<s>[INST] context: Inhibition of angiotensin-converting enzyme (ACE) reduces angiotensin II formation. As a result, those pathways that are stimulated by angiotensin II are also reduced. The most important change is a reduction in the release of aldosterone. To a lesser extent, angiotensin II also causes vasoconstriction and release of transmitter from sympathetic nerves, and these direct excitatory effects are also reduced. Finally, angiotensin II has some direct excitatory effect on antidiuretic hormone (AD H) release. Lowering angiotensin II may therefore slightly reduce ADH levels by this direct mechanism. These effects tend to reduce blood pressure and volume. This reduction is sensed by pressure and volume sensors throughout the body, leading to enhanced renin release. The effect of ACE inhibitors on ADH levels is complicated. On one hand, angiotensin II has a small direct stimulatory effect on ADH release, so blockade of angiotensin II synthesis tends to limit ADH release. Furthermore, to the extent that more salt than water is lost, plasma osmolaliry decreases, leading to a de- crease in ADH levels. On the other hand, any reduction in extracellular fluid volume tends to enhance ADH levels. In summary, only minor changes in ADH levels are expected whereas a significant rise in plasma renin levels occurs. [/INST] question: Which of the following changes is most likely to occur following administration of an ACEI? | options: A: Increased levels of rennin B: Increased levels of angiotensin C: Increased levels of aldosterone D: Increased levels of ADH | answer: A </s>