Pharmacological studies on sesame and nigella sativa fixed oils: effects on the sensitivities of the adrenoceptors baroreceptors, platelets and the uterus of the rat

The aim of this study is to unravel the effects of short-term treatment [2 weeks] with sesame oil [S.O., 6 and 12 ml Kg[-1]. Day [-1], i.p.] and Nigella sativa fixed oil [N.O. 2 and 2 ml Kg[-1] Day[-1] i.p.] on some cardiovascular, platelets and reproductive parameters in normal and/or streptozotocin hyperglycemic diabetic rats [NR and DR, respectively]. Both S.O. and N.O. significantly suppressed [alpha] -adrenoceptor-mediated phenylephrine-induced rise in the arterial blood pressure in NR only. S.O. significantly sensitized the arterial baroreceptors, whereas N.O. significantly suppressed it in NR only. None of the oils affected this parameter in the DR. Both oils significantly enhanced isoprenaline-induced hypotension in both NR and DR without any effect on isoprenaline-induced tachycardia. Both oils suppressed adenosine diphosphate [ADP]-induced platelets aggregation in both NR and DR. The suppression was more significant in DR. Both oils enhanced significantly arachidonic acid [0.714 mg Kg[1] i.v.] -induced hypotension in NR. Both oils significantly suppressed PGE[2-] and oxytocin-induced uterine contractions of the diethylstilbesterol-treated uteri of the NR. S.O. but not N.O. significantly enhanced the percentage of bias to cysts implantation in NR. None of the oils induced any teratogenic effects or induced significant changes in the gestation length, litter size, male to female ratio, resorption rate or placental weights in NR. However, N.O. significantly increased the foetal weight. In conclusion, the results point to the potential usefulness of both S.O. and N.O. in conditions that benefit from desensitization of [alpha1] adrenoceptors, [Beta2] sensitization of -adrenoceptors and uterine PGE[2] and oxytocin receptors. Furthermore, S.O.-induced sensitization of the baroreceptors may be beneficial in those conditions associated with a decrease in arterial baroretlexes. In addition, both oils seemed to be safe during pregnancy with S.O. having the additional potential advantage of enhancing the implantation rate

On the characterization of dopamine-induced contractile response of rat anococcygeus muscle preparation.

Presence of specific dopamine (DA) receptors and their characterization was attempted in rat anococcygeus muscle preparation. Dopamine (10(-6) M) and B-HT 920 (10(-6) M) produced concentration dependent contractions of the rat anococcygeus muscle preparation. The response of DA was shifted towards right in presence of haloperidol (10(-6) M; pA2 = 6.8) and sulpiride (10(-4) M) in a competitive manner. Alpha 2 antagonists yohimbine (10(-5) M) and idazoxan (10(-5) M) blocked the response to DA in a competitive manner, while alpha 1 antagonist prazosin (10(-5) M) completely blocked the response to DA. SCH 23390 (10(-5) M), a D1 DA antagonist potentiated the response to DA. Reserpinization (5 mg/kg, 24 hr prior) brought about a shift towards the right, and this response was similarly blocked by haloperidol, sulpiride and yohimbine without affecting the maximum response. Desipramine (10(-5) M) blocked the response of DA in a non-competitive manner. Pretreatment of animals with desipramine (10 mg/kg) followed by reserpine, brought about a reversal of action of reserpine. The response to B-HT 920 (10(-6) M), was blocked similarly by haloperidol and yohimbine. However, the effect of desipramine was more pronounced when compared to DA per se. SKF 38393, a D1 DA agonist, potentiated the response to B-HT 920. The findings suggest the presence of both D1 and D2 DA receptors in rat anococcygeus muscle and that DA also acts on adrenergic receptors to produce a contractile response of this muscle preparation.

In vitro study of rat uterus after chronic formaldehyde exposure.

To measure cholinergic, adrenergic and tryptaminergic receptor activity of formaldehyde (HCHO) in rat uterus, albino rats were treated with 5 and 10 mg/kg, ip HCHO for 30 days. Acetylcholine (ACh) in doses 1.33, 2 and 3 micrograms/ml produced mild to moderate contraction of isolated rat uterus in control group. HCHO had no effect on isolated rat uterus per se, however it reduced ACh and carbachol induced contraction and presence of adrenaline influences in respect of ACh and carbachol activity. Adrenaline per se had no effect in control preparations, but reduced carbachol induced contraction. Propranolol had no effect on rat uterus; but its presence in the bathing medium increased activity of adrenaline. 5-Hydroxytryptamine (5-HT) had no effect of its own on isolated rat uterus but its presence in the bathing medium enhanced contractions of carbachol and oxytocin.

