Biomedical subjects

S Akabane

Publications and source records attributed to S Akabane.

At least 19 recordsLinked to original sources

PubMed1992

Angiotensin II does not increase renal prostaglandin E2 in response to pressure reduction.

Whether angiotensin II (Ang II) stimulates renal secretion of prostaglandin E2 (PGE2) synthesized in response to pressure reduction was examined. PGE2 and Ang II in aortic and renal venous plasma were measured before and during renal arterial constriction in anesthetized dogs, with or without an intrarenal arterial infusion of an Ang II antagonist, losartan potassium (1 mg/min), or saralasin (3 micrograms/min). In other anesthetized dogs, two doses of Ang II (30 and then 300 ng/min) were infused into the renal artery, and plasma Ang II levels and renal PGE2 secretion were measured. When renal perfusion pressure was reduced to 75 and 45 mm Hg by constriction, the renal secretion of PGE2 increased seven- and fourfold, respectively. Ang II levels in the renal venous plasma increased from 6.6 +/- 1.8 to 21.7 +/- 7.4 and then 48.1 +/- 15.3 pg/ml (both P less than 0.05) as the pressure decreased. Neither losartan nor saralasin suppressed the response of renal PGE2 secretion to the pressure reduction. The intrarenal infusion of Ang II (30 ng/min) elevated the Ang II level in the renal venous plasma from 9.8 +/- 4.6 to 33.7 +/- 4.2 pg/ml (P less than 0.01), but did not increase PGE2 secretion. The higher dose (300 ng/min) of Ang II increased it, but the Ang II level in the renal venous plasma was 166 +/- 63 pg/ml. These results suggest that the greater part of the increased renal synthesis of PGE2 in response to pressure reduction is not mediated by Ang II.

Angiotensin II↗

PubMed1992

Critical degree of renal arterial stenosis that causes hypertension in dogs.

The minimum degree of renal arterial stenosis needed to cause hypertension was identified by renal arterial angiography of anesthetized dogs. The effects of renal nerves and prostanoids on the critical stenosis were also examined. The left renal artery was constricted concentrically by a radiolucent constrictor device, and the stenosis of the artery was evaluated by cineangiography with the kidney either innervated or denervated. At this time, renal blood flow, renal perfusion pressure, and systemic blood pressure were serially monitored. In another group of dogs, renal venous and aortic blood samples were taken as the stenosis increased; these were assayed for prostaglandin E2 and plasma renin activity. The same experiments were done again after treatment with a cyclooxygenase inhibitor, aspirin DL-lysine (54 mg/kg). With the kidney either innervated or denervated, systemic blood pressure began to increase when the stenosis was more than 70% of the diameter of the renal artery; the renal blood flow decreased when the stenosis was more than 75% of the diameter. Aspirin treatment attenuated the increase in blood pressure but did not affect the autoregulation of the renal blood flow when stenosis was 70% or less. Prostaglandin E2 production increased in the stenotic kidney when the stenosis was more than 70%; aspirin inhibited prostaglandin synthesis and suppressed the stimulation of renin release. These results suggest that whether there is innervation or not, the critical degree of renal arterial stenosis that causes hypertension is more than about 70% of the diameter in the presence of renal prostaglandins; in their absence, the critical point above which hypertension occurs is 75% or more.

Animals↗

PubMed1991

Effects of brain natriuretic peptide on renin secretion in normal and hypertonic saline-infused kidney.

