The value of the captopril test and the effect of captopril on renal function

We have investigated the use of captopril as a screening test for renovascular hypertension and compared the effects of captopril on renal function in patients with renovascular hypertension and those without renovascular hypertension. The captopril test and kidney gamma scintigraphy were carried out in 50 hypertensive patients, 13 with renovascular hypertension and 37 without. Blood samples were drawn for the determination of plasma renin activity and kidney gamma scintigraphy was done before and 60 minutes after 50 mg oral captopril administration. Results suggesting the diagnosis of renovascular hypertension are the following: a basal and stimulated plasma renin activity of 4 ng ml/hr or more and an absolute increase in plasma renin activity of 3 ng/ml/hr or more if basal plasma renin activity was less than 4 ng/ml/hr. Data from kidney gamma scintigraphy showed that captopril causes a decrease in clearance rate at 20 minutes in patients with renovascular hypertension but not in patients without renovascular hypertension. We conclude that the captopril test can be used to screen for renovascular hypertension, but catopril may impair the renovascular hypertensive patient's renal function.     

A prospective evaluation of a simplified captopril test for the detection of renovascular hypertension

Renovascular hypertension is potentially curable but of low prevalence. A previous retrospective study has demonstrated the use of a potentiated increase in plasma renin activity after captopril administration as a diagnostic test for renovascular hypertension; this requires two blood samples for plasma renin activity determination and three inclusive criteria for a positive test result. We applied this test prospectively to screen 100 hypertensive patients for renovascular hypertension. We evaluated 29 patients with renovascular hypertension; the remainder were diagnosed as having essential hypertension. In our patient population, a postcaptopril plasma renin activity of 5.7 ng of angiotensin per milliliter per hour (ngAl.mL-1.h-1) or greater had a 100% sensitivity and an 80% specificity for renovascular hypertension. An absolute increase in plasma renin activity with captopril of 4.7 ngAl.mL-1.h-1 or greater had a lower sensitivity of 90% and a specificity of 87%, whereas a fractional increase in plasma renin activity after captopril of 150% or higher had the lowest sensitivity of 69% and a specificity of 86%. A subgroup analysis of 38 patients who were receiving diuretic therapy demonstrated that the test sensitivity was unchanged but the specificity was reduced. In conclusion, a single postcaptopril plasma renin activity value of 5.7 ngAl.mL-1.h-1 or greater is a simplified screening test for renovascular hypertension, with excellent sensitivity and acceptable specificity. This test is well tolerated, inexpensive, and easy to perform.     

The captopril test in the detection of renovascular disease in hypertensive patients

A number of reports share the conclusion that the captopril test is an adequate screening procedure for the detection of renovascular disease among hypertensive patients. Therefore, we prospectively studied the value of this test in 149 consecutive hypertensive patients. The test was considered positive if plasma renin activity, after an oral dose of 25 mg of captopril, rose by more then 4.44 ng.L-1.s-1 (16.0 ng/mL per hour). The sensitivity of the test was 39%, the specificity was 96%, the positive predictive value was 81%, and the negative predictive value was 79%. No clinically important cutoff point identifying patients with renal artery stenosis could be detected in the values of baseline and stimulated plasma renin activity nor in baseline blood pressure or changes after captopril testing. The low sensitivity makes the captopril test unfit to be used as a screening procedure in an unselected hypertensive population.     

Stimulation of Plasma Renin Activity by Captopril in Renovascular Hypertensive Conscious Dogs

The increase in plasma renin activity induced by captopril is used in the clinical evaluation of renovascular hypertensive patients. This increase in plasma renin activity could result from either the concomitant fall in systemic pressure or other effects of captopril, such as the removal of an angiotensin II inhibitory effect on renin release, the increased production of bradykinin or prostaglandins, etc. To examine the effect captopril has on plasma renin activity, independent of changes in systemic pressure, captopril (5, 10 and 50 μg/kg iv) was administered to conscious dogs before and following the development of 1 clip-2 kidney Goldblatt hypertension. Plasma renin activity, under normal conditions remained unchanged, while during hypertension It increased 2.0, 2.8 and 3.5 fold respectively in response to the three doses of captopril. These results suggest that the development of renovascular hypertension sensitized the kidney to release renin when challenged by captopril and that the effect is independent of changes in systemic pressure.     

Captopril test: time over?