Involevements of A- and B-adrenergic receptors in the pyrethroids-induced hyperglycemia in rats

The effects of permethrin and cypermethrin on blood glucose levels, the serum insulin level and on liver glycogen content were assessed in rats. Intraperitoneal administration of cypermethrin in two dose levels [100, 200 mg/kg] caused about 2-3 fold increase of blood glucose concentration. Administration of permethrin in a low dose level [250 mg/kg] failed to produce significant changes of blood glucose concentration. Yet, in a high dose level [500 mg/kg], it increased the blood glucose concentration by about 50% of the control. The rise in blood glucose level produced by cypermethrin was greater than that produced by permethrin. Cypermethrin or permethrin significantly decreased liver glycogen content, but failed to alter serum insulin level. Simultaneous administration of either prazosin or propranolol with cypermethrin or permethrin counteracted the pyrethroids-induced hyperglycemia. These data suggested that the hyperglycemia produced by cypermethrin or permethrin is mediated by increased hepatic glycogenolysis with involvement of alpha-1 and B- adrenergic receptors

Hypothalamic adrenoceptors concerned with control of temperature, elicited by chemical stimulation.

Norepinephrine (NE) and its blockers (alpha-1, alpha-2, beta-1 and beta-2) were micro-injected into the anterior hypothalamus of male albino rats and the effects of these injections on rectal temperature were recorded. The results indicated that the thermoregulatory effects of NE were dependent on ambient temperature. The present study further demonstrated the specific involvement of beta-2 receptors present in the anterior hypothalamus concerned with thermoregulation.

Centrally mediated alpha & beta adrenoceptors controlling blood pressure in rabbits.

The effect of intracerebroventricular (icv) injection of noradrenaline (NA) on the blood pressure was studied in anaesthetised rabbits. Adrenoceptor blockers were used to study the specific adrenoceptor mediating the response. The results indicated a hypotensive response to icv injection of NA. This hypotensive response to NA was blocked by alpha-2 (yohimbine) and beta-1 (metoprolol) but not by alpha-1 (prazosin) and beta-2 (butoxamine) adrenoceptor blockers.

Estudio "in vitro" del efecto de las aminas Simpáticomimeticas sobre la reactividad vascular de la aorta de rata, en presencia de Tiroxina (hormona tiroidea) / Study \"in vitro\" of effects of the sympathomimetics amines on the rat aorta vascular reactivity with thyroxini

Se estudia el comportamiento de la aorta Torácica de rata por medio de curvas dosis-respuestas al anoradicladina en condiciones controles y en presencia Tiroxina "in vitro". Se uso cacaina en presencia y ausencia de Tiroxina, y se vió el comportamiento de la arteria con la Tiroxina

Reduced beta adrenergic responsiveness in isolated rabbit atria during hypothermia.

Beta adrenergic agonist isoprenaline (8x10(-6)M) produced a 500% increase in inotropic and 90% increase in the chronotropic responses of isolated rabbit atria at 37 degrees C. On cooling the atria to 23 degrees C, these responses were significantly reduced to 87% and 30% respectively. Similar results were obtained with adrenaline, but isoprenaline was more potent. The positive chronotropic and inotropic responses to isoprenaline were effectively blocked by propranolol and practolol at 37 degrees C whereas at 23 degrees C these beta blockers were unable to block even minor positive responses obtained by isoprenaline at this temperature. On the contrary at 23 degrees C, phenylephrine (alpha adrenergic agonist) produced marked positive chronotropic and inotropic effects indicating enhancement of alpha adrenoceptor activity at lower temperatures. This also suggests that reduced beta receptor activity at lower temperature is not due to a generalised depression of adrenoceptors as a result of hypothermia. Rewarming of atria to 37 degrees C restored the beta adrenoceptor responsiveness to previous level. It appears that ambient temperature is important im maintaining normal beta adrenergic activity of the atria.

Involvement of Central adrenergic mechanisms in the induction of cardiac arrhythmias by aconitine nitrate administered intraventricularly.

Aconitine, 10 mug, administered intraventricularly in cats produced cardiae arrhythmias. Intraventricular administration of phenoxybenzamine, propranolol and practolol abolishes the centrally induced cardiac arrhythmias. Intraventricular reserpinization also abolished these cardiac arrhythmias whereas intraventricular administration of 6-hydroxydopamine and tetrabenazine had no effect. Brain stem noradrenaline probably plays a role in these centrally induced cardiac arrhythmias by aconitine.