The use of drugs, in the cardiovascular field, which inhibit adrenergic .beta.-receptors has increased. Pronethanol, the initial drug used, was limited by unpleasant side effects. Propranolol was more effective and less toxic than pronethanol but also inhibited .beta.-receptors in the respiratory tract and in peripheral circulation. Practolol, was more specific for .beta.-receptors in the cardiac region. No subacute chronic effects for practolol were noticed in animals. Certain adverse effects were attributed to practolol: exfoliative dermatitis; micropopular, eczematous or urticerial reactions; psoriosiform and lichenoid skin eruptions; damage to the conjunctiva possibly leading to severe vision impairment; reduction in tear flow followed by corneal changes; and sclerosing peritonitis. Lymphocyte function may be capable of alteration by drugs which have receptor blocking functions and possibly practolol is capable of suppressing T[thymus-derived]-cell subpopulations which control the emergence of B [bone-marrow derived] lymphocytes with autoimmune propensities. Immunological mechanisms are probably involved in the practolol syndrome. It is not clear how this might be mediated. There is only limited evidence that these patients have become immunologically sensitized to practolol. Practolol may have a direct pharmacological effect on the control of the immune response possibly affecting T-lymphocytes control of B-lymphocytes with the ability to produce autoantibodies. The mechanism of the psorioriform eruption may be due to .beta. blockade reducing epidermal cyclic AMP leading to cell division.