The effects of brain natriuretic peptide (BNP) on renin secretion were evaluated in normal and hypertonic saline-infused kidneys of anesthetized dogs. In the normal kidney (N = 5), intrarenal infusion of porcine BNP-(1-26) (pBNP) at a dose of 50 ng/kg per min attenuated the renin secretion rate significantly to 9 +/- 27% of control without exerting a significant effect on mean arterial pressure (MAP), renal blood flow (RBF) or glomerular filtration rate (GFR); urine flow (V) was significantly increased to 260 +/- 33% of control and urinary excretion of sodium (UNaV) to 480 +/- 140% of control. In the hypertonic saline infusion group (N = 6), intrarenal infusion of hypertonic saline (20% w/v) at 0.5, 0.8, and 1.0 mEq NaCl/min caused a decrease in GFR and natriuresis in a dose-dependent manner. The renin secretion rate was attenuated by hypertonic saline infusion (1 mEq NaCl/min) to 87 +/- 31% of control. In another group (N = 6), administration of pBNP at a dose of 50 ng/kg per min during hypertonic saline infusion (1 mEq NaCl/min) increased the renin secretion rate to 196 +/- 57%, increased RBF to 160 +/- 13%, increased GFR to 137 +/- 22%, increased V to 221 +/- 29%, and increased UNaV to 218 +/- 29% of the values measured during hypertonic saline infusion. Our results indicate that BNP inhibits renin secretion through sodium delivery to the macula densa and effectively inhibits the tubuloglomerular feedback response that is activated by intrarenal hypertonic saline infusion.

Animals↗

PubMed1991

Effect of alpha 1-blockade on diminished forearm blood flow in diabetics.

An increased risk of atherosclerotic disease has been reported in patients with diabetes mellitus. The present study was therefore designed to determine forearm blood flow (FBF) in patients with essential hypertension or those with diabetes mellitus with or without hypertension. FBF determined by venous occlusion plethysmography decreased with age in controls as well as in patients with essential hypertension, whereas FBF in diabetics was significantly lower irrespective of age or blood pressure. As a result, vascular resistance was significantly higher in diabetics than in controls or patients with essential hypertension. Glycemic control in normotensive diabetics during 3 weeks significantly augmented a diminished FBF. alpha 1-Blockade by oral administration of 1 mg of prazosin also augmented the diminished FBF in diabetics, in association with a significant decrease in mean blood pressure and vascular resistance. These results suggest that FBF may be a simple and useful index for determining arterial and/or venous distensibility, and that alpha 1-blocker therapy, in addition to glycemic control, may be a first-line antihypertensive treatment for diabetics with associated hypertension.

Administration, Oral↗

PubMed1991

Effect of dietary calcium on renal prostaglandins.

The present study was designed to clarify the possible role of renal prostaglandins (PGs) on blood pressure (BP) regulation during calcium (Ca) restriction or supplementation. Twelve normotensive women with a mean age of 21.2 years participated in the study. After 1 week of normal Ca intake (mean +/- SE, 536 +/- 2 mg/day), a low-Ca diet (163 +/- 1 mg/day) was given for a further 1 week. Additional asparagine Ca (3 g as Ca/day) was also given to half of the subjects. BP, heart rate, and serum total and ionized Ca concentrations were measured at the end of each period. Levels of Ca, sodium, PGE2, 6-keto-PGF1 alpha and thromboxane (TX) B2 excreted into urine were also determined. The plasma level of ionized Ca was significantly increased without any change in total Ca in both groups. Low and high Ca intake decreased and increased urinary Ca excretion by 28% and 56%, respectively. BP was not altered after Ca deprivation or loading. However, urinary PGE2 excretion was significantly augmented from 668.9 +/- 68.1 to 959.7 +/- 183.1 ng/day by Ca loading, whereas Ca deprivation decreased PGE2 excretion (695.4 +/- 108.1 to 513.2 +/- 55.2 ng/day). No changes were observed in 6-keto-PGF1 alpha or TXB2 urinary excretion. These results suggest that renal PGE2 synthesis is stimulated or decreased by 1-week Ca loading or deprivation, indicating a possible antihypertensive role of renal PGE2 during high-Ca intake in hypertensives.

6-Ketoprostaglandin F1 alpha↗

PubMed1991

Aspirin test for differentiation of unilateral renovascular hypertension from hyperreninemic essential hypertension.

