Topic
Rauwolfia alkaloid
About: Rauwolfia alkaloid is a research topic. Over the lifetime, 290 publications have been published within this topic receiving 4998 citations.
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01 Jan 1977
TL;DR: Since there is an overall shortage of Rauwolfia drugs, increasing use is being made of the serpentine reduction method, and in roots of the fast growing Catharanthus roseus low amounts of ajmalicine, but relatively large amounts of serpentine are produced.
Abstract: The Rauwolfia alkaloid, ajmalicine, has been found to have broad application in the treatment of circulatory diseases, especially in the relief of obstruction of normal cerebral blood flow. In combination with other Rauwolfia alkaloids it has been used to lower high blood pressure. Annually an estimated 3500 kg of ajmalicine are isolated from natural sources, by pharmaceutical industries worldwide, for therapeutic use in the treatment of these diseases. To date, ajmalicine has been found to occur as a natural product in 20 species of the genus Rauwolfia, four of Catharanthus, two of Mitragyne and in Paus-inystalia yohirribe, and Stemmadenia obovata (13). For industrial purposes ajmalicine is extracted from dried Rauwolfia roots. However, it can also be prepared from the alkaloid serpentine by reduction with BH- 4. Since there is an overall shortage of Rauwolfia drugs, increasing use is being made of the serpentine reduction method. In roots of the fast growing Catharanthus roseus low amounts of ajmalicine, but relatively large amounts of serpentine are produced. This latter compound is first isolated then converted to ajmalicine. The biosynthesis of ajmalicine and serpentine has been clarified by isotope incorporation studies using differentiated plants of C. roseus (11, 4, 24). The biosynthetic sequence is shown in Figure 1 and involves the condensation of tryptamine with the iridoid glycoside, secologanin to give vincoside (19) which is subsequently, in several unknown steps, transformed to ajmalicine and finally oxidized to serpentine.
354 citations
01 Jan 1966
TL;DR: The aim of the present Chapter is to review and discuss the pertinent literature dealing with fundamental problems of Rauwolfia alkaloids and benzoquinolizines rather than to review in detail the enormous literature on the pharmacology of these agents.
Abstract: In 1955 Shore, Brodie and coworkers (Shore, Silver and Brodie 1955, Pletscher, Shore and Brodie 1955) discovered that reserpine caused a marked decrease in the concentration of 5-hydroxytryptamine (5-HT) in tissues and a concomitant rise in the urinary excretion of the 5-HT metabolite 5-hydroxyindoleacetic acid. The deep physiological significance of this discovery became even more evident when reserpine soon afterwards was found to affect tissue catecholamines in a similar manner, an effect leading to block of adrenergic transmission mechanisms (Carlsson and Hillarp 1956a, Bertler, Carlsson and Rosengren 1956). Since then numerous papers have appeared, in which the effects of Rauwolfia alkaloids and a group of similarly acting benzoquinolizines (Pletscher, Besendorf and Bachtold 1958) have been further analyzed. Particular interest has been focussed on the mechanism of action on the abovementioned amines and on the relationship between this action and the various pharmacological effects of Rauwolfia alkaloids and benzoquinolizines. It is the aim of the present Chapter to review and discuss the pertinent literature dealing with these fundamental problems rather than to review in detail the enormous literature on the pharmacology of these agents.
318 citations
TL;DR: It has been demonstrated that after the parenteral administration of relatively large doses of this drug, postganglionic sympathetic nerves are no longer able to transmit impulses across the neuroeffector junctions.
Abstract: THE rauwolfia alkaloids have been widely used in clinical practice, but relatively little information concerning the mechanism of their circulatory action in man is available. Reserpine has been extensively studied in laboratory animals, and it has been demonstrated that after the parenteral administration of relatively large doses of this drug, postganglionic sympathetic nerves are no longer able to transmit impulses across the neuroeffector junctions.1 Also, in animals, a profound fall in the concentration of norepinephrine, epinephrine and serotonin throughout the body occurs after reserpine administration,2 3 4 and the sympathetic blockade produced by reserpine in laboratory animals has been attributed to the . . .
266 citations
178 citations
Journal Article•
TL;DR: A large dose of reserpine or a prolonged cold-exposure decreased the content of ACTH in the pituitary to such an extent that the animals could not respond to an additional pituitsary stimulus.
Abstract: The effects of reserpine and cold-exposure have been compared on various indices of pituitary adrenal stimulation in rats: adrenal ascorbic acid, plasma corticosterone and FFA, and liver TPO. Both reserpineand cold-exposure elicita marked hypersecretion of ACTH. Of a number of Rauwolfia alkaloids, however, only those compounds which lowered brain stores of norepinephrine and serotonin and produced sedation, also evoked ACTH hypersecretion. A large dose of reserpine or a prolonged cold-exposure decreased the content of ACTH in the pituitary to suchan extent that the animals could not respond to an additional pituitary stimulus.
161 citations