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Assistant Professor, Pennsylvania State University College of Medicine
It is generally assumed that all receptors with which drugs combine are receptors for neurotransmitters erectile dysfunction under 25 purchase 200mg viagra extra dosage fast delivery, hormones erectile dysfunction drugs india cheap 200 mg viagra extra dosage otc, or other physiological substances erectile dysfunction doctor in patna cheap 200 mg viagra extra dosage. Thus, the discovery of a specific receptor for a group of drugs can lead to a search for previously unknown endogenous substances that combine with those same receptors. For example, evidence was found for the existence of endogenous peptides with morphinelike activity. A series of these peptides have since been identified and are collectively termed endorphins and enkephalins (see Chapter 26). It is now clear that drugs such as morphine merely mimic endorphins or enkephalins by combining with the same receptors. Since most drugs have a considerable degree of selectivity in their actions, it follows that the receptors with which they interact must be equally unique. Thus, receptors will interact with only a limited number of structurally related or complementary compounds. The end-plate region of a skeletal muscle fiber contains large numbers of receptors having a high affinity for the transmitter acetylcholine. Each of these receptors, known as nicotinic receptors, is an integral part of a channel in the postsynaptic membrane that controls the inward movement of sodium ions (see Chapter 28). Stimulation of the nerve leading to the muscle results in the release of acetylcholine from the nerve fiber in the region of the end plate. The acetylcholine combines with the receptors and changes them so that channels are opened and sodium flows inward. The more acetylcholine the end-plate region contains, the more receptors are occupied and the more channels are open. When the number of open channels reaches a critical value, sodium enters rapidly enough to disturb the ionic balance of the membrane, resulting in local depolarization. The local depolarization (end-plate potential) triggers the activation of large numbers of voltage-dependent sodium channels, causing the conducted depolarization known as an action potential. The action potential leads to the release of calcium from intracellular binding sites. The calcium then interacts with the contractile proteins, resulting in shortening of the muscle cell. The sequence of events can be shown diagrammatically as follows: 10 2 Mechanisms of Drug Action 11 Ach receptor Na influx action potential increased free Ca contraction where Ach acetylcholine. The important concept at this stage of the discussion is that specific receptive substances serve as triggers of cellular reactions. If we consider the sequence of events by which acetylcholine brings about muscle contraction through receptors, we can easily appreciate that foreign chemicals (drugs) can be designed to interact with the same process. Thus, such a drug would mimic the actions of acetylcholine at the motor end plate; nicotine and carbamylcholine are two drugs that have such an effect. Chemicals that interact with a receptor and thereby initiate a cellular reaction are termed agonists. Thus, acetylcholine itself, as well as the drugs nicotine and carbamylcholine, are agonists for the receptors in the skeletal muscle end plate.
Labetalol impotence natural treatments cheap viagra extra dosage american express, because it possesses both - and -blocking activity erectile dysfunction 55 years old buy discount viagra extra dosage 130mg on line, is useful for the preoperative management of patients with a pheochromocytoma treatment erectile dysfunction faqs buy viagra extra dosage 200mg. Adverse Effects There have been reports of excessive hypotension and paradoxical pressor effects following intravenous administration of labetalol. These latter effects may be due to a labetalol-induced blockade of neuronal amine uptake, which increases the concentrations of norepinephrine in the vicinity of its receptors. Approximately 5% of the patients who receive labetalol complain of side effects typical of noradrenergic nervous system suppression. These include postural hypotension, gastrointestinal distress, tiredness, sexual dysfunction, and tingling of the scalp. Skin rashes have been reported, as has an increase in the titer of antinuclear antibodies. Despite the latter observation, the appearance of a systemic lupus syndrome is rare. Labetalol also has been reported to interfere with chemical measurements of catecholamines and metabolites. Clinical Uses Labetalol is useful for the chronic treatment of primary hypertension. It can be used alone but is more often employed in combination with other antihypertensive agents. Labetalol also has been used intravenously for the treatment of hypertensive emergencies. Like conventional -blockers, labetalol may be useful for patients with coexisting hypertension and anginal pain due to ischemia. It is also being investigated as a possible therapeutic modality for ischemic heart disease, even in the absence of hypertension. The benefit derives from its -blocking activity, which decreases cardiac work, and from its ability to decrease afterload by virtue of its -blocking activity. Other Compounds