How does benazepril reduce systemic vascular resistance?
Benazepril lowers systemic vascular resistance by blocking the renin–angiotensin system. It is a prodrug that is converted in the body to benazeprilat, an angiotensin-converting enzyme (ACE) inhibitor [1]. By inhibiting ACE, it reduces formation of angiotensin II, which normally causes vasoconstriction. With less angiotensin II, arterioles relax and total peripheral (systemic) vascular resistance falls [1].
Why does blocking ACE lead to vasodilation?
Angiotensin II drives vascular smooth muscle contraction. Reducing angiotensin II decreases vasoconstrictor tone, so resistance vessels dilate, which reduces systemic vascular resistance [1].
Does benazepril affect bradykinin, and does that matter for vascular resistance?
ACE also breaks down bradykinin. When ACE is inhibited, bradykinin levels can rise, which contributes to vasodilation (through increased production of vasodilatory mediators). This can further support the reduction in vascular resistance [1].
What’s the overall hemodynamic result?
The net effect of decreased angiotensin II (and increased bradykinin signaling) is lower arteriolar constriction and reduced systemic vascular resistance, which contributes to the antihypertensive effect of benazepril [1].
What clinicians typically measure to confirm the mechanism?
The functional readout is a fall in blood pressure driven largely by reduced peripheral resistance, consistent with ACE inhibition reducing angiotensin II-mediated vasoconstriction [1].
Sources
1. DrugBank. Benazepril. https://go.drugbank.com/drugs/DB01111