The central nervous effects of Mitragyna africanus (Willd) stembark extract in rats.

The acute toxicity and the central effects of Mitragyna africanus (M. africanus) stembark methanol extract were studied in rats. The extract did not produce any death in the treated rats even at the highest dose (6400 mg kg(-1)) used. It produced depressant effects on the central nervous system. The stembark extract potentiated amylobarbitone sleeping time in rats dose-dependently, induced sleep in rats and also produced significant local anaesthetic effect on rabbits, the effects being comparable to that of xylocaine. The extract protected rats treated with a convulsive dose of strychnine (2 mg kg(-1)) and increased the period of onset of convulsions and decreased the number of spasms.

Failure of verapamil and diltiazem to attenuate the pressor response to hypothalamic stimulation: a possible mechanism.

The effects of verapamil or diltiazem on pressor responses to posterior hypothalamic stimulation, injected noradrenaline or tyramine were studied in urethane-anaesthetized normotensive, deoxycorticosterone acetate (DOCA), renal and spontaneously hypertensive rats at the early and established phases of hypertension. Pressor responses to the pressor stimuli were significantly enhanced in the early and established phases of hypertension when compared with the normotensives. While the magnitude of pressor responses in the established phase of renal or spontaneously hypertensive rats was significantly higher (P less than 0.05) than the corresponding value in the early phase, in contrast, the pressor response in the early phase of DOCA hypertension was significantly higher than that of the established phase. Verapamil or diltiazem significantly (P less than 0.005) inhibited pressor responses to injected noradrenaline or tyramine in all groups of rats but not that to hypothalamic stimulation, irrespective of the stage of hypertension. When the probable mechanism of the hypothalamic pressor response's resistance to the calcium antagonists was studied in-vitro, ATP significantly (P less than 0.005) inhibited the relaxant effect of the calcium antagonists in the rat aortic strips. Our data indicate that verapamil or diltiazem is ineffective in inhibiting the pressor response to posterior hypothalamic stimulation. The probable mechanism of the resistance and the clinical implication of the findings are discussed.

Anticonceptive and estrogenic effects of a seed extract of Ricinus communis var. minor.

An ether-soluble fraction of a methanol extract of Ricinus communis var. minor seeds administered subcutaneously to adult female rats and rabbits at doses up to 1.2 g/kg and 600 mg/kg, respectively, in divided doses showed anti-implantation and anticonceptive activities. Laparotomy performed on Day 10 and Day 15 of pregnancy on mated female rats and rabbits treated with the extract did not reveal any uterine implantation sites. The animals were protected against pregnancy for over three gestation periods and among those that later delivered, there was no evidence of abnormality in the pups. In ovariectomized young female rats as well as in immature mice, the extract dose-dependently increased uterine wet weight. Furthermore, the extract induced premature opening of the vagina, increased the number of epithelial cells and cornified cells and decreased the leucocyte number in the vaginal smear. The estrogen-like activities exhibited by the extract were dose-dependent and the anticonceptive effect may be due at least in part to such estrogenic action.

Effects of Ca2+ antagonists on cardiovascular responses to posterior hypothalamic stimulation in the rat.

The effects of methoxyverapamil or hydralazine on pressor responses to posterior hypothalamic stimulation and injected pressor agents were studied in normotensive male Wistar rats. Methoxyverapamil inhibited both phases of pressor responses to hypothalamic stimulation and pressor responses to injected noradrenaline or angiotensin II. Hydralazine inhibited the secondary phase (due to adrenomedullary catecholamine) and not the primary phase (due to increased sympathetic vasomotor activity) of pressor response to hypothalamic stimulation. However, it inhibited the pressor responses to exogenous noradrenaline or angiotensin II. The data indicate that hydralazine is ineffective in inhibiting the pressor response elicited by noradrenaline endogenously released at the sympathetic nerve endings.