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.     

The captopril test for identifying renovascular disease in hypertensive patients

To develop a screening test for identifying renovascular hypertension, the blood pressure and plasma renin activity responses to an oral test dose of captopril were studied in 246 quietly seated hypertensive patients. The following criteria were developed that exploit the hyperresponsiveness of renin secretion in renovascular hypertensive patients: a 60-minute post-captopril plasma renin activity of 12 ng/ml per hour or more and an absolute plasma renin activity increase of 10 ng/ml per hour or more, along with a 150 percent increase in plasma renin activity (or a 400 percent increase if the baseline plasma renin activity was below 3 ng/ml per hour). Retrospectively, the test identified, among 200 hypertensive patients without evidence of renal dysfunction, all 56 patients with proved renovascular disease. In this group, false-positive results occurred only in two of 112 patients with essential hypertension and in six with secondary hypertension. Nine untreated patients had blood pressure levels of less than 160/100 mm Hg. The test was neither as sensitive nor specific in the 46 patients with renal insufficiency. This study demonstrates that the renin response to oral captopril is a useful screening test for identifying patients with unilateral or bilateral renovascular disease. Since the test also characterizes the renin dependency of the hypertension, it may have other diagnostic and therapeutic uses.     

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.     

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.     

Effects of a single administration of captopril on hemodynamics and serum angiotensin converting enzyme activity, plasma renin activity and plasma aldosterone concentration in hypertensive patients

Hemodynamic responses and behaviors of the renin-angiotensin-aldosterone system to a single administration of captopril (50 mg) were studied in 16 hypertensive patients (essential hypertension, n = 10; renovascular hypertension, n = 3; primary aldosteronism, n = 2; Cushing's syndrome, n = 1). In 10 essential hypertensive patients, the immediate blood pressure reduction caused by decreased total peripheral resistance after the administration of captopril was observed without changes of cardiac output and heart rate. Serum angiotensin converting enzyme activity and plasma aldosterone concentration significantly decreased, whereas plasma renin activity significantly elevated 2 hours after the administration of captopril. The close relationship between the pretreatment value of plasma renin activity and the maximum decrease in mean blood pressure in 16 hypertensive patients suggests that the depressor response to a single administration of captopril could evaluate the degree of angiotensin II dependency in the maintenance of high blood pressure in various types of hypertension.     

Adenosine in renin-dependent renovascular hypertension

Our previous studies support the hypothesis that activation of the renin-angiotensin system by renal ischemia elevates adenosine levels and that adenosine acts in a negative feedback loop to limit renin release and to mitigate some of the hypertension-producing effects of angiotensin II. To further test this hypothesis, we compared the time course of caffeine-induced increases in plasma renin activity with the time course of changes in plasma levels of adenosine in two models of renin-dependent renovascular hypertension. Also, we compared the effects of caffeine on plasma renin activity and arterial blood pressure in renin-dependent versus renin-independent renovascular hypertension. In comparison to sham-operated rats, plasma levels of adenosine in the left and right renal veins and aorta were elevated severalfold in two-kidney, one clip rats (2K1C) 1 week after left renal artery clipping. However, adenosine levels declined during the second and third weeks after clipping. In 2K1C rats treated chronically with caffeine, plasma renin activity was markedly elevated during the first week after operation as compared to non-caffeine-treated 2K1C rats. However, during the second and third weeks after clipping, caffeine had lesser effects on plasma renin activity. A temporal relationship between plasma adenosine levels and caffeine-induced hyperreninemia was also observed in rats with aortic ligation. Caffeine accelerated hypertension in 2K1C rats and rats with aortic ligation (renin-dependent renovascular hypertension), but it had no effect on plasma renin activity or blood pressure in one-kidney, one clip rats (renin-independent renovascular hypertension). These results lend further support to the hypothesis that adenosine functions to mitigate the renin-angiotensin system in renin-dependent renovascular hypertension.     

