Potassium channels and prostacyclin contribute to vasorelaxant activities of Tridax procumbens crude aqueous leaf extract in rat superior mesenteric arteries.

BACKGROUND: Previous studies have shown that aqueous extract of the leaf of Tridax procuinbens is capable of lowering blood pressure through its vasodilatory effects. In the present study attempt was made to examine the biological active components of T procuinbens leaf using GC-MS methods. We further investigated the role of K+ channels in the vasorelaxation effects of Tridax procumbens using rat isolated mesenteric artery. METHODS: The superior mesenteric artery isolated from healthy, young adult Wistar rats (250-300 g) were precontracted with phenylephrine (PE) (10(-7) M) and potassium chloride (KCl) (60 mM) and were treated with Various concentrations of aqueous extract ofT procumbens (0.9.0 mg/ml). The changes in arterial tension were recorded using a force-displacement transducer (Model 7004; Ugo Basil Varese, Italy) coupled to data capsule acquisition system. RESULTS: The results of GG-MS revealed the presence of linoleic acid. The T. procumbens extract (TPE) ranging from 0.5-9.0 mg/mI significantly (p<0.05) reduced the, contraction induced by (PE) and (KCl) in a concentration-dependent manner. The extract also antagonised the calcium-induced vasoconstriction (1(-9) - 10(-5)) in calcium-free with high concentration of potassium as well as. in calcium- and potassium free physiological solutions. The vasorelaxing effect caused by TPE was significantly (p<0.05) attenuated with preincubation of potassium channels blockers (Barium chloride and apamin), NO synthaseinhibitor (L-NAME), prostacyclin inhibitor (indomethacin), atropine; propranolol, and methylene blue while it was not affected by preincubation with glibenclamide and tetra ethyl ammonium, 4-aminopyridine (4-AP) and oxadiazolo quinoxalin (ODQ). CONCLUSION: The results of this study demonstrate that T procumbens extract causes vasodilatory effects by blocking calcium channels and the vasodilatory effect of the extract may also be due to stimulation of prostacyclin production and opening of small-conductance Ga2+ activated potassium channels. The observed effect of this extract may be probably due to the presence of linoleic acid in this extract.

Effects of chronic administration of ethanolic extract of kolanut (Cola nitida) and caffeine on vascular function.

BACKGROUND: Kolanut (Cola nitida) is consumed in virtually every part of the world. The caffeine content of kolanut is scarce and the number of investigations studying the health benefits of kolanut is negligible compared to coffee. OBJECTIVE: The present study was designed to identify the caffeine content of kolanut and evaluate the effect of its chronic consumption on cardiovascular functions in rats. METHODS: The caffeine content of kolanut was determined by Gas chromatography-mass spectrometry (GC-MS). Wistar albino rats were divided into four groups (10 Rats/group). Kolanut extract (11.9 mg/kg), caffeine extracted from kolanut (7.5 mg/kg), decaffeinated of kolanut extract (6 mg/kg) and distilled water (control) was administered orally to each group for six-weeks. Effect of treatment on body weight, blood pressure and relaxation response to acetylcholine (ACh) and sodium nitroprusside (SNP) of the aortic rings was assessed. RESULTS: The total caffeine content of kolanut extract was found to be 51% and it was 96% pure from GC-MS analysis. Chronic consumption of kolanut and caffeine significantly (p < 0.05) decreased body weight. Similarly, kolanut extract decaffeinated kolanut and caffeine significantly (p < 0.05) reduced the contractile response to noradrenaline and higher potassium solution. Kolanut extract and caffeine also significantly (p < 0.05) increased the mean arterial blood pressure. Caffeine and kolanut consumption reduced the relaxation response to both acetylcholine and sodium nitroprusside. Atropine and L-NAME considerably inhibit the ACh-induced relaxation of the rat aortic ring suggesting the involvement of cholinergic mechanism. However, indomethacin (10(-4)M) also attenuated the ACh response indicating involvement of protanoids. CONCLUSION: The results suggest that treatment with both kolanut extract and caffeine had similar characteristics between the two groups with no significant differences in the ACh-induced relaxation of thering suggesting that the action of kolanut extract is due to its caffeine content.

Neurosedative and muscle relaxant activities of aqueous extract of Bryophyllum pinnatum.

The saline leaf extract of Bryophyllum pinnatum was investigated on neuropharmacological activities to ascertain claims of local use. When tested in mice, it produced a dose-dependent prolongation of onset and duration of pentobarbitone-induced hypnosis, reduction of exploratory activities in the head-dip and evasion tests. Moreover, a dose-dependent muscle in-coordination was observed in the inclined screen, traction and climbing tests. It delayed onset to convulsion in both strychnine- and picrotoxin-induced seizures in addition to minimal protection against picrotoxin seizures.

Effect of caffeine and ethanolic extract of kolanut on glucose uptake in the canine hindlimb at rest and during contraction.

