19-hydroxy-4-androstene-3-17-dione has been researched along with Body-Weight* in 2 studies
2 other study(ies) available for 19-hydroxy-4-androstene-3-17-dione and Body-Weight
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[A comparative study of C19 steroid-induced hypertension and deoxycorticosterone acetate (DOCA)-salt hypertension].
In order to evaluate the hypertensinogenic action of 19-hydroxyandrostenedione (19-OH-AD), which has been reported to be an amplifier of mineralocorticoid, the changes in several humoral factors were observed in 19-OH-AD treated rats as compared to those in DOCA hypertensive rats. Twenty-five male Wistar rats were castrated at 11 weeks of age, and the experiments were begun at 12 weeks of age. The rats were divided into 3 groups. The control group (n = 8) was given an s.c. injection of 0.2 ml of sesame oil. The 19-OH-AD group (n = 10) was injected s.c. with 10 mg of 19-OH-AD dissolved in 0.2 ml of sesame oil, and the DOCA group (n = 8) was injected s.c. with 10 mg of DOCA dissolved in 0.2 ml of sesame oil three time weekly. The urine was collected for a period of 24 hours, and the urine volume, and urinary excretions of electrolytes, prostaglandin E2 (PGE2), kinin and catecholamine were measured before and after the start of the experiment. The systolic blood pressure (S.B.P.) was measured by the tail-cuff method. The S.B.P. values before and at 9 weeks after the start of the experiments were 136.7 +/- 3.8 and 156.0 +/- 2.6 mmHg in the 19-OH-AD group, and 140.6 +/- 5.6 and 179.3 +/- 5.5 mmHg in the DOCA group, respectively. Body weight, which was elevated in both groups, was higher in the 19-OH-AD group than in the DOCA group. Water intake and urine volume were significantly (p less than 0.001) increased only in the DOCA group. The urinary Na/K ratio was significantly (p less than 0.001) elevated in the DOCA group as compared to that in the other two groups. However, there was no significant difference in urinary Na/K ratio between the control and 19-OH-AD groups. The urinary PGE2 and kinin excretions were significantly (p less than 0.01) increased in the DOCA group but did not change appreciably in the 19-OH-AD group. The urinary catecholamine excretion was significantly increased in the DOCA group. However, there were no differences in the catecholamine excretion between the control and 19-OH-AD groups.(ABSTRACT TRUNCATED AT 400 WORDS) Topics: Androstenedione; Animals; Blood Pressure; Body Weight; Desoxycorticosterone; Dinoprostone; Dopamine; Drinking; Epinephrine; Kinins; Male; Norepinephrine; Potassium; Rats; Rats, Inbred Strains; Sodium; Stimulation, Chemical | 1990 |
[A comparative study of C19 steroid-induced hypertension and deoxycorticosterone acetate (DOCA)-salt hypertension].
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. Topics: Androstenedione; Animals; Blood Pressure; Body Weight; Castration; Desoxycorticosterone; Drinking; Hypertension; Kinins; Male; Potassium; Prostaglandins E; Rats; Rats, Inbred Strains; Sodium; Sodium Chloride; Testosterone | 1984 |