluminum-containing antacids, kaolin-pectin suspensions, or bile acid sequestrants. Drugs such as histamine H 2 receptor antagonists or proton pump inhibitors that alter gastric pH may decrease the solubility and hence absorption of weak bases such as ketoconazole.

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  • Adrenergic receptors (ARs) are expressed in almost all organs and tissues and regulate a large number of diverse physiological processes upon activation by epinephrine and norepinephrine. There are three families of ARs, a1, a2, and b-ARs, with distinct pharmacological properties and functions. Since the first identification of bARs more than three decades ago, research on ARs has led to the establishment of many fundamental concepts in G protein-coupled receptor (GPCR) pharmacology.

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  • The topic of pharmacology usually escapes the attention of many college students by virtue of the fact that pharmacology itself is rarely taught on the undergraduate level. It generally is reserved for postbaccalaureate students who are enrolled in health curricula associated with medicine, dentistry, nursing, and the veterinary sciences; however, certain upper level undergraduates are interested in the subject. This book is the product of teaching undergraduates the principles of pharmacology over the last 20 years.

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  • What is ‘biochemical pharmacology’? • A fancy way of saying ‘pharmacology’, and of hiding the fact that we are sneaking a subject of medical interest into the UW biochemistry curriculum. • An indication that we are not going to discuss prescriptions for your grandmother’s aching knee; we will focus on the scientific side of things but not on whether to take the small blue pill before or after the meal. What is it not? • A claim that we accurately understand the mechanism of action of each practically useful drug in biochemical terms.

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  • The incidence of cardiovascular disease has decreased in the last several years with a better understanding of the pathophysiology of acute coronary syndromes (ACS), widespread implementation of lipid lowering drugs, improved surgical treatments such as stent placements, and new therapeutic regimens such as the statins, low molecular weight heparins, and platelet glycoprotein IIb/IIIa receptor inhibitors. Nevertheless, it remains today as the leading cause of morbidity and mortality in the Western world....

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  • It has been nearly 20 years since the last Humana Press book devoted to serotonin (5-hydroxytryptamine; 5-HT) receptors has appeared. Since then, the field of 5-HT receptors has undergone a revolution due to the discovery of many additional 5-HT receptors. Although 5-HT was chemically elucidated in 1948 by Page and colleagues (Rapport et al.

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  • This book is intended to provide an overview of the pharmacology of neurotransmitter release. Neurotransmitter release initiates synaptic transmission, the major mechanism by which neurons communicate with each other and with effector cells.

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  • Mechanisms of Dyspnea Respiratory sensations are the consequence of interactions between the efferent, or outgoing, motor output from the brain to the ventilatory muscles (feed-forward) and the afferent, or incoming, sensory input from receptors throughout the body (feedback), as well as the integrative processing of this information that we infer must be occurring in the brain (Fig. 33-1). A given disease state may lead to dyspnea by one or more mechanisms, some of which may be operative under some circumstances but not others. ...

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