A group of researchers is studying secondary hypertension in porcine models of renal artery stenosis. During an experiment, a clip is placed that constricts the right renal artery to 30% of its original cross-sectional area. A few days later, hemodynamic and biochemical measurements are recorded and compared to measurements obtained before clip placement. Which of the following changes is most likely to be seen in the experimental animals?

Question

A group of researchers is studying secondary hypertension in porcine models of renal artery stenosis.  During an experiment, a clip is placed that constricts the right renal artery to 30% of its original cross-sectional area.  A few days later, hemodynamic and biochemical measurements are recorded and compared to measurements obtained before clip placement.  Which of the following changes is most likely to be seen in the experimental animals?

Quizplus · Accepted Answer

11ec160b_3cff_53b8_9249_655a98dfd57d_MD0001_00 Unilateral renal hypoperfusion (due to renal artery stenosis or clipping) causes activation of the renin-angiotensin-aldosterone system (RAAS). In response to low perfusion pressures, the juxtaglomerular cells of the kidney synthesize renin, which converts angiotensinogen (synthesized in the liver) to angiotensin I. Angiotensin-converting enzyme, which is synthesized largely in the lungs, then converts angiotensin I to its active form, angiotensin II. Angiotensin II has multiple actions to increase systemic blood pressure. It directly increases systemic vascular resistance through generalized arteriolar vasoconstriction (Choice B). It also increases sodium and water reabsorption both directly, by increasing sodium reabsorption in the proximal tubule, and indirectly, by stimulating aldosterone synthesis in the adrenal cortex and antidiuretic hormone in the hypothalamus (Choice A). Elevated systemic pressure and blood volume help overcome the decreased perfusion pressures in the stenotic kidney and maintain a near-normal filtration rate. However, the unaffected kidney is exposed to elevated systemic pressures, resulting in increased sodium excretion due to a pressure natriuresis effect. Although this helps reduce circulating volume, many patients with renal artery stenosis have chronic hypertension due to persistent hyperreninemia and angiotensin II-induced vasoconstriction caused by the stenotic kidney. (Choice C) After placement of the clip, glomerular filtration rate will drop in the stenotic kidney, triggering compensatory RAAS activation. This increases the perfusion pressure of the stenotic kidney, helping to normalize glomerular filtration rate. However, like most compensatory responses, the increase in filtration caused by RAAS activation is not enough to overcome the initial drop in filtration caused by clip placement. Therefore, the filtration rate remains less than normal in the stenotic kidney. (Choice D) Renin production is suppressed in the unaffected kidney due to its exposure to elevated systemic pressures. Educational objective: Unilateral renal artery stenosis causes hypoperfusion and activation of the renin-angiotensin-aldosterone system. Angiotensin II causes arteriolar vasoconstriction and increases aldosterone and antidiuretic hormone synthesis. The resultant hypertension helps reduce the decline in glomerular filtration rate in the affected kidney, but causes a pressure natriuresis with increased sodium excretion in the unaffected kidney.

A Group of Researchers Is Studying Secondary Hypertension in Porcine