By J. X. Thomas Jr. Ph.D., M. W. Gerdisch (auth.), Gerd Heusch, John Ross Jr. (eds.)
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Schomig and G. Richardt 77. Malliani A, Schwartz PJ, Zanchetti A (1980) Neural mechanisms in life-threatening arrhythmias. Am Heart J 100: 705-715 78. Martins JB, Kerber RE, Marcus ML, Laughlin DL, Levy DM (1980) Inhibition of adrenergic neurotransmission in ischaemic regions of the canine left ventricle. Cardiovasc Res 14: 116-124 79. McGrath BP, Lim SP, Leversha L, Shanahan A (1981) Myocardial and peripheral catecholamine responses to acute coronary artery constriction before and after propranolol treatment in the anaesthetised dog.
J Mol Cell Cardiol 20: 75-82 141. Verrier RL, Thompson PL, Lown B (1974) Ventricular vulnerability during sympathetic stimulation: role of heart rate and blood pressure. Cardiovasc Res 8: 602-610 142. Videbaek J, Christensen NJ, Sterndorff B (1972) Serial determination of plasma catecholamines in myocardial infarction. Circulation 46: 846-855 143. Vigue P, Frelin C, Cragoe Jr EJ, Lazdunski M (1983) Ethylisopropylamiloride: A new and highly potent derivative of amiloride for the inhibition of the Na +/H+ exchange system in various cell types.
This seminal contribution has subsequently led to a plethora of studies dealing with the development of specific agents which block these receptors, and to more recent findings indicating that there are additional subclasses for both the IX- and p-adrenergic receptor [51, 79]. More recently, IX- and p-adrenergic receptor subtypes have been cloned and their structures within membranes have been proposed based on hydrophobic exclusion studies [14, 40, 41, 61]. Results over the last decade have also indicated that these adrenergic receptor subtypes can exist in a variety of different states and can be cycled intracellulariy, leading to both sensitization and desensitization of the receptor .
Adrenergic Mechanisms in Myocardial Ischemia by J. X. Thomas Jr. Ph.D., M. W. Gerdisch (auth.), Gerd Heusch, John Ross Jr. (eds.)