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Recently, it has been recognized that 19-hydroxyandrostenedione (19-OH-AD), one of the C19 steroids, acts to amplify the mineralocorticoid activity and to elevate blood pressure. However, there is no detailed report about the pressor mechanism and the effects on several humoral depressor factors, i.e., kallikrein, kinin and prostaglandins etc. Therefore, we studied the differences in the pressor mechanisms and the changes in urinary prostaglandin E (PGE) and kinin excretions among deoxycorticosterone acetate (DOCA)-salt hypertension, 19-OH-AD induced hypertension, and testosterone induced hypertension. In this study, DOCA, 19-OH-AD and testosterone were administered subcutaneously to castrated male rats (Wistar rats, 12 weeks) at a dose of 10 mg/body/week for the first 6 weeks. Then the doses were increased to 30 mg/body/week for the next 5 weeks. These experiments were done in metabolic cages. It was found that 19-OH-AD induced hypertension earlier than DOCA and testosterone. However, 19-OH-AD and testosterone had no effect on the levels of urinary kinin and PGE excretions, while DOCA significantly increased urinary kinin and PGE excretions immediately after the onset of hypertension. Furthermore, DOCA increased the urinary Na/K ratio, while 19-OH-AD and testosterone did not change the ratio. It is suggested that 19-OH-AD might induce the pressor action due to the changes in the vascular reactivity rather than the mineralocorticoid activity.

A Comparative Study of C19 Steroid-Induced Hypertension and Deoxycorticosterone Acetate (DOCA)-Salt Hypertension