Introduction

Pharmacology can be defined as the study of chemicals (drugs), which can influence and, by this means, change the activity of living structures, i.e. the cells of the body. Consider three types of cell: (i) a typical human cell, (ii) a bacterial cell (as a representative of micro-organisms which may cause disease in humans) and (iii) a tumour cell (see Fig. 4.1). Drugs have been designed to influence each of these cells.

Fig. 4.1 • Basic cell types: (i) a typical human cell; (ii) a bacterial cell; (iii) a tumour cell

Drugs can manipulate the multitude of biochemical reactions which underpin the very life of cells. In the human cell we aim to use drugs to alter particular aspects of cell function to, in turn, improve the activity of body systems and thereby achieve the desired change in body health status. In the bacterial cell the aim of drugs is to kill the cell or at least disable it, in order to facilitate its destruction by our immune system. In this case we design drugs which are essentially damaging. They disrupt a process in the bacterial cell which is not found in human cells, e.g. the wall of a bacterial cell can be targeted. In this way we can damage the bacterial cells while leaving our own cells, in theory, undisturbed. In other words we aim for selective toxicity which, hopefully, minimises the side effects for us. Lastly, in the tumour cell, we can use drugs to target a crucial characteristic of this large, and somewhat metabolically greedy cell; its rapid rate of cell division. Drugs designed to inhibit the process of mitosis can be employed to reduce tumour growth. Unfortunately body cells, which are also normally dividing, are vulnerable, e.g. those lining the gut or hair root cells. In this situation selective toxicity is more difficult to attain.

Pharmacodynamics and pharmacokinetics

Pharmacology can be sub-divided into two topics of interest; firstly how drugs interact with our body cells – Pharmacodynamics – and, secondly, the factors we should consider when we want to find the best route of administration of a drug, how it is carried around the body, metabolised and then excreted – Pharmacokinetics.

We shall begin by considering pharmacodynamics and reconsider the structure of our human cell in order to describe more clearly the targets of drug action.

Our cells can be likened to highly organised factories contained within a barrier, the cell membrane. The internal organelles house the biochemical processes of the cell orchestrated by complex arrays of enzymes. Figure 4.2 shows a diagrammatic view of a human cell and the various targets of drug action detailed below.

Fig. 4.2 • Diagrammatic representation of the human cell and drug targets

The first potential cell target we will describe for drugs are the cell enzymes (labelled A on Fig. 4.2). It is possible for a drug to inhibit these biological catalysts to bring about a change in cell activity. For example, the liver cells of the body contain an enzyme responsible for the production of cholesterol. By inhibiting the enzyme in this cell using the statin drugs, less cholesterol is produced, the build up of cholesterol in blood vessels is reduced and the benefit for the individual is reduced cardiovascular disease risk.

Other drugs which influence enzymes in the body are aspirin and the ACE inhibitors – you may have heard of the latter in the context of the renal system and regulation of blood pressure.

You will also recall the role of the cell membrane. It acts as a selective barrier controlling what can and cannot enter the cell. Drugs can act on the cell membrane in several ways; firstly, by acting on structures within the membrane important to the passage of material in and out of the cell and, secondly, on structures called receptors.

In the first group we can include carriers (sometimes referred to as transporters) and ion channels. Carriers are often protein structures which the cell uses to transport material into the cell. Drugs can be used to block the activity of these structures, i.e. the compound is not taken into the cell (see Fig. 4.2

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