Normal renin uremic hypertension. Study of cardiac hemodynamics, plasma volume, extracellular fluid volume, and the renin angiotensin system.

Studies were undertaken in 33 uremic patients with or without hypertension, 11 normal subjects, and 15 essential hypertensive patients to assess cardiac hemodynamics, plasma volume, extracellular fluid volume, and peripheral renin levels. Cardiac output and intraarterial blood pressure were measured and peripheral vascular resistance index calculated. These studies suggest that uremic hypertension with normal renin values and hypervolemia is hemodynamically sustained by an increase in peripheral resistance rather than by an increased cardiac output. The renin angiotensin system plays a secondary role as compared to overexpansion in the genesis of hypertension in normoreninemic uremic hypertension.     

The physiology of renin secretion in essential hypertension. Estimation of renin secretion rate and renal plasma flow from peripheral and renal vein renin levels

From renin measurements made in blood collected simultaneously from renal veins, aorta and vena cava, an equation was developed for estimating renin secretion rates in patients with three renin subtypes of essential hypertension. From these data a second equation was derived for estimating differential renal plasma flow in patients with unequal kidney perfusion. The latter equation achieves maximum precision when there is no renin secretion from one side.Plasma renin activity was identical in blood collected from the aorta or the vena cava. It was also similar, but higher, in blood collected from either right or left renal veins. The ratio of renin from the two renal veins, an expression of the variability in renal vein renin measurements in essential hypertension, was 1.5 or less in 87 per cent of patients and less than 1.63 in 95 per cent.Renal vein renin content remained proportional to arterial renin over the range of peripheral renin levels found in essential hypertension, so that renal vein renin concentration from each kidney was consistently 124 per cent of arterial renin. The constancy of this relationship complements previous observations indicating that the metabolic clearance rate of renin is proportional to arterial renin levels. The observed equality of renin values between renal veins suggests that differential renal plasma flow is fairly equal and constant in patients with essential hypertension. Moreover, since renal plasma flow from each kidney is inversely related to the increment in renal vein renin concentration relative to arterial renin input [(V-A)/A], differential changes in (V-A)/A can be used to identify differential changes in renal plasma flow.These derived interrelationships are relevant to an analysis of renovascular hypertension since, with this approach, reductions in renal plasma flow can be estimated using only renal vein and arterial renin measurements and adequacy of sampling can be assessed from the sum of (V-A)/A from each kidney.There was no measurable difference in plasma renin substrate in the three renin subgroups of patients with essential hypertension so that observed differences in plasma renin activity levels appear entirely due to differences in renal renin secretion. Under conditions of this study renal renin secretion per minute was 144 times the arterial renin level.     

The role of renal hemodynamics in the antihypertensive effect of captopril

To evaluate the role of regional hemodynamics in mediating the long-term depressor effect of the converting enzyme inhibitor, captopril, at a low dose (37.5 mg/day), for 2 weeks, its systemic, renal, and forearm circulatory actions were determined in 12 patients with mild to moderate essential hypertension. After administration of captopril, there was a significant decline in mean blood pressure (average -12.1 +/- 1.9%) accompanied by a decrease in systemic vascular resistance (-9.1 +/- 3.3%), but cardiac output did not change. Although forearm vascular resistance was not altered, renal vascular resistance decreased considerably (-17.1 +/- 5.0%). Moreover, there was a highly significant (r = 0.891) correlation between the changes in mean blood pressure and renal vascular resistance. Plasma renin activity increased after therapy as plasma aldosterone decreased, while plasma norepinephrine slightly increased. The change in renal vascular resistance significantly (r = -0.617) correlated with the pretreatment level of plasma renin activity. These findings suggest that suppression of the renin-angiotensin system in essential hypertension induces selective vasodilation in the renal vasculature, which may play an important role in the long-term antihypertensive effect of the converting enzyme inhibitor. This renal vasodilator action appears to be the feature that distinguishes the converting enzyme inhibitor from conventional vasodilator drugs.     

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.     