OBJECTIVE: The role of non-invasive tests for the detection of renovascular hypertension is still a matter of controversy. The 'captopril test' is widely used; its clinical usefulness, however, remains questionable. The aim of the current study was therefore to report our own experience and to review the published data on the diagnostic significance of the test. PATIENTS AND METHODS: Data from 485 hypertensive patients who underwent a captopril test in consecutive order at our institution were analysed retrospectively. After a 30-min resting period in the supine position 50 mg of captopril was given orally. Blood was collected before and 90 min after dosage for the determination of plasma renin concentration (normal range 3.5-8.0 ng/ml/h). An increase by 100% or more of the baseline value was considered a positive response. Blood pressure was recorded at baseline and at 90 min. RESULTS: A positive response was present in 62 patients; further diagnostic work-up revealed significant renal artery stenosis in 11 of these patients. In the 423 patients with a negative response renal artery stenosis was found in three cases. With some limitations of retrospective analyses in mind, sensitivity and specificity of the test were calculated as 79% and 89%, respectively. No severe complication occurred during the test. CONCLUSION: Our data on the diagnostic indices and the safety of the captopril test are in good agreement with most published series. Altogether, available data suggest that the captopril test has a limited diagnostic accuracy as a screening test for the detection of renovascular hypertension. New radiologic non-invasive techniques with greater diagnostic value are therefore likely to challenge the clinical role of the test in the future.     

Reversible renin-dependent renovascular hypertension successfully treated with percutaneous transluminal renal angioplasty and stenting

A 37-year old woman was suspected of having renovascular hypertension because of recent onset severe hypertension (blood pressure 220/135 mmHg; compared to 132/65 mmHg two years earlier) and an abdominal bruit. A captopril renal scan indicated the presence of right renal artery stenosis. Additionally, a captopril plasma renin activity (PRA) provocation test showed a positive result for renovascular hypertension (baseline PRA = 291 microU/mL; 1 hour post-captopril PRA = 1444 microU/mL). Selective renal angiography demonstrated a severe critical stenotic lesion at the distal portion of the right renal artery. Blood pressure (BP) decreased to 136/80 mmHg one day after successful percutaneous transluminal renal angioplasty and stenting. Repeat renal angiography six months after the procedure revealed no evidence of in-stent restenosis. Blood pressure (BP = 137/76 mmHg) and plasma renin profile (baseline PRA = 23.8 microU/mL; 1 hour post-captopril PRA=22.3 microu/mL) also were normal six months following initial revascularization. Moreover, blood pressure (137/84 mmHg) and renin profile remained normal 2.5 years after the procedure (baseline PRA = 24.3 microU/mL; 1 hour post-captopril = 25.6 microU/mL). The results of this study have thus demonstrated a case of renin-dependent renovascular hypertension in which both the blood pressure and plasma renin activity profile normalized following successful percutaneous transluminal angioplasty and stenting.     

Diagnostic value of the captopril test in patients with arterial hypertension

In 30 patients with renovascular hypertension, 50 with hypertension in a course of arteries, 71 hypertensive subjects with coexisting parenchymal nephropathy and in 63 with primary hypertension the captopril test was performed after 8 hours night rest and within high sodium diet. Positive test result was stated in 76.67% of patients with renovascular hypertension, in 70.59% of patients with arteritis, in 53.52% of patients with hypertension and coexisting parenchymal nephropathy and in 63.49% of patients with primary hypertension. Significant correlation between increase of plasma renin activity and blood pressure decrease after captopril administration was only stated in patients with renovascular hypertension and in those with arteritis. Results of performed studies impaired the captopril test value in diagnostics of renin-dependent hypertension.     

The captopril test for identification of renovascular hypertension: value and immediate adverse effects

Abstract. To develop a screening test for identification of renovascular hypertension, the blood pressure and plasma renin concentration responses to an oral test dose of captopril (6.25 mg) were studied in 47 hypertensive patients of mean age 61 years (range 34-85 years). Blood pressure was measured at 15-min intervals for 90 min after administration of captopril. Blood samples for plasma renin determination were drawn immediately before and 90 min after drug administration. Eleven patients had renal artery stenosis. The fall in diastolic blood pressure in these patients was greater, on average, than in patients with other forms of hypertension (30 mmHg vs. 14 mmHg, P < 0.01), as was the increase in plasma renin concentration (188 mU l^?1 vs. 2 mU l^?1, P < 0.01). This study demonstrates that the short-term captopril test is useful for distinguishing patients with renovascular disease from those with other forms of hypertension. During the test, 7 patients (15%) exhibited reversible cerebral symptoms. In two of these subjects digital subtraction angiography was performed, which revealed stenosis of the carotid artery. Consequently, it is suggested that captopril should not be used in patients with arteriosclerotic stenoses of the carotids.     