Hemodynamic effects of captopril in essential hypertension, renovascular hypertension and cardiac failure: correlations with short- and long-term effects on plasma renin

The hemodynamic effects of captopril were investigated in 22 patients with essential hypertension, 22 with hypertension and renal artery stenosis and 14 with refractory chronic heart failure. The effects of a first dose of captopril, 50 mg orally, were observed for 2 hours, and the effects of repeated doses, 450 mg/day in combination with mild dietary sodium restriction, for at least 4 weeks.Short-term captopril treatment caused similar reductions in blood pressure in the three patient groups, that is, 21 ± 3 mm Hg in essential hypertension, 29 ± 6 mm Hg in renovascular hypertension and 21 ± 2 mm Hg in heart failure (mean ± standard error of the mean) despite large differences in pretreatment plasma renin. Heart rate and cardiac output did not change in hypertensive patients, and cardiac filling pressures decreased. The changes in right atrial pressure, pulmonary artery pressure and pulmonary capillary wedge pressure in essential hypertension and in renovascular hypertension did not differ. Heart rate decreased and cardiac output increased in heart failure, whereas cardiac filling pressures decreased. Blood pressure responses to long-term captopril therapy in essential and in renovascular hypertension were similar and, as with short-term treatment, changes in blood pressure were largely determined by changes in peripheral resistance. Several measurements of extracellular fluid volume showed no evidence of fluid retention by the kidneys.Short-term but not long-term blood pressure responses were correlated with pretreatment plasma renin (percent change in mean arterial pressure, short-term, versus log renin, r = 0.47, p < 0.001, n = 14). Both short- and long-term responses of total peripheral resistance were correlated with plasma renin (percent change in resistance, short-term versus log renin, r = 0.64, p < 0.001, n = 40; percent change in resistance, long-term versus log renin, r = 0.56, p < 0.001, n = 31). The correlations were weak and probably not important for clinical practice. These data indicate that other factors besides circulating renin are important in captopril's hypotensive effect. The favorable hemodynamic effects of converting enzyme inhibition warrant further consideration of this principle of therapy in the clinical management of most forms of hypertension and also in the treatment of chronic heart failure.     

Aspirin lowers blood pressure in patients with renovascular hypertension

To clarify the role of renal prostanoid in hyperreninemia and high blood pressure in human renovascular hypertension, we measured prostaglandin E2 and renin activity in renal venous and abdominal aortic plasma before and after the intravenous administration of the cyclooxygenase inhibitor, aspirin DL-lysine. Subjects were six patients with unilateral renovascular hypertension and six with essential hypertension. In patients with renovascular hypertension, prostaglandin E2 concentration in renal venous plasma from the stenotic kidney was 9.25 +/- 1.48 pg/ml, which was significantly higher (p less than 0.01) than the concentration in the renal venous plasma from the normal kidney (4.97 +/- 1.02 pg/ml) or in the aortic plasma (2.59 +/- 0.15 pg/ml). Plasma renin activity was also higher in the renal vein of the stenotic kidney than in the other two sites. The stenotic side/normal side ratio of the renal venous prostaglandin E2 correlated significantly with a renin ratio greater than 1.5 (r = 0.8211, p less than 0.05). Intravenous injection of aspirin DL-lysine (18 mg/kg) 30 minutes later markedly suppressed prostaglandin E2 and renin levels at all sites and clearly lowered arterial blood pressure (mean: from 120 +/- 6 to 110 +/- 5 mm Hg, p less than 0.01). The reduction in blood pressure correlated significantly with the suppression of plasma renin activity in the aorta (p less than 0.05) and in the renal vein of the stenotic kidney (p less than 0.01). Conversely, in patients with essential hypertension, aspirin had little effect on renin levels and increased mean blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Effect of angiotensin blockade and converting enzyme inhibition on renovascular hypertension: comparison between unilateral and bilateral renal artery stenosis

The response to angiotensin II analog infusion during sodium deletion and the effects of a one-month captopril treatment were compared between 15 renovascular hypertensive patients with unilateral and 6 with bilateral renal artery stenosis. Plasma renin activity, its response to sodium depletion, and the renal vein renin ratio during sodium depletion were greater in unilateral than in bilateral stenosis. A fall in diastolic blood pressure induced by analog infusion during sodium depletion was correlated with the preinfusion plasma renin activity and with the renal vein renin ratio. Treatment with captopril showed a comparable hypotensive effect in unilateral and bilateral stenosis. The reduction in blood pressure was not correlated with the pretreatment renin levels or changes in blood pressure observed during analog infusion. Plasma renin activity rose and plasma aldosterone level fell in all patients. These results indicate that the mechanism maintaining high blood pressure is more renin dependent in unilateral than in bilateral stenosis and that the long-term effect of captopril does not depend solely on the suppression of the renin-angiotensin-aldosterone system.     

