Acetylcholine and Nicotine agonist - Essay Example

The effect of Salbutamol on the response of Ileum to Acetylcholine Response to question Nicotine is a component that exerts its influence through interacting with the receptors of nicotinic that exist in many subtypes with different pharmacology. The subunits of the mRNA expression are normally wide spread, whereas the pattern of expression of other components is limited to few regions. Nicotine is responsible in the modulation of neurotransmitters release through the presynaptic activation. The many behavioural and physiological influences of nicotine could lead to the release of a variety of neurotransmitters through the activation of acetylcholine (nAChR) at the terminals of presynaptic on the neurons.

The evaluation potential of many functions of presynaptic NAChRs would help in finding out how nicotine bring changes to the brain. Considering a cholinergic projection from MHb (medial habenula) by retroflexus fasciculus to the IPN (interpeduncular nucleus) would exist. In this regard, the ability for nAChr functional diversity is extensive in the IPN. This implies that presynaptic IPN could modulate the production of acetylcholine within the IPN. Different studies have confirmed that the facilitation of nicotine by presynaptic would agonist the release of acetylcholine out of the IPN.

The prime characteristic of this process includes effects of alpha-conotoxins, agonist and agonist investigation, B2 mutation null effects, and the dopamine nAChR mediated release. Response to question 2. Salbutamol could be referred to as am adrenergic agonist receptor, which is used to reduce on the effects of bronchospasm in situations like asthma. It is also used in the treatment of cystic fibrosis, pulmozyme, acetylcysteine, and iprptropium that is linked to DOK-7. As an example of a beta2-agonist, sulbutanol can also be used in obstetrics.

The salbutamol that is intravenous could be utilized as a tocolytic in relaxing the smooth muscles of the uterus hence delay premature labor. This has made sulbutamol be the most preferred agent. In the context of this experiment, Salbutamol antagonist’ caused parallel shift of the given dose response curve. This implies that Salbutamol antagonist’ can elicit a slight and dose-dependent contractile response in the ileum that is induced by acetylcholine. While the Salbutamol agonist’ potentiated the effect of Nicotine and shifted its associated dose response curve towards the left as shown in the graph, it did not affect wholly the contractile effects of the acetylecholyne.

This implies that Salbutam agonist as proven by the iochemical studies, tend to act selectively. As far as EC50 of the agonist is concerned, it is clear from the data, as well as the graph that there is a significant change in the EC50 of the agonist. Since this experiment entailed investigating the effects of salbutamol treatment on response of ileum to acelytecholine, it is certainly clear from the graph that the use of acetylecholine did cause a decrease in the ileum sensitivity to the contractile action of agonist Nocotine.

This desensitization was purely characterized by increasing values of EC (50) of nicotine without a change in its maximal effect. Treatment of ileum with salbutamol caused a slightly small increase in the contractile response to Nicotine when measure at a time prior to being exposed to acetylcholine. As observed from the shift in the graph, after exposure to the acetylcholine, there was little desensitization was seen in the ileum treated with salbutamol. This implies that salbutamol treatment caused some small increase in the Nicotine-mediated phoshoinositide hydrolysis.

On the other hand, salbutamol treatment caused a large decrease in Nicotine mediated inhibition of the forskolin stimulated cAMP accumulation inside the muscles of the ileum. Thus, exposure of ileum to the chemical acetylecholine did not have any desensitizing effect on the ability of Nicotine to elicit any phosphoinositide hydrolysis. Table 1: The effect of Salbutamol on the response of Ileum to Acetylcholine. Acetylcholine FBC (M) V1 V2 Response (g) % Response Acetylcholine + Salbutamol 1e-4 or 2e-9M (1×10-2) M V1 V2 Response (g) % of MAX AGONIST Response 1.00E-09 0.697 0.936 0.239 5.

164217805 1.00E-09 1.685 1.644 0.041 0.901891773 3.00E-09 0.697 1.166 0.469 10.13396716 3.00E-09 1.685 1.743 0.058 1.275846898 1.00E-08 0.697 1.619 0.922 19.92221262 1.00E-08 1.685 2.138 0.45 9.964804223 3.00E-08 0.697 2.599 1.902 41.09766638 3.00E-08 1.685 3.497 1.812 39.85921689 1.00E-07 0.697 4.188 3.492 75.45375972 1.00E-07 1.685 5.168 3.483 76.61680598 3.00E-07 0.697 4.781 4.084 88.2454624 3.00E-07 1.685 6.222 4.537 99.80202376 1.00E-06 0.697 5.325 4.628 100 1.00E-06 1.685 6.231 4.546 100 3.00E-06 0.697 5.004 4.307 93.

06395851 3.00E-06 1.685 6.091 4.406 96.92036956 1.00E-05 0.697 4.361 3.665 79.19187554 1.00E-05 1.685 5.218 3.533 77.716674 3.00E-05 0.697 3.793 3.096 66.8971478 3.00E-05 1.685 4.543 2.86 62.84645842 Table 2: The effect of Salbutamol on the response of Ileum to Nicotine Nicotine FBC (M) V1 V2 Response (g) % Response Nicotine + Salbutamol 1e-4 or 2e-9M (1×10-2) M V1 V2 Response (g) % of MAX AGONIST Response 1.00E-06 1.273 1.496 0.222 4.937722 1.00E-06 1.726 1.652 0.074 1.695692 3.00E-06 1.273 2.401 1.128 25.08897 3.00E-06 1.726 2.706 0.98 22.45646 1.00E-05 1.273 4.757 3.483 77.46886 1.00E-05 1.726 5.564 3.837 87.92392 3.00E-05 1.273 5.77 4.496 100 3.00E-05 1.726 6.091 4.364 100 References Brown, MJ., 2005. Novel double-isotope technique for enzymatic assay of catecholamines, permitting high precision, sensitivity and plasma sample capacity.

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