Clinical evaluation of the captopril screening test for primary aldosteronism

In order to investigate the validity of angiotensin converting enzyme inhibition with captopril as a screening test for primary aldosteronism (PA), 50 mg of captopril were administered orally to 7 patients with PA, 17 with essential hypertension (EH), 5 with renovascular hypertension (RVH), 2 with renoparenchymal hypertension (RH) and 8 normal volunteers. The plasma aldosterone concentration (PAC) was suppressed to less than 15 ng/dl in all of the EH, RVH and RH patients and normal subjects 90 min after administration of captopril, but not suppressed in 6 of 7 patients with PA. In addition, the plasma renin activity (PRA) was increased to greater than 1 ng/ml/h in 10 of 17 patients with EH and in all with RVH, RH and the normal controls, but to less than that in 6 of 7 PA and the remaining EH patients. The PAC to PRA ratio after captopril was greater than 20 in all patients with PA, while it remained below 20 in EH, RVH and RH patients and normal controls. From these results, we conclude that the PAC to PRA ratio in the captopril administration test is a simple and useful tool to detect PA in hypertensive patients. In addition, the test has a great advantage in that it can be safely applied to outpatients with relatively severe hypertension.     

Sensitivity and specificity of screening tests for renal vascular hypertension.

To facilitate the identification of patients with renal vascular hypertension, we evaluated four potential screening tests: rapid-sequence urography, systolic-diastolic abdominal bruit, upright plasma renin activity (PRA), and response to saralasin infusion. Our study included 379 normal subjects, 199 essential hypertensive patients with normal renal angiograms, and 64 patients with surgically responsive renal vascular hypertension. Thirty-nine percent of patients with renal vascular hypertension had systolic-diastolic bruits, 76% abnormal urograms, and 27% a PRA greater than 30 ng of angiotensin 1/mL.3 h. Only one half of the 23 patients with renal vascular hypertension tested had a depressor response to saralasin, as did two of 13 essential hypertensive patients. In essential hypertensive subjects, 1% had systolic-diastolic bruits, 2% abnormal urograms, and 5% upright renin values greater than 30 ng of angiotensin 1/mL.3 h. The screening combination of urogram, bruit, or upright renin value offered a test sensitivity of 93%, with a specificity of 92%. The results of saralasin infusion failed to increase the diagnostic yield.     

Use of Captopril in the Diagnosis of Renal Hypertension

Abstract: 1 . The effects of a single 25 mg oral dose of captopril on blood pressure, heart rate and circulating renin, angiotensin I, angiotensin II, bradykinin and catecholamine levels were examined in untreated patients with essential (n = 10, Group I), accelerated (n = 6, Group II) and renal hypertension (n = 8, Group III) studied on a normal sodium diet .
2 . Mean blood pressure fell only slightly in Group I patients, (113 ± 3 to 109 ± 3 mmHg at 60 minutes) but a greater fall was observed in Group II (153 ± 8 to 135 ± 11 mmHg) and a marked fall in Group III, (136 ± 3 to 114 ± 5 mmHg). There were no significant changes in heart rate in any group .
3 . Plasma angiotensin II levels were significantly reduced 30 minutes after captopril in all three groups and returned toward resting values after four hours. The falls in plasma angiotensin II levels were accompanied by reciprocal increases in blood angiotensin I and plasma renin, but blood bradykinin and plasma catecholamine concentrations remained unchanged .
4 . Resting plasma renin levels showed considerable overlap in the three groups and the mean renin values were not significantly different in the three groups. After captopril a marked rise in plasma renin concentration (>2.5 ng/ml/hr) was observed in seven patients in Group III, including all six patients with renovascular disease. In contrast, none of the patients with essential hypertension and only one patient with accelerated hypertension had such an increase. Determination of the acute renin and blood pressure responses to converting enzyme inhibition with a single oral dose of captopril appears to be useful in identifying patients with renovascular hypertension .     