促红细胞生成素导致高血压的临床研究

通过对４０例不同年龄、不同病因的尿毒症维持性血透患者，应用不同剂量的促红素治疗、观察血色素、血粘度、血浆肾素、血管紧张素、心排出量、外周血管阻力以及血压变化等临床指标，发现促红素对肾性贫血的疗效为９０％，但高血压的发生也达３７．５％。高血压的发生与促红素的剂量、患者的年龄；以往有无高血压等有关。高血压发生的时间大部分随着血色素的增加而增高，但少数与此无关，血粘度和心排出量的增加，血浆肾素和血管紧张素的变化在这类高血压的发生中不占主要地位。高血压发生的主要机理是外周血管阻力的增加。     

Systemic and renal effects of a new angiotensin converting enzyme inhibitor, benazepril, in essential hypertension

Seventeen essential hypertensive patients with normal renal function were treated with a new non-sulphydryl orally active angiotensin converting enzyme (ACE) inhibitor, benazepril, 10 mg given once or twice daily, according to diastolic blood pressure levels, for 6 weeks. In all patients, changes in blood pressure, systemic and renal hemodynamics, plasma renin activity and urinary aldosterone and albumin excretions were assessed at the end of a 2-week placebo run-in period and at the end of the study. Benazepril monotherapy controlled blood pressure well. No changes in cardiac output, heart rate or stroke volume were observed, while peripheral vascular resistance was significantly decreased (-11%, P less than 0.05). Plasma volume was unaltered. The glomerular filtration rate was stable, but effective renal plasma flow was increased because of the marked reduction in renal vascular resistance (-35%) and, therefore, the filtration fraction was decreased. Urinary albumin excretion remained unchanged. A significant increase in plasma renin activity (P less than 0.001) and a decrease in urinary aldosterone excretion were seen. No side effects were observed during the treatment period. In conclusion, our results suggest that benazepril alone is an effective antihypertensive agent in patients with essential hypertension. The blood pressure lowering effect is due mainly to systemic vasodilation and is observed up to 24 h after administration of the drug. The vasodilation appears to be more consistent in the renal than in the systemic circulation.     

Hypertension after successful renal transplantation

Thirty-three renal allograft recipients who had high blood pressure (mean arterial pressure more than 105 mm Hg) at least one year after their successful transplant operation were compared with 23 normotensive kidney transplant recipients (mean arterial pressure less than 105 mm Hg) at the General Clinical Research Center. The patients with higher blood pressure had markedly and significantly higher (96 percent) renal vascular resistance and significantly lower (41 percent) renal plasma flow. Responses to salt loading and restriction were suggestive of marked activity of the renin-angiotensin system as were plasma renin activity measurements. Subsequent follow-up has revealed chronic rejection or renal artery stenosis as a probable cause of hypertension for 11 of the 33 patients. The remaining 22 patients had increased renal vascular resistance and decreased renal plasma flow indistinguishable from that in the 11 patients in whom follow-up revealed a cause for their persistent hypertension; however, 21 of these 22 patients have their native kidneys in place.     

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     

Vasodilators, antihypertensive therapy and the kidney

Both traditional and newer treatments of essential hypertension are discussed in relation to kidney function and renal perfusion. In essential hypertension, renal vascular resistance is routinely increased and renal blood flow is often decreased. Reduced sodium intake as a form of therapy will cause a decrease in both renal blood flow and glomerular filtration, most likely due to an angiotensin-induced renal vasoconstriction caused by the reactive increase in renin release. Treatment with diuretics produces the same effects, also angiotensin-mediated. The addition of a beta-adrenergic blocking agent to prevent renin release may be a good choice, but individual agents within this class must be examined for direct renal vasoconstriction. The effects of "nonspecific" vasodilators on renal perfusion and renal sodium handling vary with the patient but may produce antinatriuresis, sodium retention and decrease in glomerular filtration. Studies with calcium antagonists have shown promising results. Nifedipine studies show a substantial increase in renal plasma flow, a well-maintained glomerular filtration rate and a brisk diuresis and natriuresis. However, patients with the lowest baseline renal flow do not show these benefits. Diltiazem has shown a potentiated renal vascular response in normotensive patients of hypertensive parents. Angiotensin converting enzyme inhibitors such as captopril and enalapril have produced increased renal blood flow and well-maintained glomerular filtration in patients with essential hypertension. The agents available for treating hypertension have improved dramatically in the past decade. A salutary effect on the kidney will remain high on the list of important characteristics to be considered in choosing one of these agents.     

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.     