Several other -adrenoceptor antagonists, similar to labetalol, exhibit some degree of -receptor antagonism. Which of the following actions of epinephrine would be antagonized by prazosin but not by propranolol Which of the following adrenoceptor antagonists will reduce responses mediated by both - and receptors Shown is the effect of applying norepinephrine on the arterial pressure of an isolated (in vitro) segment of artery from an experimental animal before and after adding drug X to the tissue. Drug X is most likely: (A) Guanethidine (B) Propranolol (C) Cocaine (D) Prazosin (E) Atropine 5. The responses being measured are an increase in heart rate of a human subject and relaxation of an in vitro strip of human bronchiolar smooth muscle. The adrenoceptors that epinephrine acts on to affect heart rate, renin release, bronchiolar tone, and glycogenolysis are -receptors. The radial smooth muscle in the iris has -receptors that when activated, contract the radial muscle which dilates the pupil. Propranolol and metoprolol are selective for receptors, whereas prazosin and phenoxybenzamine are selective for -receptors. Labetalol is the only antagonist in this list that has the ability to reduce responses mediated by both - and -receptors. What is shown is an increase in pressure caused by norepinephrine and the reduction of the effect by drug X.
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In contrast erectile dysfunction 43 generic viagra extra dosage 150 mg on line, the levels of weak organic acids will probably be lower than those in plasma erectile dysfunction niacin order viagra extra dosage 130 mg line. Low-molecularweight un-ionized water-soluble drugs will diffuse passively across the mammary epithelium and transfer into milk injections for erectile dysfunction after prostate surgery purchase cheap viagra extra dosage on line. There they may reside in association with one or more milk components, for example, bound to protein such as lactalbumin, dissolved within fat globules, or free in the aqueous compartment. Substances that are not electrolytes, such as ethanol, urea, and antipyrine, readily enter milk and reach approximately the same concentration as in plasma. Compounds used in agriculture also may be passed from cows to humans by this route. Finally, antibiotics such as the tetracyclines, which can function as chelating agents and bind calcium, have a higher milk than plasma concentration. In addition, composition of the milk will be affected by the maternal diet; for example, a high-carbohydrate diet will increase the content of saturated fatty acids in milk. The greatest drug exposure occurs when feeding begins shortly after maternal drug dosing. Additional factors determining exposure of the infant include milk volume consumed (about 150 mL/kg/day) and milk composition at the time of feeding. Fat content is highest in the morning and then gradually decreases until about 10 P. A longer feed usually results in exposure of the infant to more of a fat-soluble drug, since milk fat content increases somewhat during a given nursing period. In general, the ability to oxidize and conjugate drugs is low in the neonate and does not approach full adult rates until approximately age 6. It follows, therefore, that drug accumulation should be less in an older infant who breast-feeds than in a suckling neonate. Although abnormalities in fetal organ structure and function can result from the presence of certain drugs in breast milk, it would be quite inappropriate to deny the breast-feeding woman appropriate and necessary drug therapy. Breast-feeding should be discouraged when inherent drug toxicity is known or when adverse pharmacological actions of the drug on the infant are likely. Infant drug exposure can be minimized, however, through short intermittent maternal drug use and by drug dosing immediately after breastfeeding. Concerning the renal excretion of drugs: (A) Drugs that are ionized in the renal tubule are more likely to undergo passive reabsorption than those that are unionized (B) Low-molecular-weight drugs are much more likely to be actively secreted than filtered. When one inhibits the action of a drug-metabolizing enzyme (A), one would expect an increase instead of a decrease in drug concentrations, since less is being metabolized. Induction of an enzyme (B) would have the opposite effect, since there would be more enzyme available to metabolize the drug. C is correct, since the most common mechanism of enzyme induction is through synthesis of new enzyme protein, which does not occur immediately. Finally, mechanism-based inactivation (D) is also correct, since this is irreversible, leaving the enzyme inactive and eventually it is degraded by the body. The conjugate, however, usually maintains the same pharmacological mechanism of action, although frequently of a lesser magnitude. Conjugation with glucuronic acid makes a drug molecule more water soluble (A), and glucuronic acid conjugates are more likely to be eliminated by secretion into the bile (C) than are unconjugated compounds. These glucuronide conjugates, once secreted into the bile, may be cleaved by -glucuronidases to liberate the parent compound, which can then be reabsorbed (D). Plasma proteins are too large to be filtered by the glomerulus, so that any drug molecules bound to these plasma proteins will not undergo filtration.
