Why would you want it as low as possible? Are you assuming that a lower blood pressure is always a better blood pressure?
While it is true that ACE inhibitors and ARBs can lead to decreases in hematocrit, and AAS usage can increase hematocrit which might increase the risk of trombosis, this is not an argument to always use BP-lowering medication. For one, not all AAS users experience hematocrit increases to the extent that it significantly increases the risk of trombosis. Second, even if it does, this risk needs to be weighed against the risks of a potential form of treatment. (Mild increases in hematocrit in low-risk populations, especially otherwise healthy nonsmoking young adults, aren't really of concern.) Third, ACE inhibitors and ARBs don't consistently decrease hematocrit. They do so in certain populations in which RAAS activation is an excerbating or causal factor for increased hematocrit. While there are some uncertainties surrounding the mechanism it does so, it converges on an increase in EPO. The AAS-induced increase in hematocrit is most likely due to suppression of hepcidin rather than an increase in EPO. And even in the case of the latter, it's the question whether RAAS activation plays sufficient of a role in this to the extent that ARBs or ACE inhibitors lower hematocrit. There's no evidence to indicate that these drugs lower hematocrit in said population.
While BP-lowering medication can indeed help against certain structural changes of the heart, in particular LV hypertrophy, this is again not to say all AAS users should use BP-lowering medication. First, not all AAS users experience LV hypertrophy. Second, the regression of LV hypertrophy seen with the use of BP-lowering medication is predominatenly due to its BP-lowering effect per se. This can be derived by the fact that all classes of BP-lowering medication lead to regression of LV hypertrophy, and calcium channel blockers showing similar efficacy as ARBs and ACE inhibitors. As such, hypertension is a prerequisite for this to work. And as stated earlier, not all AAS users are hypertensive. Finally, the LV hypertrophy that can be caused by AAS is most likely not, or only to a small extent, the result of increased blood pressure. These changes occur too rapid for that and they coincide with other structural changes that aren't necessarily seen in hypertensive populations. Moreover, the average BP increase due to AAS users is too mild in comparison to the structural changes of the heart that are seen.
As such, I feel it's misguided to say that all AAS users should use some form of BP-lowering medication.