Disparate cardiovascular effects of obesity and arterial hypertension

Since obesity and essential hypertension frequently coexist, a study was designed to analyze some of their cardiovascular effects. Twenty-eight obese patients, half of whom were normotensive and half with established hypertension, were matched for mean arterial pressure with 28 corresponding lean subjects. Systemic and renal hemodynamics, intravascular volume, plasma renin activity, and circulating catecholamine levels were measured. Obese patients had increased cardiac output (p less than 0.001), stroke volume (p less than 0.001), central blood volume (p less than 0.02), plasma and total blood volume (p less than 0.01), and decreased total peripheral resistance (p less than 0.001). In contrast, cardiac output, central blood volume, and stroke volume of hypertensive patients were normal, but they had increased total peripheral (p less than 0.001) and renal vascular resistance (p less than 0.001) and a contracted intravascular volume. Left ventricular stroke work was elevated to a similar level in obesity (p less than 0.001) and hypertension (p less than 0.02), but the increase was caused by an expanded stroke volume in the former and by an increase in systolic pressure in the latter. It is concluded that the disparate effects of obesity and hypertension on total peripheral resistance and intravascular volume counteract and may even offset each other. Thus, obesity may mitigate the effects of chronically elevated total peripheral resistance (and therefore end-organ damage) in essential hypertension. Since both entities affect the heart through different mechanisms, their presence in the same patient results in a double burden to the left ventricle, thereby gently enhancing the long-term risk of congestive failure.     

Relation of renin status to neurogenic vascular resistance in borderline hypertension.

The relation of renin-angiotensin status to general hemodynamics and to neurogenic vascular resistance was studied in patients with border-line hypertension. Plasma renin activity during standing was referred to a standard renin-urinary sodium nomogram derived from 18 normal subjects. Among 22 patients with borderline hypertension the renin level was high in 8, low in 4 and within normal limits in the remaining 10. In patients with borderline hypertension and high or normal levels of plasma renin activity, the blood pressure elevation was due to increased total peripheral vascular resistance. In contrast, in patients with low renin borderline hypertension, total peripheral resistance was not significantly elevated; the blood pressure elevation reflected a cardiac index 12 percent higher than that in normal subjects. The neurogenic contribution to total peripheral vascular resistance was assessed by studying the effects of alpha adrenergic blockade with phentolamine, after prior autonomic blockade of the heart with atropine (0.04 mg/kg body weight) and propranolol (0.2 mg/kg). Phentolamine (15 mg) produced an immediate reduction in total peripheral resistance of 12.0 +/- 6.7 percent in patients with high renin borderline hypertension (P less than 0.01) but no change in normal subjects or those with borderline hypertension and normal or low renin levels. Normalization of the blood pressure followed "total" autonomic blockade with atropine, propranolol or phentolamine only in patients with high renin borderline hypertension. It is concluded from these preliminary data that in high renin borderline hypertension the blood pressure elevation is sustained by neurogenic mechanisms. The elevated renin level in these patients is probably an expression of increased sympathetic nervous activity. Although the elevated plasma renin level may possibly be contributing to the generation of higher sympathetic tone, or data do not support a direct role of circulating angiotensin in the maintenance of the elevated vascular resistance.     

Plasma renin and blood pressure during treatment with methyldopa

Blood pressure and plasma renin activity and concentration were studied before and during administration of alpha methyldopa to normal and hypertensive subjects. Methyldopa produced no significant decrease in renin levels and caused only inconsistent changes in blood pressure in subjects with normal pressure, patients with low renin essential hypertension regardless of severity, or patients with normal renin essential hypertension of mild degree. In contrast, a significant reduction in blood pressure and marked lowering of plasma renin levels were observed after administration of methyldopa in patients with normal renin essential hypertension of moderate to severe degree and in those with hypertensive terminal renal failure. In moderate to severe essential hypertension, methyldopa-lnduced decreases in blood pressure and plasma renin activity were significantly correlated. These data are consistent with the possibility that the hypotensive action of methyldopa may be partially related to Its effect on the renin-angiotensin system. They also lend support to the value of plasma renln determinations In selecting appropriate antlhypertensive drugs for individual patients.     

The pattern of plasma renin activity and aldosterone secretion in normal and hypertensive subjects before and after saline infusions

The pattern of plasma renin activity and aldosterone secretion was studied in 56 unselected patients with essential hypertension and in 10 hypertensive patients with renal complications. The results were compared to responses found in 17 normal subjects and 6 patients with verified primary aldosteronism. In all cases, plasma renin activity and aldosterone secretion rates were measured under precise conditions of metabolic balance, initially during dietary salt restriction and then after physiologic saline infusions.

