A wide range of medications have been found to be associated with xerostomia, the subjective symptom of dry mouth. The assessment of medication-induced xerostomia (MIX) is usually made through a subject's responses to relevant questions or the use of visual analogue scales whereby the subject is asked to rate the severity of their oral dryness. It is uncertain how much MIX is accompanied or can be ascribed to medication-induced salivary gland hypofunction and reduced secretion of saliva. MIX in older age groups is associated with the number of medications being taken and is higher than seen in the younger subjects. Many medications cause xerostomia as a side effect, but some of these, for example, selective serotonin reuptake inhibitors, do not appear to cause salivary gland hypofunction. However, there have been relatively few studies assessing objective changes in salivary fl ow in response to medications. The salivary refl ex has peripheral and central components which can be the targets of medications, leading to interruption of the refl ex and medication-induced salivary gland dysfunction (MISGD) characterized by reduced production of saliva. The principal peripheral target is the cholinergic muscarinic (M3) receptor of salivary gland acinar cells which is blocked by antimuscarinic drugs used in the treatment of, for example, irritable bladder and chronic obstructive pulmonary disease. Tricyclic antidepressants not only have targets in the central nervous system but interact with and block muscarinic receptors in the periphery. Sympathetic nervemediated stimuli enhance salivary secretion, and there is no peripheral inhibition. Although adrenergic antagonists cause MIX, there is no evidence that they reduce salivary secretion. However, antihypertensive β-adrenoceptor blockers