Investigation of the influence of the endothelium on the actions of acetylcholine and nitroprusside.

Results (a) Estimate the maximum responses (Emax) and EC50 values for phenylephrine with the two types of arterial ring. Put this data in a single, self-explanatory table.

Table1. Emax and EC50 values for phenylephrine. Phenylephrine | Emax in grams tension | EC50 in nM | Endothelium intact | 2.2 | 40 | Endothelium denuded | 2.9 | 10 |

(c) Estimate the EC50 values for the effects of acetylcholine and nitroprusside in both types of arterial ring, and present these in a table. Table 2. EC50 values for the effect of acetylcholine and nitroprusside. EC50 in nM | …show more content…

On vascular endothelial cells activation of muscarinic receptors with acetylcholine mediates the synthesis of nitric oxide and causes vasodilation followed by smooth muscle relaxation. M3 receptors are also present on the membranes of vascular smooth muscle cells that represent only a minor fraction of total muscarinic receptor in most smooth muscles. In endothelium denuded rings acetylcholine directly stimulates M3 receptors on the smooth muscle cells and triggers direct contractions of smooth muscle by increasing intracellular calcium level. The response is not significant due to the minor fraction of M3 receptors involved. (g) Why is there a difference in the sensitivity to the relaxant effects of nitroprusside in the two preparations? Along with secreting relaxing factors an endothelium also plays a major role in the control of smooth muscle proliferation. (Paul.M et al, 1994) Consequently, in response to the endothelium independent vasodilator nitroprusside a healthy endothelium releases vasoconstriction factors (α-adrenoreceptor agonists) such as Angiotensin II, Endothelin-1, PGF2α and 5HT. Activation of adrenoreceptors by these agents leads to inactivation of the cAMP and thus induces smooth muscle constriction. To overcome the effect caused by adrenoreceptor agonists higher