Angiotensin I converting enzyme activity in hypertension. Relationship to blood pressure, renin-sodium profiles, and antihypertensive therapy

The activity of the angiotensin I converting enzyme was measured in 55 patients with untreated essential hypertension, 11 patients with untreated renovascular hypertension, five patients with untreated primary aldosteronism, and 23 normotensive subjects. Converting enzyme activity was significantly higher (p less than 0.025 or less) in essential hypertension (28 +/- 1 units/ml) and renovascular hypertension (28.5 +/- 3 units/ml) when compared with the activity in the normotensive subjects (21 +/- 1.5 units/ml). Seventeen (31 percent) of the patients with essential hypertension and three (27 percent) patients with renovascular hypertension had an elevated converting enzyme activity above the mean +2 standard deviations value of the normotensive subjects (32.8 units/ml), ranging from 33 to 55.8 units/ml. Converting enzyme activity was similar in black and white patients and in male and female patients, but it tended to decrease with increasing age in both the hypertensive and the normotensive subjects. In the untreated patients with essential hypertension (n = 55), converting enzyme activity was inversely related to mean arterial pressure and age (r = -0.34, p less than 0.01) and positively related to plasma renin activity (r = 0.31, p less than 0.05). Converting enzyme activity was always decreased during captopril therapy, and it was not affected by beta blockers, but it was increased by diuretics. These findings indicate that converting enzyme activity is elevated in patients with essential and renovascular hypertension.     

High renin hypertension in the elderly

This paper describes clinical features of high renin hypertension in the elderly. Peripheral plasma renin activity ranged from 0 to 20.1 ng/ml/hr in 59 hypertensive in-patients aged 70 to 86. The patients were divided into 2 groups: 9 cases with plasma renin activity greater than or equal to 3.0 ng/ml/hr (high renin group) and the remaining 50 with plasma renin activity less than 3.0 ng/ml/hr (control group). The development of hypertension differed between the 2 groups. Six of the high renin group (66.7%) had a history of acceleration of previously mild hypertension, while only 3 of the control group (6.0%) had this history (p less than 0.01). The frequencies of high diastolic blood pressure (greater than or equal to 120 mmHg), massive proteinuria (at least 3.0 g/day), hypokalemia (serum potassium less than or equal to 3.0 mEq/L) and high serum cholesterol (greater than or equal to 250 mg/100 ml) were significantly greater in the high renin group than in the control group (p less than 0.01, respectively). Renovascular hypertension was suspected in 6 patients from the high renin group (66.7%), as compared with 1 of the control group (2.0%) (p less than 0.001). There was massive proteinuria in 3 of 6 patients with renovascular hypertension in the high renin group and 2 showed nephrotic syndrome. Thus, two-thirds of the elderly patients with high renin hypertension had probable renovascular hypertension with a history of rapid progression of hypertension.     

Conversion of inactive renin to active renin following acute angiotensin converting enzyme inhibition in essential hypertension and renovascular hypertension

The physiological role of inactive renin, especially the question of whether and how a conversion to active renin takes place in vivo, remains controversial. In order to show the dynamic alterations from inactive to active renin following acute ACE-inhibition, both forms of renin were investigated in both renal veins and the peripheral circulation of 20 patients with essential hypertension and 20 patients with renovascular hypertension before and 1 h after 25 mg of captopril. Active and inactive renin were determined indirectly as plasma renin activity (PRA, unit: ng/ml x h). In vitro activation of inactive renin was achieved with trypsin (1 mg/ml plasma), followed by a further determination of PRA (= total renin). Subtraction of the active renin from the total renin yields the amount of inactive renin. In patients with essential hypertension, the mean values of active renin increase equally in both renal veins (1.4 and 1.3 before, 1.9 and 1.8 after captopril) and the peripheral circulation (0.9 and 1.3) (p less than 0.002), whereas the inactive renin decreases correspondingly. Renal veins: 7.6 and 8.2 before, 7.2 and 7.6 after captopril; peripheral circulation: 7.7 before and 7.0 after captopril (p less than 0.05). In all patients with renovascular hypertension, there is basally a marked lateralization of active renin (6.4 vs 3.5; p less than 0.01) and inactive renin (20.5 and 18.9, p less than 0.03) towards the side of the ischemic kidney. After captopril, the values for total renin and active renin increase (p less than 0.001), and the side difference for active renin becomes still more pronounced (33.0 vs 14.2; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Captopril-stimulated renin in the diagnosis of restenosis after percutaneous transluminal renal angioplasty