Responses of renin release and blood pressure to aspirin DL-lysine (ASP) were examined to find out if the responses could help in the differentiation between unilateral renovascular hypertension (RVH) and hyperreninemic essential hypertension (EHT). The two studies involved ten patients with unilateral RVH, eight with hyperreninemic EHT, and five with hyporeninemic EHT. In a radiological study, before and 30 min after an intravenous injection of ASP (18 mg/kg), renal venous and abdominal aortic plasma was sampled and assayed for prostaglandin (PG) E2 and plasma renin activity (PRA). Systemic blood pressure was measured serially. The reproducibility of the responses to ASP was confirmed in a bedside study. In unilateral RVH, ASP suppressed renin release from the stenotic kidney and reduced the renal vein PRA ratio to less than 1.5 via the inhibition of PG synthesis, which is accelerated in that kidney. The mean suppression of aortic PRA at this dose of ASP was 35% in these patients, and their blood pressure decreased in proportion to the suppression of PRA. However, in the two EHT groups, ASP elevated the mean blood pressure. The renal synthesis of PGE2 was inhibited by ASP in all patients, but the suppression of PRA, while small, was significant (19% in the aorta) in the patients with hyperreninemic EHT, and not significant in patients with hyporeninemic EHT. The different responses of blood pressure and PRA to ASP between RVH and EHT were reproducible in the bedside study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Effects of ouabain and verapamil on endothelin-1-induced contraction of mesenteric artery in young spontaneously hypertensive rats.

We studied the effects of ouabain and verapamil on endothelin-1(ET-1)-induced contraction of the mesenteric artery in prehypertensive spontaneously hypertensive rats (SHRs) and age-matched Wistar-Kyoto (WKY) rats. Rings of mesenteric artery of SHRs and WKY rats aged 4 weeks were superfused with physiological saline solution and isometric tension was measured. ET-1 (10(-9) or 10(-8) M)-induced contractions were significantly larger in WKY rats than in SHRs. ET-1 (10(-7) M)-induced contractions were not significantly different between SHRs and WKY rats. Verapamil markedly inhibited ET-1 (10(-7) M)-induced contractions both in SHRs and in WKY rats. Although the percent inhibition tended to be larger in SHRs than in WKY rats, the difference was not significant. Ouabain significantly increased ET-1 (10(-7) M)-induced contraction in the presence of verapamil both in SHRs and in WKY rats. The increase was significantly greater in SHRs than in WKY rats. As a result, ET-1 (10(-7) M)-induced contractions were significantly greater in SHRs than in WKY rats in the presence of verapamil and ouabain. These results suggest that in ET-1-induced arterial contraction, [Na+]i-mediated [Ca2+]i regulation such as the Na+/Ca2+ exchange system might be greater in SHRs than in WKY rats, and that this might be, at least in part, involved in the pathogenesis or maintenance of hypertension in SHRs.

Animals↗

PubMed1991

Differential effects of endothelin-1 and big endothelin on canine kidneys.

Renal effects of endothelin-1 (ET-1, human, 1-21) and the equivalent molar concentration of big ET (human, 1-38) and the contributions of prostaglandins and endothelium-derived relaxing factor to these actions were examined. Intrarenal infusion of ET-1, at a dose of 0.4 pmol/kg/min, decreased renal blood flow (RBF), glomerular filtration rate (GFR), and urine output (V) to 62, 70, and 45% of control values, respectively. Additional aspirin-DL-lysine (ASP) treatment (25 mg/kg) caused marked decreases in RBF, GFR, and V to 20, 14, and 9% of control values, respectively. During ET-1 infusion, intrarenal infusion of NG-monomethyl-L-arginine (L-NMMA, 1 mumol/min) caused decreases in RBF, GFR, and V. In another group, intrarenal infusion of big ET at a dose equivalent to that of ET-1 did not significantly affect RBF, GFR, or urine output, which were 95, 107, and 84% of control values, respectively. Additional ASP treatment decreased these values to 78, 69, and 52% of control values, respectively. L-NMMA infusion during big ET infusion showed little effect on renal function. Our study demonstrated that intrarenal infusion of ET-1, at a dose of 0.4 pmol/kg/min, caused significant hemodynamic and functional changes in the canine kidney compared with an equivalent molar concentration of big ET.