The study investigated the effects of caffeine and ethanolic extract of kolanut (EEK) on glucose uptake in the canine hindlimb at rest and during contraction. Thirty male anaesthetized mongrel dogs [11-13 kg] were divided into six groups [5 dogs/group] Caffeine [6 mg/kg], EEK [5 mg/kg], or normal saline [control] was administered intravenously to each group at rest. Arterial and venous blood samples were collected at 0, 5, 10, 15, 20, 25, 30, 45, 60, 75 and 90 minutes after drug administration. Blood glucose was measured by glucose oxidase method. Arteriovenous [A-V] glucose difference was calculated and venous blood flow [VBF] was measured during the sampling period. Hindlimb glucose uptake [HGU] was calculated as the product of [A-V] glucose and blood flow. After sampling at rest, the experiments were repeated with the right femoral nerve stimulated using electrical stimulator at 5 Hz. At rest, A-V glucose increased significantly [P<0.05] from 4.2+/-0.2 mg/dl to 29.8+/-8.6, and 24.4+/-2.6 for caffeine and EEK respectively. VBF decreased to 2.0+/-0.9 and 6.0+/-0.6 ml/min for caffeine and EEK respectively. However, HGU significantly increased from 34.8+/-0.1 mg/min to 74.5+/-3.2 mg/min and 175.8+/-3.4 mg/min for caffeine and EEK, respectively. Contraction of the hindlimb muscle alone significantly increased the [A-V] glucose [68%], VBF [26%] and HGU [120%] when compared with the control. During contraction, [A-V] glucose increased from 4.3 +/-1.5 mg/dl to 35.6+/-3.0 mg/dl, and 27.0+/-2.2 mg/dl for caffeine and EEK respectively. VBF also increased from 8.4+/-0.3 ml/min to 12.8+/-0.3 ml/min for EEK. Although, contraction improves VBF [7.3+/-0.5 ml/min] to the hindlimb in response to caffeine, the value was significantly [P<0.05] lower than that of control [8.4+/-0.5 ml/min]. Contraction also significantly increased HGU from 35.8+/-3.6 mg/min to 249.0+/-3.3 and 286.72+/-2.0 mg/min for caffeine and EEK, respectively. The results showed that caffeine and EEK significantly increased HGU and that these effects are due to the increases in glucose extraction [A-V glucose] caused by caffeine and EEK.

Role of adrenergic receptors in the caffeine-induced increase in glucose uptake by the canine hindlimb.

The present study was designed to investigate the effects of alpha and beta adrenergic receptor blockers on caffeine-induced increase in canine hindlimb glucose uptake. The study was carried out on fasted male anaesthetized dogs divided into five groups [5 dogs per group]. Each dog was given a bolus injection of normal saline, caffeine [6 mg/kg] caffeine after pretreatment with prazosin [0.2 mg/kg], caffeine after pretreatment with propranolol [0.5 mg/kg] or caffeine after pretreatment with a combination of prazosin [0.2 mg/kg] and propranolol [0.5 mg/kg]. The experiments were carried out under resting and exercising conditions of the hindlimb. Hindlimb glucose uptake [HGU] was calculated as the product of blood flow and arterio-venous glucose difference. Blood glucose was determined by the glucose oxidase method and blood flow to the hindlimb was determined by time-collection method. The results showed that pretreatment of the animal with either prazosin or propranolol significantly reduced caffeine-induced hyperglycemia, glucose extraction and hindlimb glucose uptake at rest. The two blockers also separately reduced caffeine-induced hyperglycemia during contraction of the hindlimb. Prazosin or propranolol did not however influence the effect of caffeine on glucose extraction and hindlimb glucose uptake during contraction of the hindlimb. It was therefore concluded that alpha and beta adrenergic receptors are involved in caffeine induced responses at rest and not during hindlimb contraction.

Influence of nitric oxide on histamine and carbachol-induced gastric Acid secretion in the common african toad - bufo regularis.

The study aimed to determine the influence of nitric oxide (NO) on the action of histamine and carbachol on acid secretion in the common African toad - Bufo regularis. Gastric acidity was determined by titration method. The acid secretion was determined when nitric oxide was absent following administration of NO synthase inhibitor; N-nitro-L-arginine methyl ester (L-NAME) and when nitric oxide was in excess by administration of exogenous NO donor, sodium nitroprusside (SNP). Histamine or carbachol increased acid secretion in the toad. Acid output increased from 0.32 +/- 0.04 mEq/15min to 0.56 +/- 0.08 and 0.61 +/- 0.05 mEq/15min for histamine and carbachol respectively [P < 0.05]. Pretreatment of the toad with L-NAME produced further increases in histamine (0.62 +/- 0.06 mEq/15min) or carbachol (0.74 +/- 0.06 mEq/15min) induced acid secretion respectively. SNP however, completely abolished the acid secretion stimulated by either histamine or carbachol. It was therefore concluded that nitric oxide has a negative influence on the histamine or carbachol-stimulated acid secretion in the toad - Bufo regularis.