Beta Antagonists

Relative extraction efficiencies of polar polymeric neutral, cation, and anion exchange sorbents (HLB, MCX, and MAX) for 11 beta antagonists and 6 beta agonists in human whole blood were probed.109 Initial characterization of MCX and MAX for acidic and basic load conditions, respectively, showed that both the agonists and antagonists were well retained on MCX, while they were recovered from MAX in the wash with either methanol or 2% ammonia in methanol (see Table 1.6). Blood samples were treated with ethanol containing 10% zinc sulfate to precipitate proteins and the supernatants loaded in 2% aqueous ammonium hydroxide onto the sorbents. After a 30% methanol and 2% aqueous ammonia wash, the analytes were eluted with methanol (HLB), 2% ammonia in methanol (MCX), or 2% formic acid in methanol (MAX). The best recoveries were observed with MCX under aqueous conditions or blood supernatant (after protein precipitation) spiked sample load conditions (see Table 1.7). Ion suppression studies by post-column infusion showed no suppression for propranolol and terbutaline with MCX, while HLB and MAX exhibited suppression (see Figure 1.6). 

Bompart et al. [125] reported the synthesis of composite nanoparticles of approximately 500 nm diameter consisting of a polymer core, a layer of gold nanoparticles attached to the core, and a few nanometers thick MIP outer layer (Fig. 13). These particles were used as individually addressable nanosensors, where surface-enhanced Raman spectroscopy was used to detect the binding of the target analyte, the beta-antagonist propranolol. A l,000x improved detection limit was... 

The general clinical applications of alpha and beta antagonists are presented below. Specific agents within each major group are also discussed. 

Beta antagonists are generally administered for their effect on the beta-1 receptors that are located on the heart.31 When stimulated, these receptors mediate an increase in cardiac contractility and rate of contraction. By blocking these receptors, beta antagonists reduce the rate and force of myocardial contractions. Consequently, beta antagonists are frequently used to decrease cardiac workload in conditions such as hypertension and certain types of angina pectoris. Beta blockers may also be used to normalize heart rate in certain forms of cardiac arrhythmias. Specific clinical applications of individual beta blockers are summarized in Table 20-2. 

Clinically useful beta antagonists are classified as beta-l-selective if they predominantly affect the beta-1 subtype they are classified as beta-nonselective if they have a fairly equal affinity for beta-1 and beta-2 receptors (see Table 20-2). Beta-l-selective drugs are also referred to as cardioselective because of their preferential effect on the myocardium. Even if a beta antagonist is nonselective (i.e., blocks both beta-1 and beta-2 receptors), the beta-1 blockade is clinically beneficial. When stimulated, beta-2 receptors, which... 

When nonselective beta blockers are used, some antagonism of beta-2 receptors also occurs.2,31 The antagonism of beta-2 receptors on bronchiole smooth muscle often leads to some degree of bronchoconstric-tion and an increase in airway resistance. Although this event is usually not a problem in individuals with normal pulmonary function, patients with respiratory problems such as asthma, bronchitis, and emphysema may be adversely affected by nonselective beta antagonists. In these patients, one of the beta-1-selective drugs should be administered. 

Beta blockers that bind to both beta-1 and beta-2 receptors (nonselective agents, see Table 20-2) may induce bronchoconstriction in patients with asthma or similar respiratory problems. These patients should be given one of the more cardioselective beta antagonists, such as atenolol (Tenormin) or metoprolol (Lopressor, others). Beta blockers may also produce excessive cardiac depression in individuals with certain types of cardiac disease. Beta blockers are generally well tolerated in most patients, however, and major problems are infrequent. 

Beta antagonists are effective in the treatment of both supraventricular and ventricular arrhythmias (see Chapter 14 Agents Used in Cardiac Arrhythmias). It has been suggested that the improved... 

Libretto SE (1994) A review of the toxicology of salbutamol (albuterol). Archives of Toxicology 68(4) 213-216. Spangler DL (1989) Review of side effects associated with beta antagonists. Annals of Allergy 62 59-62. 

O Keeffe MJ, O Keeffe M, Glennon JD. Supercritical fluid extraction (SFE) as a multi-residue procedure for beta-antagonists in bovine liver tissue. Analyst 1999 124 1355-1360. 

FIGURE 43 Stimulation of die dopamine receptors in renal and mesenteric arteries causes vasodilation, which is not blocked by propranolol (beta antagonist) but is blocked by a dopamine-receptor-blocking agent such as chlorpromazine. 

Hypotension, heart block, heart failure, bronchospasm, nausea, scalp tingling, paradoxical pressor response may not be effective in patients receiving alpha- or beta-antagonists... 

As for nearly all beta antagonists, the main cardiovascular indications for pindolol are hypertension, angina pectoris, and arrhythmias. The usual warnings and precautions for beta antagonists also apply to pindolol (see also Figure 69). 

These partial agonist drugs (e.g., pindolol, acebutolol. carteolol, celiprolol, and penbu-tolol), like the beta antagonists, are useful in the therapy of hypertension and angina. They do, however, tend to cause less bradycardia and lipid abnormalities than do beta antagonist drugs. 

Esmolol is a beta antagonist with a short half-life. Thus, it is most useful in the therapy of acute arrhythmias, and as an adjunct to surgical procedures. 

Pindolol is a beta antagonist with high membrane-stabilizing (local anesthetic) activity Timolol lacks the local anesthetic effects of propranolol... 

I. Pharmacology. Labetalol is a mixed alpha- and beta-adrenergic antagonist after intravenous administration, the nonselective beta-antagonist properties are approximately sevenfold greater than the alpha-1 antagonist activity. Hemodynamic effects generally include decreases in heart rate, blood pressure, and systemic vascular resistance. Atrioventricular conduction velocity may be decreased. After intravenous injection, hypotensive effects are maximal within 10-15 minutes and persist about 2-4 hours. The dmg is eliminated by hepatic metabolism and has a half-life of 5-6 hours. 

Asthma (25) Long acting agents for patients with frequent use of short acting beta antagonists Chronic Medication Underuse... 

Dumasia, M.C., and Houghton, E. (1991) Screening and confirmatory analysis of beta-agonists, beta-antagonists and their metabolites in horse urine by capillary gas chromatography-mass spectrometry. Journal of Chromatography, 564,503-513. 

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