Animals↗

PubMed1991

Immunoreactive endothelin-1 contents in brain regions from spontaneously hypertensive rats.

To investigate the possible role of brain endothelin-1 (ET-1) in hypertension of spontaneously hypertensive rats (SHRs), we measured immunoreactive (ir) ET-1 contents in brain regions as well as plasma ir-ET-1 levels in SHRs aged 4-5 and 12-14 weeks and age-matched Wistar-Kyoto rats (WKY) with a radioimmunoassay for ET-1. Systolic blood pressures of SHR aged 4-5 and 12-14 weeks were significantly higher than those of corresponding WKY. Significant amounts of ir-ET-1 were detectable throughout the discrete brain regions analyzed in both strains; higher ir-ET-1 contents in structures such as thalamus, hypothalamus, midbrain, pons, medulla, and cerebellum, with the lowest in cerebral cortex, were observed. A reverse-phase high-performance liquid chromatography of the brain extracts revealed the presence of both a major component identical to the elution position of synthetic ET-1 and a minor component possibly corresponding to its oxidized form. When compared, ir-ET-1 contents in all brain regions analyzed were lower in SHRs than in WKY rats. This strain-related change of ir-ET-1 contents was significant in the medulla at 4-5 weeks of age, and in all brain regions except hypothalamus at 12-14 weeks of age. Plasma ir-ET-1 levels, in contrast, were comparable between SHRs and WKY rats. These results suggest that brain ET-1 may be involved in the development and the maintenance of hypertension in SHRs.

Aging↗

PubMed1991

Acute and chronic effects of anti-endothelin-1 antibody on blood pressure in spontaneously hypertensive rats.

To evaluate the significance of endogenous endothelin (ET) in the maintenance of blood pressure in hypertensive and normotensive conditions, we examined the acute and chronic effects of anti-ET-1 antibody in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats. Immunoglobulin (Ig) solution purified from anti-ET-1 rabbit serum was injected intravenously in conscious rats aged 12-14 weeks (SHR: n = 7, WKY: n = 7). In the control group (SHR: n = 5, WKY: n = 4), Ig prepared from nonimmune rabbit serum was administered. One week after the first injections of Ig, second intravenous injections were given. After the intravenous injections of ET-1 antibody, there were no significant changes in directly measured blood pressure (BP) for up to 60 min in both strains. On the first, third, and seventh days after the first administration of ET-1 antibody, as well as on the first, third, and seventh days after the second injection, there were no appreciable differences in BP between SHR treated with anti-ET-1 antibody and SHR with control Ig. No significant changes in BP were observed throughout the observation period in WKY groups. Plasma levels of immunoreactive ET-1 were similar in SHR and WKY. This study suggests that circulating ET may not play a significant role in the maintenance of hypertension in SHRs or in the regulation of blood pressure in WKY rats.

Animals↗

PubMed1991

Effect of dietary calcium on serum BGP (osteocalcin).

The present study was designed to clarify the effects of dietary calcium (Ca) intake on serum BGP (osteocalcin) levels. Twelve women with a mean age of 21.2 years participated in the study. After one week of normal Ca intake (mean +/- SE, 535 +/- 2 mg/day), a low-Ca diet (163 +/- 1 mg/day) was given for one further week. Additional asparagine Ca (3 g as Ca/day) was also given to half of the subjects. Serum total and ionized Ca concentrations as well as BGP, PTH and 1,25(OH)2D3 were measured at the end of each period. Amounts of Ca and hydroxyproline excreted in urine were also determined. The plasma level of ionized Ca was significantly increased without any change in total Ca in either group. Low and high Ca intake decreased and increased urinary Ca excretion by 28% and 56%, respectively. Serum levels of BGP and 1,25(OH)2D3 were significantly augmented along with a transient increase in urinary hydroxyproline excretion after Ca deprivation. These results suggest that serum BGP is increased after one week of Ca restriction in healthy subjects.

Adult↗

PubMed1991

[Noninvasive evaluation of arteriosclerotic changes in patients with diabetes mellitus].