Abnormally low responses in plasma renin activity to salt restriction were found in 13 patients with essential hypertension (25 percent), and in 4 there was no significant increase with standing. The expected increase in aldosterone secretion also failed to occur in 9 patients, 6 of whom demonstrated low plasma renin activity. The great majority of patients with essential hypertension responded normally to saline infusions with decreased plasma renin activity and aldosterone secretion, but in 4 patients the latter was greater than 300 μg/day after saline infusion. The response of hypertensive patients with renal complications was not different from that seen in uncomplicated cases.

Although there was great variation in the responses seen in individual patients with essential hypertension, the combination of suppressed plasma renin activity and autonomous, excessive aldosterone secretion was found in only 1 patient. In this unselected series, the maximal incidence of primary aldosteronism (using the currently accepted criteria) was less than 5 percent.     

Renin as a risk factor in essential hypertension: More evidence

When patients with essential hypertension are classified into three major subgroups according to their plasma renin levels, they appear to exhibit different physiologic and epidemiologic characteristics. The present study extends previous observations which have suggested that low renin patients are relatively protected from development of heart attacks and strokes.Low renin patients despite the fact that they are older, exhibit lower blood urea levels than patients in the other two groups. These data are in keeping with the idea that low renin patients have relatively less renal vascular involvement.Young hypertensive blacks, known to be most prone to severe hypertension with vascular complications, practically always fall into the normal renin subgroup, whereas, in contrast, a vast majority of those blacks above the age of 50, with relatively milder hypertensive disease, exhibit low renin levels.These new findings which further associate vascular sequellae with the normal or high renin state provide more support for the concept that low renin patients have a relatively benign type of hypertensive disease.Nonhomogeneity of the low renin hypertensive population and differences in methodologic and physiologic approaches used to define such patients may provide the basis for conflicting observations from certain laboratories.     

Furosemide and plasma renin activity in essential hypertension.

Changes in arterial blood pressure, renal electrolyte excretion, and plasma renin activity in response to repeated doses of furosemide were measured in 12 patients with essential hypertension admitted to the medical service for electrolyte balance studies. Eighty and 120 mg/day furosemide in divided doses for 5 to 10 days produced a prompt increase in renal sodium excretion. Urinary Na/K concentration ratios, which were elevated during peak natriuresis, returned to control levels following the initial diuretic response. In 2 patients with high initial levels of plasma renin activity, arterial blood pressure was not reduced by furosemide, and more potent antihypertensive agents were required to control the blood pressure. In the remaining patients, furosemide produced a significant decrease in systolic and diastolic blood pressure. There was a general upward shift of plasma renin levels in terms of 24-hour renal sodium excretion in those who demonstrated an antihypertensive response to the drug. However, the average increase in plasma renin activity after repeated doses of furosemide was not statistically significant and no correlation was demonstrated between the level of plasma renin activity after furosemide and the blood pressure lowering effect of the drug.     

Acute responses to urapidil in hypertensive persons

Urapidil is a new antihypertensive agent involving both a peripheral and a central mode of action. To evaluate the acute effects of this drug on renal vascular tone and on pressor systems a randomized placebo-controlled crossover study was conducted in 10 patients with uncomplicated essential hypertension. Each subject received, on 2 separate days 1 week apart, an intravenous injection of either placebo or urapidil (25 or, if necessary, 50 mg). Before and after this injection blood pressure and heart rate (Dinamap), renal plasma flow (125I-hippuran), active plasma renin concentration, angiotensin II, aldosterone and catecholamines in plasma were measured. The results show that urapidil, when compared with placebo, greatly reduced blood pressure, while increasing heart rate, renal blood flow, and noradrenaline and adrenaline levels. However, dopamine levels were suppressed. Whereas renin and angiotensin II were only mildly stimulated, aldosterone levels increased significantly. It is concluded that urapidil, given intravenously, has an immediate blood pressure-lowering effect associated with a decrease in renal vascular tone and an increase in renal perfusion. Consequently, both the sympathetic and renin-angiotensin systems are stimulated, although the latter only to a mild degree. The increase in aldosterone may be partially related to the decrease in dopamine levels.     