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.     

Long-Term Effects of Converting Enzyme Inhibitors on Split Renal Function in Renovascular Hypertension

Long-term effects of angiotensin converting enzyme inhibitors on split renal function were studied using a noninvasive radioisotopic method in five patients with renovascular hypertension. In the stenotic side the glomerular filtration rate which acutely decreased following captopril, tended to return toward pretreatment levels on prolonged captopril administration (up to 2 years), while the value remained unchanged in the nonstenotic side of the kidney. Effective renal plasma flow increased in both sides. During long-term captopril treatment, there were no significant changes in serum creatinine, sodium, potassium, and blood pressure control was maintained at the same level in an acute period. These results suggest that the glomerular filtration in the stenotic kidney of renovascular hypertension, which was acutely reduced, will not further deteriorate, but will increase after prolonged captopril treatment.     

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 .     

Renal venous renin in patients with renovascular hypertension.

Renal venous and peripheral plasma renin activities were determined in 29 operated patients with renovascular hypertension and in 10 patients with essential hypertension. The majority of patients with renovascular hypertension exhibited elevated peripheral plasma renin activity, but the most striking increase of renin activity was demonstrated in the venous effluent of the involved kidney. Using data obtained in patients with essential hypertension, the ratio of renal vein renin activity not exceeding 1.4 was assumed normal. In patients with renovascular hypertension, the values above 1.4 were accepted as lateralizing ratios. In 78.6 % of patients with unilateral renal artery stenosis and a lateralizing renal vein renin ratio, normotension or improvement of blood pressure control were obtained post-operatively. The discussion emphasis the importances of renal vein renin estimations with the calculation of renal vein ratio for determining the functional significance of renal artery stenosis and for predicting the surgical outcome     

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)     

Endogenous adenosine restrains renin release in conscious rats

The purpose of this study was to test the hypothesis that endogenous adenosine functions to restrain the renin release response to pharmacological and pathophysiological stimuli. To achieve this objective, we examined the effects of an adenosine receptor antagonist, 1,3-dipropyl-8-(p-sulfophenyl)xanthine (DPSPX), on the renin release response induced by acute administration of hydralazine or by chronic clipping of the left renal artery (renovascular hypertensive rats). In conscious, unrestrained rats, DPSPX significantly increased plasma renin activity (PRA) in control rats, in rats treated with hydralazine, and in renovascular hypertensive rats. The effect of DPSPX on PRA was significantly greater in rats treated with hydralazine or in renovascular hypertensive rats compared with control rats. DPSPX did not influence arterial blood pressure in any group, did not affect the measurement of PRA, and did not alter the elimination of renin activity from the circulation. Additional experiments were performed in the in situ autoperfused kidney so that the effects of DPSPX on renal hemodynamics and renal excretory function could be assessed. In this experimental model, DPSPX also increased PRA in hydralazine-treated rats and in renovascular hypertensive rats without affecting arterial pressure, renal blood flow, or sodium excretion. In a final set of studies in conscious, unrestrained rats, adenosine deaminase increased PRA in a dose-dependent manner in hydralazine-treated rats and significantly increased the slope of the relation between PRA and the depressor response to hydralazine. We conclude: 1) Although the kidney has both A1 and A2 adenosine receptors mediating inhibitory and stimulatory actions, respectively, on renin release, the dominant effect of endogenous adenosine on renin release is inhibitory. 2) Even under basal physiological conditions, endogenous adenosine tonically inhibits renin release. 3) This inhibitory effect is augmented whenever the renin-angiotensin system is stimulated regardless of the approach used to activate renin release. 4) Endogenous adenosine negatively modulates renin release by a direct effect on juxtaglomerular cells.     