In order to evaluate atherosclerotic changes in diabetes mellitus (DM), pulse wave velocity (PWV), forearm blood flow (FBF: by venous occlusion strain gauge plethysmography), forearm vascular resistance (VR: mean arterial pressure/FBF) and radial artery blood velocity (RABV: by ultrasonic Doppler) were determined noninvasively in healthy controls (n = 15) as well as age-matched diabetic patients with (DMHT, n = 11) or without hypertension (DMNT, n = 21). Both in controls and diabetic subjects, PWV demonstrated a significant positive correlation with age. Diabetics tended to show higher, although not significantly higher, PWV in comparison with controls. In controls, but not in diabetics, FBF and VR respectively demonstrated a significant negative and positive relationship with age. Diabetics younger than 50 years had a lower FBF and a higher VR in comparison with age-matched controls. In the DMHT group, FBF was significantly attenuated. There was no difference in RABV between controls and diabetic group. PWV did not correlate with FBF or VR. However, FBF did show a significant negative correlation with VR. RABV negatively correlated with FBF in diabetics, indicating that FBF may reflect distensibility in forearm arteries and veins. These results suggest that FBF may be a better arteriosclerotic index for resistance vessels and DM or hypertension may accelerate arteriosclerotic changes.

Arteriosclerosis↗

PubMed1991

Aspirin injection test to predict angioplasty outcome in unilateral renovascular hypertension: preliminary report.

We examined the usefulness of aspirin DL-lysine for prediction of the outcome of renal artery angioplasty in renovascular hypertension. The study was carried out in eight hypertensive patients with unilateral renal artery stenosis: six were free from azotemia and two had slight azotemia. Before and 30 min after an intravenous injection of aspirin DL-lysine (18 mg/kg), renal venous and abdominal aortic plasma was sampled and assayed for prostaglandin E2 and plasma renin activity. Blood pressure and heart rate were serially measured at this time. Renal angioplasty was later performed and was technically successful in all patients. In the six patients without azotemia, aspirin inhibited renal prostaglandin E2 synthesis and suppressed renin release from the ischemic kidney, resulting in lowered blood pressure. Renal angioplasty caused plasma renin activity to become normal and lowered high blood pressure. The reduction in blood pressure by angioplasty was correlated with the responses of blood pressure and renin release to aspirin. However, in the two patients with azotemia, aspirin neither suppressed renin release nor lowered blood pressure. Their hypertension was not reduced by the angioplasty. These results indicate that an aspirin injection test could be useful for prediction of the outcome of angioplasty in unilateral renovascular hypertension.

Adult↗

PubMed1990

Mechanisms of intracellular pH regulation in the hamster inner medullary collecting duct perfused in vitro.

To examine the mechanisms of H+ transport in the mid-inner medullary collecting duct of hamsters, we measured the intracellular pH (pHi) in the in vitro perfused tubules by microscopic fluorometry using 2',7'-bis(carboxyethyl)-carboxyfluorescein (BCECF) as a fluorescent probe. In the basal condition, pHi was 6.74 +/- 0.04 (n = 45) in HCO3(-)-free modified Ringer solution. Either elimination of Na+ from the bath or addition of amiloride (1 mM) to the bath produced a reversible fall in pHi. After acid loading with 25 mM NH4Cl, pHi spontaneously recovered with an initial recovery rate of 0.096 +/- 0.012 (n = 23) pH unit/min. In the absence of ambient Na+, after removal of NH+4, the pHi remained low (5.95 +/- 0.10, n = 8) and showed no signs of recovery. Subsequent restoration of Na+ only in the lumen had no effect on pHi. However, when Na+ in the bath was returned to the control level, pHi recovered completely Amiloride (1 mM) in the bath completely inhibited the Na(-)-dependent pHi recovery. Furthermore, elimination of Na+ from the bath, but not from the lumen, decreased pHi from 6.97 +/- 0.07 to 6.44 +/- 0.05 (n = 12) in the HCO3-/Ringer solution or 6.70 +/- 0.03 to 6.02 +/- 0.5 pH unit/min in the presence of CO2/HCO3-, whereas it did not recover in the absence of CO2/HCO3-.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗

PubMed1990

Possible role of renal prostaglandin E2 in natriuresis associated with supraventricular tachycardia.