Recurrence of hypertension is reported in a considerable percentage of renovascular hypertensive patients treated by percutaneous transluminal angioplasty (PTRA); among the possible mechanisms for these failures, restenosis of the renal artery is the only correctable one. Since captopril stimulates renin secretion to a greater extent in renovascular than in essential hypertensive patients, we determined if it could be used to unmask significant restenosis in the patients with hypertension recurring after PTRA. Follow-up study was performed in 28 patients treated with PTRA. We found that captopril caused a greater increase in peripheral plasma renin activity in 8 of 8 cases who had recurrence of hypertension and restenosis than in 13 of 15 of the patients who did not. We suggest that the determination of captopril-stimulated renin may provide a useful, simple and economical tool for the detection of restenosis after PTRA.     

Dynamic evaluation of the renin-angiotensin system with captopril in screening for renovascular hypertension

In 69 hypertensive with suspected renovascular hypertension the response of plasma renin and angiotensin I to a single oral dose of Captopril (Captopril test) was determined. In 15 of the 16 patients found to have renal artery stenosis at angiography and cured by either revascularization or nephrectomy, Captopril stimulated both plasma renin activity and plasma angiotensin I to a far greater extent than in the majority of the 53 classified as essential hypertensives. False positives were limited to 8. Sensitivity and specificity were 94% and 85%, respectively. In the same series sequential renal angiophotoscan showed 100% sensitivity but a lower specificity (75%). In comparison, both the sensitivity and the specificity of rapid-sequence intravenous pielography, isotopic renogram and recumbent plasma renin activity were far less satisfactory. It is concluded that this simple, safe and economical test should be preferred to the other diagnostic procedures in the screening of renovascular hypertension. Its use in combination with renal angiophotoscan improves diagnostic reliability.     

Predicting cardiac morbidity

Captopril was administered for 6 days to 26 severely hypertensive hospitalized patients, 17 with essential hypertension and 9 with renovascular hypertension. All the patients were on a low sodium diet and were treated after the 3rd day in the hospital with progressively increasing doses of captopril (75 to 450 mg/day). Mean blood pressure decreased from 142 ± 20 to 117 ± 18 mm Hg in essential hypertension and from 136 ± 11 to 106 ± 10 mm Hg in renovascular hypertension. Plasma renin activity and aldosterone as well as urinary aldosterone and vasopressin were higher in renovascular hypertension than in essential hypertension. In both groups, captopril decreased similarly plasma aldosterone and urinary aldosterone and vasopressin, whereas plasma renin activity increased.These identical changes in blood pressure and hormonal variables were accompanied by different modifications in urinary sodium excretion, plasma volume and plasma creatinine. Urinary sodium excretion was higher (3.06 ± 1.38 mmol/mmol of urinary creatinine) in treated essential hypertension than in treated renovascular hypertension (1.77 ± 1.01, p < 0.05). Plasma volume was unchanged in essential hypertension and increased by 7.75 ± 7 percent of the normal values (p < .0.2) in renovascular hypertension. Plasma creatinine was slightly but significantly increased in essential hypertension (+6.7 ± 10.7 μmol/liter, p <0.02) and was much more elevated in renovascular hypertension (+45.2 ± 38.3 μmol/liter, p < 0.01).These data demonstrate that captopril is able to decrease similarly the activity of the renin-angiotensin-aldosterone-vasopressin system in essential and renovascular hypertension, whereas its renal effects are different. Marked increases in plasma creatinine were observed among patients with renal artery stenosis. These observations suggest caution in the use of converting enzyme inhibitors in patients with renovascular hypertension, especially those on a low sodium diet.     