Angiotensin II is a necessary component for the development of hypertension in the two kidney, one clip rat

The current study was undertaken to define the role of the renin-angiotensin system in the development of hypertension in the two kidney, one clip Goldblatt rat. Captopril was administered orally (100 mg/kg/day) to two groups of rats (n = 8 each) 24 hours before and each day after unilateral renal artery clipping (0.2 mm internal diameter): the drug was given for either 16 weeks (group I) or 24 weeks (group II). Sham-operated (n = 5) and Goldblatt (n = 8) rats not receiving captopril were prepared for comparisons of plasma renin activity and systolic blood pressure. Indomethacin (20 mg/kg/day subcutaneously) was administered for 48 hours concomitantly with captopril to the rats in group I. In group II, systolic blood pressure was monitored for 7 weeks after cessation of captopril. Continual captopril administration to Goldblatt rats completely prevented the rise in systolic blood pressure, a rise that was observed in Goldblatt rats not receiving captopril. Whereas systolic blood pressure of captopril-treated rats approximated 100 mm Hg throughout the study, that of Goldblatt rats not receiving the drug increased to nearly 180 mm Hg within 6 weeks after clipping. Systolic blood pressure of sham-operated rats remained normal. Indomethacin did not change systolic blood pressure in the drug-treated rats in group I. On cessation of captopril therapy in group II, systolic blood pressure increased gradually in a manner that paralleled the development of the disease in the Goldblatt rats that did not receive captopril. Plasma renin activity was determined in Goldblatt and sham-operated rats at either 16 weeks (group I) or 24 weeks (group II) after clipping; the rats from either group with mild hypertension (systolic blood pressure less than 180 mm Hg) had normal plasma renin activity whereas those with severe hypertension (systolic blood pressure greater than 180 mm Hg) had greatly elevated plasma renin activity. In summary, captopril can completely prevent the increase in systolic blood pressure for up to 24 weeks in Goldblatt rats, and this hypotensive effect is not mediated by the prostaglandins. It is concluded that the renin-angiotensin system is a necessary component of the hypertensive process in this experimental model.     

Active and inactive renin after a single dose of captopril in hypertensive patients

In 25 hypertensive patients (15 with renal artery stenosis and 10 with essential hypertension), captopril, in a single 12.5 mg dose, caused a prompt decrease in arterial pressure without changing the heart rate. Plasma active and trypsin-activated renin significantly increased, whereas inactive renin and plasma aldosterone decreased. The plasma active/ inactive renin ratio was also increased, suggesting that captopril, together with a release of active renin, may induce an in vivo activation of inactive renin.No correlations were found between blood pressure changes and both pretreatment and captopril-induced variations of active, inactive and trypsin-activated renin or the active/inactive ratio. However, the percent decrease in mean arterial pressure was significantly related to the increase in the active/inactive renin ratio in a group of patients whose blood pressure was brought to normal (r = ?0.78; p < 0.001). This finding suggests the possibility that vasodilating substances, in addition to inhibiting angiotensin II formation, might play some role both in exerting a full effect of captopril on blood pressure and in triggering the in vivo mechanisms of inactive renin activation.     

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.     

Oral angiotensin-converting enzyme inhibitor in long-term treatment of hypertensive patients.

The antihypertensive effect of the orally active angiotensin-converting enzyme inhibitor captopril (SQ 14225) was assessed in 22 hypertensive patients of whom 17 were followed for periods ranging from 1 to 7 months. Of these, eight had essential hypertension, eight had renovascular hypertension, and six had hypertension associated with chronic renal failure. Blood pressure decreased markedly in all patients, including those with low renin levels. Nevertheless, the magnitude of blood pressure reduction correlated with the base-line plasma renin activity (r = 0.58, P less than 0.01). Increasing the dose of captopril from 25 to 200 mg did not enhance the amplitude of the antihypertensive effect but did increase its duration. Patients' blood pressure remained well controlled and free of side-effects with a maximal daily dose of up to 200 mg by mouth twice daily. Despite the blood pressure reduction, sodium excretion tended to increase, probably because of reduced aldosterone secretion. There was no evidence of orthostatic hypotension, and no escape from the antihypertensive effect was observed. These results indicate that chronic inhibition of the angiotensin-converting enzyme with an orally active compound offers a new, efficient, and well-tolerated approach to the treatment of hypertension.