We investigated the possible role of renal prostaglandin (PG) E2 in natriuresis associated with supraventricular tachycardia (SVT). In five female patients with paroxysmal tachycardia, SVT was artificially induced and then stopped 60 min later. Before, during, and after SVT, plasma levels of arginine vasopressin and atrial natriuretic peptide (ANP) and the urinary excretion of sodium and PGE2 were measured. Polyuria was observed during SVT. However, natriuresis did not occur until immediately after the termination of SVT. During SVT, the plasma levels of arginine vasopressin tended to decrease. When SVT was terminated, the vasopressin levels increased significantly (p less than 0.01). Urinary excretion of PGE2 tended to decrease during SVT and then increased significantly (p less than 0.01) after SVT ended. Urinary excretion of sodium was correlated (r = 0.699, p less than 0.001) with the urinary excretion of PGE2. Plasma ANP increased during SVT, but there was no correlation with urinary sodium excretion. These results suggest that renal PGE2, the biosynthesis of which may be stimulated by a increase in plasma vasopressin, is an important factor contributing to the natriuresis observed after the end of SVT.

Adult↗

PubMed1990

A comparison of lisinopril with enalapril by monitoring plasma angiotensin II levels in humans.

The present study was designed to examine and compare the acute effects of lisinopril (20 mg) and enalapril (10 mg) after a single oral administration on the inhibition of the renin-angiotensin system (RAS) in eight normal subjects. Serum concentration of lisinopril and enalaprilat, an active metabolite of enalapril, reached the respective maximal levels at 6 and 4 hr after administration of the drugs. At 24 hr, the serum concentration of lisinopril was higher than that of enalapril; thus the rate of disappearance of lisinopril was retarded, in comparison to that of enalapril. The reduction of serum angiotensin I converting enzyme (ACE) activity was consistent with the pattern of increase of concentration of the drugs in the serum. However, with these two drugs, the concentration of plasma ANG II was decreased in a similar manner, and it returned to the pretreatment level within 24 hr. Thus, there was no significant difference in ANG II levels throughout the 24 hr-study between the lisinopril and enalapril treatment. The results indicate that a single administration of 20 mg lisinopril and 10 mg enalapril show similar potency for lowering the circulating ANG II level, although lisinopril exerts a more sustained inhibition of serum ACE activity. The measurement of ANG II provides useful informations for evaluating the efficacy of ACE inhibitors for the inhibition of circulatory RAS.

Administration, Oral↗

PubMed1989

Alterations in cerebrospinal fluid angiotensin II by sodium intake in patients with essential hypertension.

1. Angiotensin (ANG) levels were measured in the cerebrospinal fluid of 15 patients with essential hypertension on a high sodium diet for 1 week and on a low sodium diet for a further week. ANGs were determined using a system of extraction by Sep-Pak cartridges followed by h.p.l.c. combined with radioimmunoassay. 2. Sodium depletion resulted in increases of ANG II in the cerebrospinal fluid from 1.16 +/- 0.38 (SEM) to 1.83 +/- 0.43 fmol/ml (P less than 0.01) and of ANG III from 0.65 +/- 0.11 to 0.86 +/- 0.15 fmol/ml (P less than 0.01). 3. The ANG II level in the cerebrospinal fluid was found to be unchanged and recovery of added ANG II was approximately 90%, even after incubation for 3 h, on both diets. Thus, it is unlikely that ANG II is produced or degraded in the cerebrospinal fluid in vitro. 4. There was no significant correlation between the cerebrospinal fluid and the plasma ANG II concentration on the low sodium diet. 5. These results suggest that the cerebrospinal fluid ANG II level increases with sodium depletion, and that the effect of the level of ANG II on the activity of the angiotensin-forming system in the central nervous system may be assessed by determination of ANG II in the cerebrospinal fluid in patients with essential hypertension.

Adult↗

PubMed1989

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)

Adult↗