The amino group of the adrenergic drug can be substituted with a bulkier amino substituents to enhance beta activity. OH groups can also be added to positions 3 and 5 of the benzene ring of the drug to cause beta 2 selectivity.
It can have one less OH group than catecholamines. The new structure will not be recognised by metabolic enzymes so the drug will not be degraded by COMT.
Although these drugs are structurally similar to amphetamine, they cause less sensation of stimulation, and are less suited for use in conditions characterized by lack of adrenergic stimulation.
Antiadrenergic drugs decrease or block effects of sympathetic nerve stimulation, endogenous catecholamines (e.g. epinephrine), and adrenergic drugs.
The most common side effects of adrenergic amines are nervousness, agitation, and wakefulness
increase bp and heart rate
Tsuneyoshi Tanabe has written: 'Cardiac glycosides and adrenergic activity' -- subject(s): Physiological effect, Drugs, Adrenergic mechanisms, Glucosides, Heart
This is done through several mechanisms: - Stimulating noradrenaline to be released - Mimicking noradrenaline's action on the receptors -Preventing noradrenaline to be broken down and reuptaken
Alpha1-adrenergic blockers are drugs that work by blocking the alpha1-receptors of vascular smooth muscle, thus preventing the uptake of catecholamines by the smooth muscle cells.
Drugs that decrease ADH levels include alcohol, beta-adrenergic agents, morphine antagonists, and phenytoin (Dilantin).
They work on the eye the same way as the nasal decongestants. A-adrenergic receptors are stimulated on small arterioles in the eye and conjuctival congestion is temporarily relieved through arteriolar vasoconstriction.
Selective breeding
Since the alkyl substituent is made bulkier, the beta activity of the drug will be enhanced.