Changes in active and inactive renin and in angiotensin II across the kidney in essential hypertension and renal artery stenosis

Investigations were performed in 26 patients with essential hypertension and 24 with unilateral renal artery stenosis. In each patient blood was drawn simultaneously and in triplicate, from both renal veins and aorta, for measurement of plasma concentrations of active and inactive renin and of angiotensin II. In 19 patients estimates of individual renal plasma flow were obtained in order to calculate secretion rates for active and inactive renin, and to assess the contribution of renin secretion rate and of renal plasma flow to the renal vein renin ratio. In patients with essential hypertension there was evidence that the kidney secreted active renin (18% mean increase in renal vein concentration above that of arterial plasma; P less than 0.001), but no evidence of secretion of inactive renin (4% mean increase; NS). There was a tendency for the kidney to extract angiotensin II (8% mean decrease in renal vein concentration below that of arterial plasma; P = 0.07). The affected kidney in patients with renal artery stenosis showed marked secretion of active renin (364% mean increase; P less than 0.001) and also secreted inactive renin (80% mean increase; P less than 0.05) with net generation of angiotensin II across the renal circulation (100% mean increase; P less than 0.05). The contralateral kidney exhibited suppressed secretion of active renin (3% mean increase; NS) with no evidence of secretion of inactive renin (2% mean increase; NS), and marked extraction of angiotensin II (50% mean decrease; P less than 0.001). The correlation between combined secretion rate of active renin by both kidneys and the arterial concentration of active renin in patients with essential and renovascular hypertension taken together was strongly positive (r = 0.82; P less than 0.01). The same correlation for inactive renin was weak (r = 0.32; NS). The correlation between the combined secretion rates of active renin by both kidneys and the circulating plasma concentration of angiotensin II (r = +0.60; P less than 0.05) was both significant and positive. By contrast, the total 'secretion' rate of angiotensin II by both kidneys was inversely related to arterial plasma angiotensin II (r = -0.92; P less than 0.001). This latter relationship suggests an important role for the kidney in clearing angiotensin II from the circulation, this being more marked the higher the arterial angiotensin II concentration.(ABSTRACT TRUNCATED AT 400 WORDS)     

Renal vascular resistance in essential hypertension: duplex-Doppler ultrasonographic evaluation

Duplex Doppler ultrasonography has been validated as a noninvasive method to evaluate hemodynamic features of renal blood flow in renal and intrarenal arteries in patients with various renal diseases. The significance of duplex Doppler sonography in the evaluation of renal vascular resistance in essential hypertension has not yet been clearly determined. The aim of the present study was to evaluate the renal vascular resistance in patients with essential hypertension by measuring intrarenal arterial resistance (RI) and to correlate RI with renal functional tests and other clinical and laboratory data. Duplex Doppler ultrasonography was used to measure RIs in intrarenal arteries in 128 patients with essential hypertension and 61 age-matched normotensive control examinees. The renal vascular resistance index (RI) was determined by use of Doppler ultrasound. Hypertension was classified according to the 1997 Joint National Committee Guidelines (JNC-VI). Mean RI in hypertensive patients was 0.66 +/- 0.05 (+/- sd) and in healthy controls 0.60 +/- 0.03 (+/- sd) (p = 0.0001). RI correlated significantly with patient's age (r = 0.577, p = 0.001), duration of hypertension (r = 0.335, p= 0.001), stage of hypertension according to the JNC-VI classification (r = 0.315, p = 0.006), creatinine clearance (r = -0.383, p = 0.001), systolic blood pressure (SBP, r = 0.41, p = 0.001) and mean blood pressure (MBP, r = 0.30, p = 0.002). RI values did not correlate significantly with plasma renin concentration (r = -0.198 NS), diastolic blood pressure (DBP, r = 0.17, p = 0.06), and cardiac pulse (r = -0.10, p = 0.16). Multiple regression analysis showed that independent variables for RI were the patient's age (multiple R = 0.53, signif. F = 0.001) and systolic blood pressure (multiple R = 0.57, signif. F = 0.03). The renal Doppler resistance index (RI) is increased in essential hypertension and it correlates with renal functional tests as well as with patient's age, duration of hypertension, with a stage of hypertension according to the JNC-VI classification, and with systolic and mean blood pressure. The increased renal vascular resistance (RI) in hypertensive patients could be a sign of developing hypertensive nephrosclerosis and consequently renal failure. The utilization of the renal vascular resistance index (RI), provides a new noninvasive parameter in the followup of patients with essential hypertension.     

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)