The application of a subthreshold stimulus (#1) produces a depolarizing current that fails to result in excitation of the myocardial cell erectile dysfunction pump how do they work buy cheap viagra extra dosage on-line. Major transmembrane currents carried by specific ions entering the cell through selective ion channels are depicted to the right erectile dysfunction medication injection discount viagra extra dosage 120mg overnight delivery. The membrane potential at which this occurs may be calculated using the Nernst equation: Ex 61 log([x]i/[x]o) In this equation erectile dysfunction drugs research discount 200mg viagra extra dosage overnight delivery, x is the ion in question, [x]i is the concentration inside the cell, and [x]o is the concentration outside the cell. The contribution of other ionic species to the resting membrane potential is smaller because of the low transmembrane permeability at hyperpolarized resting membrane potentials. An examination of the relationship of [K]o] and [K]i] in the Nernst equation shows that an increase in the [K]o will result in a decrease in the membrane resting potential (less negative). Changes in the extracellular concentration of another ion (Na, Ca, Mg, Cl) may also modify the resting potential. To produce membrane depolarization, a current stimulus of sufficient intensity to exceed the outward K current must be applied to the cell. If the depolarizing stimulus raises the membrane potential above a threshold value, sodium channels within the sarcolemmal membrane change their conformation and open their ion-selective pore, allowing Na to enter the cell driven by the electrochemical gradient. The open sodium channels raise the membrane potential toward the equilibrium potential of sodium (65 mV) and set into motion the intricate and precisely coordinated series of ion channel openings and closings leading to the characteristic action potential. The action potential has been divided into five phases, rapid depolarization (phase 0), early repolarization (phase 1), plateau (phase 2), rapid repolarization (phase 3) and finally the resting phase in myocytes or slow diastolic depolarization (phase 4). The last is a property in cells with the potential for automaticity (defined later). The interval during which the myocyte cannot be stimulated is the absolute refractory period. After the myocyte returns to a hyperpolarized resting potential, the channels cycle through the inactivated state back to the rested or closed conformation and again are available to open in response to a stimulus of sufficient intensity. The refractory period defines the maximal rate at which the cardiac cells will respond to applied stimuli and propagate impulses to neighboring cells. The density of available sodium channels in the cell membrane also determines the rate at which an impulse is conducted from one cell to another. The maximal upstroke velocity of phase 0 (Vmax) is a major determinant of the speed of impulse conduction within the myocardium and therefore is important in initiation and maintenance of arrhythmia. Phase 1 At the peak of the action potential upstroke, a short rapid period of repolarization occurs and the membrane potential returns toward 0 mV. The distribution of Ito is heterogeneous throughout the myocardium and varies from species to species. Within the ventricle, Ito is present in the epicardium and absent in the endocardium. Abnormalities in the function of Ito have been implicated in Brugada syndrome, a potentially lethal genetic disease resulting in ventricular tachycardia and fibrillation. Ionic Basis for the Membrane Action Potential Phase 0: Rapid Depolarization Phase 0 of the action potential encompasses the rapid depolarization of the myocyte induced principally by the opening of voltage gated sodium channels. The sodium channels open rapidly in response to membrane depolarization and close within 1 to 2 milliseconds in a time-dependent fashion. The conformation of the channels changes, and they enter an inactivated state in which they cannot be recruited to participate in generating a subsequent action potential for a defined inter- Phase 2: Action Potential Plateau Phase 2 is characterized by a net balance between inward (depolarizing) and outward (repolarizing) ion currents maintaining the myocyte in a depolarized state. During this phase, Ca enters the cell, causing Ca release from intracellular stores and linking electrical depolarization with mechanical contraction. Interestingly, the current flow during the plateau phase is small, and therefore, perturbations in any of the currents participating in this phase (either through genetic mutations 16 Antiarrhythmic Drugs 163 or pharmacologically) may result in profound alterations in the action potential.
