Clinical Experiences With Reserpine (Serpasil) in Hypertension

Abstract

1 We are indebted to Elva Hiscock, B.S., for the careful dietary management and handling of patients.The root of the plant, Rauwotfia serpentina, has been mentioned in the literature of India for centuries as a useful agent in the treatment of anxiety and hyperactive mental states. Although its use in the treatment of hypertension was first described in 1933 (1), it received little attention in the American literature until very recently. Attempts to isolate the active principle from crude Rauwol~a serpentina began at the end of the last century, but the first crystalline alkaloid was not isolated until 1931 (2). Today, some 14 substances have been extracted from the crude plant. Most of these have proved to be pharmacologically inert. In 1952, however, Muller, Schlittler, and Bein (3) isolated an active alkaloid from the plant which they named reserpine. Reserpine possesses both the sedative and hypotensive properties of the whole root and is believed to be the principal active component (4). PHARMACOLOGYThe pharmacology of reserpine has been rather extensively studied. It has been found to have a unique sedative effect, inasmuch as a dosage many times greater than the effective sedative dosage does not produce narcosis (5). Reserpine does not produce the electroencephalographic changes characteristic of barbiturate administration, thus indicating that the sites of action are different for these two drugs (6). Again, in contrast to the barbiturates, reserpine lowers the convulsive threshold in animals subjected to electroshock (7). With acute intravenous administration of reserpine, sedation occurs before any hypotensive effect is observed (8). Furthermore, no correlation has been noted between the degrees of sedative and hypotensive response. It would, therefore, seem that these two effects of reserpine are distinct from each other.With regard to its hypotensive effect, a mass of evidence has been accumulated which indicates that reserpine's site of action is central rather than peripheral. Experimentally, it suppresses hypertension resulting from stimulation of afferent fibers of the vagus and sciatic nerves and from pressure changes in the carotid sinus (5). The absence of any marked postural hypotension following reserpine administration suggests that it produces no ganglionic blockade (4,9). The possibility of a peripheral site of action is precluded by the absence of sig-