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Endothelin is a vasoactive peptide involved in a variety of processes, including the control of blood flow. Endothelin is capable of binding to two different receptors. There are receptors for endothelin located on smooth muscle (ETA) and receptors for endothelin located on vascular endothelium (ETB). When endothelin binds to ETA, it initiates vasoconstriction by narrowing blood vessels. However, when endothelin binds to ETB, vasodilation occurs due to the widening of blood vessels. The activity of the ETB receptor seems to counterregulate the ETA effects and prevents excessive vasoconstriction. Drug $X$ is a selective receptor antagonist for endothelin. It is designed to bind preferentially to certain endothelin receptors. Drug $\mathrm{Y}$ is another selective receptor antagonist for endothelin. It is also designed to preferentially bind to one of the endothelin receptors. Researchers are hopeful that drugs $\mathrm{X}$ and $\mathrm{Y}$ will be of value in the treatment of conditions such as pulmonary arterial hypertension (PAH). In PAH, excess endothelin is produced, which causes an increase in blood pressure within the pulmonary arteries. Normal pressure in the pulmonary arteries is expected to be about $14 \mathrm{~mm} \mathrm{Hg}$, and pressure at or above $25 \mathrm{~mm}$ Hg constitutes PAH. Both drugs have been tested in patients with PAH. There were five patients in each group. At the end of the study, the percent decrease in mean pulmonary artery pressure was measured for each patient and reported in the table. \begin{tabular}{cccc} \hline Patient & Drug X & DrugY & Placebo \\ \hline 1 & $+10 \%$ & $-10 \%$ & $+5 \%$ \\ 2 & $+3 \%$ & $-5 \%$ & $0 \%$ \\ 3 & $-5 \%$ & $+2 \%$ & $+13 \%$ \\ 4 & $+2 \%$ & $0 \%$ & $-4 \%$ \\ 5 & $0 \%$ & $-7 \%$ & $-2 \%$ \\ Average decrease & $+2 \%$ & $-4 \%$ & $+2.4 \%$ \\ \hline \end{tabular} In addition to regulation of vessel diameter, ETA is known to have other roles in the body. When activated by a specific type of endothelin, ETA can synergize with growth factors to cause rapid cell proliferation. Based on this information, it is MOST likely that ETA can be involved with: Options: A. an increase in metabolism B. the development of cancer C. immune system hypersensitivities D. increased stress to the kidneys and liver

The question suggests that ETA can be activated by certain types of endothelin, which causes ETA to synergize with growth factors to increase cell proliferation rates. Growth factors are one of many mechanisms used to regulate the cell cycle. Of the choices listed, A, C, and D can be eliminated as they have nothing to do with growth factors and cell proliferation. The only reasonable answer is choice B since one of the many characteristics of cancer is increased cell proliferation. The correct answer is B.