Final answer:
ACE inhibitors decrease kidney perfusion in bilateral renal artery stenosis by reducing angiotensin II levels, leading to dilation of efferent arterioles and a drop in glomerular filtration pressure, potentially exacerbating renal issues.
Step-by-step explanation:
ACE inhibitors can lead to a decrease in kidney perfusion in patients with bilateral renal artery stenosis by inhibiting the production of angiotensin II, which is a vasoconstrictor. This causes dilation of efferent arterioles and a decrease in glomerular filtration pressure.
The systemic regulation of blood pressure and kidney perfusion involves the complex renin-angiotensin-aldosterone system (RAAS). When blood pressure drops or when the kidney requires more blood flow, renin is released from juxtaglomerular cells. Renin converts angiotensinogen into angiotensin I, which is then converted to angiotensin II by the action of ACE. Angiotensin II normally acts to constrict blood vessels and increase blood pressure. However, ACE inhibitors block this conversion, reducing angiotensin II levels and subsequently lowering both systemic blood pressure and intraglomerular pressure.
With bilateral renal artery stenosis, the arterioles leading to the kidneys are narrowed, impairing blood flow. The kidneys compensate for this by increasing renin production to maintain GFR through the RAAS. When ACE inhibitors are used in this case, they prevent the usual compensatory vasoconstriction mediated by angiotensin II, leading to a further decrease in perfusion pressure and a potential reduction in glomerular filtration rate (GFR). Thus, although ACE inhibitors may be useful in treating high blood pressure, they can exacerbate renal problems in patients with renal artery stenosis by reducing the kidney's ability to maintain adequate GFR.