P-receptor blocking agents

Although not beneficial for numerous sports, P-blockers have been recognized to be performance-enhancing in archery and shooting through their antagonistic properties that inhibit the normally adrenaline-mediated sympathetic actions. Consequently, symptoms of anxiety 

TABLE 3.6 Characteristic Fragment Ions of Selected P-blockers after Derivatization Using EI° 

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M. Enquist and J. Hermansson, Separation of the enantiomers of P-receptor blocking agents and other cationic drugs using the CHIRAL-AGP column. Binding properties and characterization of... 

Due to the need of extensive derivatization for GC-MS analysis (see Chapter 3), P-receptor blocking agents such as atenolol, bupranolol, metoprolol, and propranolol (Fig. 4.23,1-4) have been early subjects of LC-MS/MS analysis. The presence of a secondary amino function in all P-blockers provides sufficient proton affinity for positive ESI, and core structure-specific as well as individual product ions are derived from target analytes using low energy CID as summarized in Table 4.7. 

Stimulants/narcotics/P2-Agonists/p-Receptor Blocking Agents... 

RNHCH.CH(OHlCH— R R P Adrenergic receptor blocking agents 473... 

Communication with the profession was at first maintained by continuing (until January 1985) the Adverse Reaction Series leaflets started by CSD, and later by a regularly published bulletin on Current Problems . The first issue of Current Problems in September 1975 led with the adverse oculo-cutaneous effects and sclerosing peritonitis associated with p-adrenergic receptor blocking agents and also included items on loss of consciousness associated with prazosin and on the risks of anti-inflammatory agents and asthma. 

The cardiovascular response to dopamine in humans depends on the concentration infused. Low rates of dopamine infusion can produce vasodilation in the renal, mesenteric, coronary, and intercerebral vascular beds with little effect on other blood vessels or on the heart. The vasodilation produced by dopamine is not antagonized by the p-adrenoceptor blocking agent propranolol but is antagonized by haloperidol and other dopamine receptor-blocking agents. 

The actions of p-blockers on blood pressure are complex. After acute administration, blood pressure is only slightly altered. This is because of the compensatory reflex increase in peripheral vascular resistance that results from a (3-blocker-induced decrease in cardiac output. Vasoconstriction is mediated by a-receptors, and a-receptors are not antagonized by (3-receptor blocking agents. Chronic administration of (3-blockers, however, results in a reduction of blood pressure, and this is the reason for their use in primary hypertension (see Chapter 20). The mechanism of this effect is not well understood, but it may include such actions as a reduction in renin release, antagonism of (3-receptors in the central nervous system, or antagonism of presynaptic facilita-tory (3-receptors on sympathetic nerves. 

Suzman, M.M. Use of p-adrenergic receptor blocking agents in psychiatry. In Palmer,... 

The p-adrenergic blocking agents suppress the activation of the heart by blocking [It receptors (see p. 73). They also reduce the work of the heart by decreasing cardiac output and causing a slight decrease in blood pressure. Propranolol (see p. 74) is the prototype of this class of compounds, but other (3-blockers, such as metoprolol and atenolol are... 

Clinical reports - Organic nitrates and the p-adrenergic receptor blocking agents constitute the mainstay of therapy.54-58 The mechanism of action of nitroglycerin remains uncertain. Although recent evidence tends to underline its peripheral vascular activity,5 >55 several studies have also implicated a direct coronary artery or collateral response.43 46,52, 59>60 Clinical data generally support the hypothesis that primary coronary vasodilators are of limited value in this disease since vessels in ischemic areas are already dilated. -2 However, beneficial results have been reported in patients with the vasodilators chromonar (22)° and lidoflazine (j ).62 6 ... 

Answer D. The effectiveness of labetalol in the management of hypertension and in severe hypertensive states appears to be due to a combination of antagonistic actions at both alpha and beta adrenoceptors. Labetalol is not a P selective blocking agent (unlike atenolol and metoprolol), and (unlike pindolol and acebutolol) it lacks intrinsic sympathomimetic activity. Labetalol is available for both peroral and parenteral use unfortunately, it blocks p2 receptors in bronchiolar smooth muscle. 

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