The ophthalmologist has to be alert to the possibility of interaction between his therapy, be it topical or systemic, and the drugs which the patient may be receiving for other conditions. Adverse ocular reactions due to systemic drug therapy will be discussed together in a future volume; much of this information is, however, currently to be found in the various chapters of Meyler’s Side Effects of Drugs.

The mechanism of the hypotensive effect during beta-adrenergic blockade in hypertension was studied in 50 patients with renal or essential hypertension using the new cardioselective beta blocker, Tenormin. A subsequent follow-up on an outpatient basis of 25 of the patients showed that when the active generic was replaced by a placebo blood pressure rose again, confirming that the initial fall in arterial hypertension was a genuine effect. The autonomic nervous system is divided into the parasympathetic and sympathetic systems, with three types of adrenergic receptors: alpha (smooth muscle contraction), beta1 (cardiac acceleration and fatty acid mobilization) and beta2 (smooth muscle relaxation). Substances affecting the function of the adrenergic system are the agonists or stimulators, which mimic the effects of endogenous norepinephrine or epinephrine, and antagonists or blockers, which block the receptors and prevent stimulation by the agonists. Autonomic stimulation in the eye mediates various changes which apparently affect outflow facility and rate of formation of aqueous humor. Alteration of either or both of these factors by autonomic agonists or antagonists may have a direct or an indirect effect on intraocular pressure. Beta-adrenergic blocking substances have been used to treat a variety of diseases. Some of the effects of these generics are attributable to properties other than beta blockade, such as intrinsic sympathomimetic activity and local anaesthetic activity. Side effects of this class of generic drugs require caution in cases of congestive heart failure and in asthmatics. Autonomic agents used in the cure of ocular hypertension and glaucoma include pilocarpine, a cholinergic agonist, epinephrine, an adrenergic agonist, and various beta adrenergic blockers or antagonists including propranolol, atenolol and timolol. The physico-chemical properties and pharmacokinetics of timolol are reviewed. Data showing a significant reduction in intraocular pressure as a result of ocular instillation of timolol are presented. Reduction of the rate of aqueous formation appears to be the mechanism of action. A low incidence of non-serious side effects is reported.

The pathogenesis of migraine is not completely understood but may involve vasodilation of cerebral blood vessels and/or the release of vasoactive neuropeptides (ie, norepinephrine) from the perivascular axons in the dura mater after activation of the trigeminovascular system. Many environmental factors and physiologic influences may provoke a migraine or increase its severity. The typical migraine headache without aura is unilateral, pulsating, of moderate-to-severe intensity, and aggravated by physical activity. Migraine prevention is best achieved by avoidance of known migraine triggers or enhancers and by reducing the amount of lifestyle stressors. Pharmacotherapeutic options in the cure of migraine are discussed herein.

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