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The effect of Salbutamol on the response of Ileum to Acetylcholine - Essay Example

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From the graph, the EC50 of Acetylcholine is 4.00E-08, while the EC50 of Salbutamol + Acetylchline is 4.00E-08. The values for the Ec50 of Nicotine are 5.5E-06, and the EC50 OF Salbutamol + Nicotine is 5.00E-06…
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The effect of Salbutamol on the response of Ileum to Acetylcholine
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The effect of Salbutamol on the response of Ileum to Acetylcholine Response to question From the graph, the EC50 of Acetylcholine is 4.00E-08, while the EC50 of Salbutamol + Acetylchline is 4.00E-08. The values for the Ec50 of Nicotine are 5.5E-06, and the EC50 OF Salbutamol + Nicotine is 5.00E-06. This clearly implies that there is no significant effect of sulbutamol on the way the ileum responds to acetylechline. However, there is a significant effect of the sulbutamol on the way ileum responds to nicotine. This desensitisation was purely characterised by increasing values of EC (50) of nicotine without a change in its maximal effect. This thus implies that treatment of ileum with salbutamol after exposure to the acetylcholine, had little desensitisation while treatment of ileum with salbuamol after exposure to nicotine caused some larger increase in the Nicotine-mediated phoshoinositide hydrolysis. Response to question 2. Salbutamol could be referred to as an adrenergic agonist receptor, which is used to reduce the effects of bronchospasm in diseases 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 utilised as a tocolytic in relaxing the smooth muscles of the uterus, and hence delay premature labour. This has made sulbutamol be the most preferred agent. In the context of this experiment, salbutamol antagonist’ caused a 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 biochemical studies, tends 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 that caused a slightly small increase in the contractile response to nicotine when measured at a time prior to being exposed to acetylcholine. As observed from the shift in the graph, the use of acetylecholine did cause a decrease in the ileum sensitivity to the contractile action of agonist nicotine. This desensitisation was purely characterised by increasing values of EC (50) of nicotine without a change in its maximal effect. Treatment of ileum with salbutamol after exposure to the acetylcholine, there was little desensitisation 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 desensitising 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. Clin Sci (Lond);61(5):591–598. [PubMed] Bergendal K., 2004. Salmeterol, formoterol, and salbutamol in the isolated guinea pig trachea: the difference in maximum relaxant effects and the potency but not in functional antagonism. Thorax ;48(4):547–553. Lipworth, B., & McDevitt, D. 2008. Beta-adrenoceptosr response to inhaled salbutamol in the normal subjects. Eur J Clin Pharmacol; 36(4):239–265. Norgaard A., Botker H.,& Klitgaard, N, 2007. Digitalis always enhances exercise-induced hyperkalaemia. Eur J Clin Pharmacol;41(8):609–611. O'Donnell SR, 1998. Examinations for some -adrenoreceptor stimulants for the selectivity using an isolated trachea and atria of the guinea pig. Eur J Pharmacol,19(3):371–379. O'Donnell, S, & Wanstall, J, 2003.. Evidences that efficacy of the fenoterol is higher than that of salbutamol on the beta-adrenoceptors in guinea-pig trachea. Eur J Pharmacol;47(3):333–340. Struthers, D, Quigley, L., & Brown, M, 2002. Rapid changes in the plasma potassium during a game of squash. Clin Sci (Lond);74(6):397–401. [PubMed Wheeldon, N., McDevitt. D., & Lipworth. B., 20006. Cardiac effects of the beta 3-adrenoceptor agonists BRL35135 in man. Br J Clin Pharmacol; 37(4):373–369. Waller, D., 2006. Beta-adrenoceptor partiallly agonists: a renaissance in the cardiovascular therapy? Br J Clin Pharmacol.:157–171.] Wagner J., & Schumann H, 2004. Comparison of bronchodilator and cardiovascular actions of isoprenaline, Th 1165a, terbutaline and salbutamol in cats and isolated organ preparations. Res Exp Med (Berl);162(3):49–65. Williams, M, & Gervino, E., 2000. Catecholamine modulation of the rapid potassium shifts during exercise. N Engl J Med.28; 312(13):823–827. [PubMed] Wilson , L., 1999. Beta-adrenoceptor subtypes in human, guinea pig, and rabbit atria. J Cardiovasc Pharmacol,1216–1221. [PubMed] Read More
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