The methanolic bark extract of Khaya senegalensis was investigated for its effects on the cardiovascular system. The extract increased the blood pressure of chloralose anaesthetized rats. The increase in rate and force of contraction of isolated, spontaneous rabbit atria evoked by the extract were dose dependent and less pronounced than those produced by isoprenaline. The chronotropic effects of the extract and isoprenaline were antagonized by propranolol which also abolished the ionotropic effect of the extract and antagonized isoprenaline-induced ionotrophy. The vasoconstrictor effect of the extract observed with isolated spiral strips of rabbit aorta was dose dependent, less potent than noradrenaline and was abolished by prazosin. These findings indicate that the hypertensive effect of the methanolic bark extract of K . senegalensis is partly due to the stimulation of flreceptors and a-adrenoceptors.
This study examined the influence of overnight storage on endothelium-independent contractions to 5-hydroxytryptamine (5-HT), endothelium-dependent contractions to NG-nitro-L-arginine methyl ester (L-NAME), and endothelium-dependent relaxations to substance P (SP) and L-arginine, using the porcine isolated splenic artery. In endothelium-intact (E+) segments from fresh porcine isolated splenic arteries or segments from the same vessels stored overnight at 4 degrees C, either in Krebs-Henseleit saline or in Krebs-Henseleit saline containing 1 mM L-arginine, 5-HT caused concentration-related contractions that were similar under all three conditions. Overnight storage enhanced contractions of the splenic artery to L-NAME, an effect not observed if the vessels were co-stored with 1 mM L-arginine. L-NAME failed to contract endothelium-denuded (E-) segments from fresh tissues or tissues stored overnight, indicating that its constrictor effects were endothelium-dependent. SP caused concentration-related, endothelium-dependent relaxations of the splenic artery that were inhibited by 100 microM L-NAME, indicating that the relaxations could be attributed to the stimulated release of NO from endothelial cells. Established contractions to 100 microM L-NAME in E+ segments from fresh tissues, or segments from the same tissues stored overnight at 4 degrees C, either in Krebs-Henseleit saline or in Krebs-Henseleit saline containing 1 mM L-arginine, were all reversed by 1 mM L-arginine to similar extents, indicating that overnight storage did not affect endothelium-dependent dilator responses to L-arginine.(ABSTRACT TRUNCATED AT 250 WORDS)
The nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), produced large endothelium-dependent contractions in isolated segments of the porcine splenic artery, equivalent to approximately 30% of the maximum responses to 5-hydroxytryptamine (5-HT). These responses were inhibited by 1mM L-arginine, but not by either 1mM D-arginine or the superoxide anion scavenger, superoxide dismutase. However, L-NAME-induced contractions were markedly inhibited by the cyclooxygenase inhibitor, flurbiprofen, and the lipoxygenase inhibitor, 2,3,5-tri-methyl-6-(12-hydroxy-5,10-dodecadiynyl)1,4-benzoquinone (AA-861). The combined cyclooxygenase and lipoxygenase inhibitor 3-amino-1-[m-(trifluoromethyl)phenyl]-2-pyrazoline (BW-755C) abolished L-NAME-induced contractions. These findings suggest that suppression of endothelial nitric oxide synthase in the porcine isolated splenic artery results in activation of arachidonic metabolism and production of vasoconstrictor eicosanoids.
Changes in the response to acetylcholine of expansor secundariorum muscles from chicks have been analysed by pharmacological techniques and by [3‐3H]‐quinuclidinyl benzilate ([3‐3H]‐QNB) binding to quantify the muscarinic receptor population.
The expansor secundariorum muscle responded to acetylcholine up to the age of 30 days; the response declined thereafter. This developmental decrease in response to acetylcholine was prevented by surgical denervation.
In chicks aged less than 25 days, denervation did not affect the sensitivity of the expansor muscle to acetylcholine. In older chicks (above 40 days) denervation gradually restored the sensitivity of the expansor muscle to acetylcholine. Responses of the expansor muscle were always abolished by atropine (1 μm) indicating they were mediated by muscarinic receptors.
Binding studies with [3‐3H]‐QNB showed that changes in response of expansor muscles to acetylcholine were primarily due to changes in the muscarinic receptor population.
It is suggested that the noradrenergic innervation of the expansor muscle influences the number of muscarinic receptors expressed in the tissue.
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