Oral calcium treatment lowers blood pressure in renovascular hypertensive rats by suppressing the renin-angiotensin system

The effects of calcium supplementation on blood pressure and its mechanisms were investigated in two-kidney, one clip renovascular hypertensive rats. Two series of experiments were performed: one was begun just after renal artery constriction, the other after the onset of hypertension. Calcium supplementation significantly attenuated the development of hypertension (systolic blood pressure: 183 +/- 8 vs 130 +/- 2 mm Hg) and was found to abate existing renovascular hypertension (systolic blood pressure: from 183 +/- 8 to 151 +/- 4 mm Hg). Calcium treatment did not cause significant alterations in fluid intake, urine volume, or urinary sodium excretion in either study. However, increased plasma renin activity and plasma aldosterone concentration were suppressed to the basal levels at the end of 3 weeks of calcium treatment (14 +/- 3 vs 8 +/- 2 ng angiotensin I/ml/hr; 530 +/- 50 vs 380 +/- 40 pg/ml). Blood pressure of calcium-treated renovascular hypertensive rats responded poorly to blockade of the renin-angiotensin system with captopril injection and angiotensin II analogue (saralasin) infusion. Further, in rats with chronic established renovascular hypertension, calcium treatment attenuated the enhanced pressor response to norepinephrine, but not to angiotensin II. These results suggest that the blood pressure-lowering actions of calcium supplementation are related primarily to suppression of renin secretion and secondarily to alteration of pressor response to norepinephrine in two-kidney, one clip renovascular hypertensive rats.     

Prospective study on the prevalence of secondary hypertension among hypertensive patients visiting a general outpatient clinic in Japan.

Secondary hypertension (SH) including endocrine hypertension has been reported to be uncommon. We estimated the prevalence of SH among hypertensive patients. We prospectively studied 1,020 hypertensive patients. As an initial screening, we measured plasma aldosterone concentration, plasma renin activity, serum cortisol concentration and plasma catecholamine concentration and conducted abdominal ultrasonography (US). As a secondary screening, we performed furosemide plus upright test, captopril renography, dexamethasone suppression test, 24-h urine catecholamine measurement and abdominal CT. Finally, primary aldosteronism with the exception of idiopathic hyperaldosteronism, pheochromocytoma, and Cushing's syndrome were diagnosed by histopathological examination of surgical specimens. Idiopathic hyperaldosteronism was clinically diagnosed by adrenocorticotrophic hormone (ACTH)-stimulated adrenal venous sampling and renovascular hypertension by renal arteriography. There were 61 patients with primary aldosteronism, 5 with renovascular hypertension, 11 with Cushing's syndrome, 10 with preclinical Cushing's syndrome and 6 with pheochromocytoma, and the prevalence of SH was 9.1% among 1,020 hypertensive patients. In 76 (82%) of 93 patients with SH, hypertension was cured or improved after unilateral adrenalectomy, transsphenoidal pituitary adenectomy or percutaneous transluminal angioplasty. With the exception of US and CT, all initial and secondary screening tests were found to be sensitive and specific for differentiating SH from essential hypertension (EH). In conclusion, the measurement of various hormone concentrations was very sensitive for ruling out SH--a condition for which, in the present study, there were few specific signs or symptoms--while CT and US examinations were not always useful for differentiating SH from EH. The prevalence of curable SH among hypertensive subjects was higher in this study, which was conducted by our simple method of screening tests, than in previous reports. Hypertensive patients should be screened for SH and the underlying disease treated appropriately to avoid long-term use of antihypertensive drugs and risks of atherosclerotic complications.     

Effects of converting enzyme inhibition on split renal function in renovascular hypertension

The effects of captopril on effective renal plasma flow and glomerular filtration rate were studied using a noninvasive radioisotopic method on individual kidneys in eight patients with renovascular hypertension and 12 patients with essential hypertension with various renin levels. Four patients with renovascular hypertension had unilateral while three had bilateral renal artery stenosis. The effective renal plasma flow and glomerular filtration rate were determined by using 131I-iodohippurate sodium and 99mTc-diethylenetriamine pentaacetic acid, respectively. Glomerular filtration rate and effective renal plasma flow were significantly reduced in the stenotic kidneys of patients with renovascular hypertension compared with values in nonstenotic kidneys (p less than 0.01). Treatment with captopril, 37.5 to 75 mg/day for 1 to 48 weeks, further reduced the glomerular filtration rate only in stenotic kidneys, and effective renal plasma flow increased in both kidney types. In two of the three renal hypertensive patients with bilateral renal artery stenosis, captopril produced a reversible azotemia that was unrelated to the fall in blood pressure, as evidenced by the lack of azotemia seen after a moderate blood pressure reduction induced by other antihypertensive medications. These results indicate that endogenous angiotensin II is essential in maintaining the glomerular filtration rate in stenotic kidneys and suggest that a reduction in glomerular filtration rate during captopril administration could indicate the presence of renal artery stenosis.