Table 1.

Sex-specific responses to established and novel pharmacological therapeutic formulations targeting the renin-angiotensin system in clinical populations.

Therapeutic Agent	Mechanism of Action	Sex-Specific Responses
ACE inhibitors	Decrease Ang II formation	Men demonstrate better blood pressure control [117], with women having increased susceptibility to side effects [119,120].
Angiotensin receptor blockers (ARBs)	Block Ang II effects at AT1R	Women exhibit greater antihypertensive effect and require lower drug dosage [121,122,110]. Improved survival in women with CHF when compared to ACE inhibitors [110].
Mineralocorticoid antagonists	Block aldosterone effects at mineralocorticoid receptors	More effective to lower blood pressure in women and in obesity-related hypertension [123,124].
Direct Renin Inhibitors	Antagonize renin to prevent downstream activation of the RAS	Similar blood pressure lowering efficacy in hypertensive men and women treated with aliskiren [67].
MasR Agonists	Increase activity of Ang-(1–7) mas receptors	Unknown
ACE2 Activators	Decrease Ang II and increase Ang-(1–7) levels	Unknown
Recombinant human ACE2	Decrease Ang II and increase Ang-(1–7) levels	Unknown

ACE, angiotensin converting enzyme; ACE2, angiotensin converting enzyme 2; Ang, angiotensin; AT₁R, angiotensin II type 1 receptor; CHF, congestive heart failure; MasR, angiotensin-(1–7) mas receptor; RAS, renin-angiotensin system.