Drug-Receptor Interactions

Drug Receptor:  any functional macromolecule in a cell to which a drug binds to produce its effects.  at receptors, drugs mimic or block the action of the body's own regulatory molecules.  

Receptors and Selectivity of Drug Action : If a drug interacts with only one kind of receptor, and if that receptor regulates just a few processes, then the effects of the drug will be limited.

Even though a drug is selective for one type of receptor, it can still produce a variety of effects.

Selectivity does not guarantee safety.

Theories of Drug-Receptor Interaction

- Simple Occupancy Theory:  Two factors - The intensity of the response to a drug is proportional to the number of receptors occupied by that drug, and the maximal response will occur when all available receptors have been occupied.

- Modified Occupancy Theory:  Assumes that all drugs acting at a particular receptor are identical with respect to the ability to bind to the receptor and the ability to influence receptor function once binding has taken place.

•    Affinity:  The strength of the attraction between a drug and its receptor.  Affinity is reflected in potency.  (Drugs with high affinity are very potent).

•    Intrinsic Activity:  The ability of a drug to activate a receptor following binding.  Reflected in the maximal efficacy (drugs with high intrinsic activity have high maximal efficacy).

Calcium Channel Blocking Agents 

• Act on contractile and conductive tissues of the heart and on vascular smooth muscles 
• Prevent movement of extracellular calcium into the cell 
– Coronary and peripheral arteries dilate
– Myocardial contractility decreases 
– Depress conduction system

Therapeutic Actions
• Inhibit movement of calcium ions across the membranes of myocardial and arterial muscle cells. Altering the action potential and blocking muscle cell contraction 
• Depress myocardial contractility 
• Slow cardiac impulse formation in the conductive tissues 
• Cause a fall in BP 
 

Neurolept Anesthesia
An antipsychotic agent such as droperidol plus an opiate analgesic agent such as fentanyl or sufentanil. This latter agent is approximately eight to ten times more potent than fentanyl.

Diclofenac

Short half life (1‐2 hrs), high 1stpass metab.,  accumulates in synovial fluid after oral admn., reduce inflammation, such as in arthritis or acute injury

Mechanism of action

inhibition of prostaglandin synthesis by inhibition of cyclooxygenase (COX). There is some evidence that diclofenac inhibits the lipooxygenase pathways, thus reducing formation of the

leukotrienes (also pro-inflammatory autacoids). There is also speculation that diclofenac may inhibit phospholipase A2 as part of its mechanism of action. These additional actions may explain the high potency of diclofenac - it is the most potent NSAID on a molar basis.

Inhibition of COX also decreases prostaglandins in the epithelium of the stomach, making it more sensitive to corrosion by gastric acid. This is also the main side effect of diclofenac and other drugs that are not selective for the COX2-isoenzyme.

Oxytetracycline

Treats Oxytetracycline is a medicine used for treating a wide range of infections including infections of the lungs, urinary system, skin and eyes. It may also be used to treat sexually transmitted infections, infections caused by lice, rickettsial infections, cholera and plague. It is very occasionally used to treat leptospirosis, gas gangrene, and tetanus.

Neomycin

used as a topical preparation

Neomycin is not absorbed from the gastrointestinal tract, and has been used as a preventative measure for hepatic encephalopathy and hypercholesterolemia. By killing bacteria in the intestinal tract, it keeps ammonia levels low and prevents hepatic encephalopathy, especially prior to GI surgery. It is not given intravenously, as neomycin is extremely nephrotoxic (it causes kidney damage), especially compared to other aminoglycosides.