By H. Jick (auth.), E. Grundmann (eds.)
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The development of de- 46 pendence and the appearance of withdrawal symptoms can be explained often on the basis of modified post-synaptic sensitivity not adequately compensated by pre-synaptic sensitivity. The recent discovery of enkephalin receptors on catecholaminergic nerve endings in the CNS may greatly contribute to an improved understanding of the mechanisms involved in the manifestations of the narcotic abstinence syndrome. Schwartz and associates (1978) have proposed that tolerance and dependence to opi ate drugs develop as a consequence of post-synaptic super sensitivity secondary to presynaptic inhibition of transmitter (including catecholamines) release in different area of the brain.
Y) Disease In view of the crucial role of the liver in drug disposition, the rate of drug metabolism could be expected to be impaired in patients with hepatic disease. The reasons for this are at least twofold: 1. hepatocellular disease can result in reduced drug-metabolizing enzyme activity and 2. disruption of the normal vascular architecture of the organ may decrease the availability of the drug at the metabolic sites. A number of studies have confirmed that drug metabolism is impaired in patients with various types of liver disease.
Interactions among drugs which act primarily on the autonomic nervous system are well known and include blockade of the /3-agonist effects of adrenaline by propranolol, or of the a-agonist effects of noradrenaline by phenoxybenzamine. Less well recognized is the possibility that similar interactions occur with drugs which produce secondary phannacological effects on the same system. Phenothiazine drugs and tricyclic antidepressants, for example, possess significant a-adrenergic blocking properties and may enhance the activity of other a-blockers used in combination.