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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Purpose of this study has been to compare the results obtained using two different procedures in blood sampling from the renal veins for measuring renal venous renin. The first is the classical procedure which employs three catheters for simultaneous sampling from both renal veins and from the inferior vena cava, or from an artery. The other one is a simplified procedure which employs a single catheter that allows blood to be collected in the following rapid sequential manner: right renal vein, inferior vena cava, left renal vein, inferior vena cava. We have studied 13 patients (8 with essential hypertension, 5 with unilateral renal artery stenosis). Two catheters were introduced through a femoral vein and inserted into both renal veins; a third catheter was inserted into the femoral artery; then the blood sampling was performed strictly simultaneously. Soon after, the blood sampling was repeated according to the above mentioned sequential single catheter procedure. PRA was measured by Angiotensin I radioimmunoassay, then the Renal Vein Ratios (RVRR) were calculated. Even though as average of less than 20 seconds elapsed between the blood sampling in a renal vein and that in inferior vena cava, our results demonstrate that the release of renin can vary so quickly that erroneous informations may be obtained unless a strictly simultaneous sampling of blood is performed. In conclusion, our study demonstrates that the only reliable renal vein renin sampling procedure must employ the simultaneous renal venous and arterial (or inferior vena cava) blood collection.
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PMID:[Methodology of renal vein renin study: comparison between simultaneous and sequential sampling (author's transl)]. 700 41

Vasoconstriction-volume analysis postulates that arteriolar vasoconstriction is the mechanism of blood pressure elevation in patients with "high-renin" essential hypertension while a volume expanded state with relatively dilated arterioles sustains "low renin" essential hypertension. To test this hypothesis we carried out hemodynamic and PRA studies in 43 essential hypertensives. Cardiac index was directly related to PRA (r=0,41; p less than 0,01), by contrast, peripheral vascular resistances and plasma volume were unrelated to PRA. The data do not support the bipolar hypothesis since vasoconstriction and volume expansion are associated with unpredictable changes in PRA. The direct relationship between CI and PRA may be interpreted as the result of a common factor (presumably sympathetic nervous system) governing both functions.
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PMID:[Functional relationships between plasma renin activity and hemodynamic indices in essential arterial hypertension]. 700 11

In view of the possible role of prostaglandins /PG/ in the pathogenesis of hypertension we have determined PGE2 and PGF2 alpha levels simultaneously with plasma renin activity/PRA/ in renal venous and caval venous blood in 13 patients with unilateral renal artery stenosis/RAS/ and in six untreated patients with unilateral parenchymal renal disease/PRD/. Four patients with essential hypertension were the control group. PG levels and PRA were estimated by RIA. In patients with RAS the mean PGE2 level as well as PRA was higher on the side of the stenosis. No such difference was found in the PGF2 alpha level. There was a significant correlation between the renal vein PGE2 ratio and renin ratio /stenotic side versus contralateral side/ r=0.520, 0.02 less than p less than 0.05. In patients with PRD prostaglandin levels in venous blood of the affected kidney were similar to that of venous caval blood, but markedly elevated in the venous blood of the contralateral kidney. PRA was similar on both sides. The data obtained in this study indicate, that prostaglandins in renal venous blood behave differently in hypertensive patients with RAS and PRD. In patients with RAS augmented PGE2 release may serve as a protective mechanism. In patients with PRD, the increased PG level in the non-affected kidney may reflect a compensatory mechanism in spite of the atrophic process in the affected kidney.
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PMID:Prostaglandin levels and renin activity in renal venous blood of patients with renal hypertension. 701 74

Hemodynamic effects of [Sar1, Ile8] AII, an angiotensin II analog, were studied in 30 patients with essential hypertension, who were subdivided into 11 low renin, 10 normal renin and 9 high renin groups according to low, normal and high PRA values both before and after furosemide administration (80 mg, orally) plus 4 h of ambulation, respectively. [Sar1, Ile8] AII infusion (600 ng/kg/min) produced significant increases in mean blood pressure (MBP) and total peripheral resistance index (TPRI) in normal renin and low renin groups and significant decreases in MBP and TPRI in high renin group, while the cardiac index and heart rate remained unchanged during the infusion in these three groups. Change in MBP at 30 min of [Sar1, Ile8] AII infusion correlated significantly with alteration in TPRI in 23 patients with essential hypertension, who completed the 30-min infusion. The response of both MBP and TPRI to [SAR1, Ile8] AII also correlated significantly with basal PRA. These results suggest that blood pressure response to [SAR1, Ile8] AII in essential hypertension is primarily due to alteration in total peripheral resistance and that direction and amplitude of the response of both MBP and TPRI are practically dependent on basal PRA levels.
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PMID:Hemodynamic effects of [Sar1, Ile8] AII, an angiotensin II analog, in the renin subgroups of essential hypertension. 701 85

The angiotensin I-converting enzyme inhibitor, captopril (SQ 14225) was proposed as first treatment in 12 cases of uncomplicated essential hypertension maintained on unrestricted sodium intake (group I). Arterial pressure was normalized in 7 patients (subgroup Ia) whilst hydrochlorothiazide was added to captopril in 5 patients (subgroup Ib). A significant dose-response curve between the dose of captopril (range 75 to 450 mg/day) and the antihypertensive effect was obtained with a maximum at 300 mg/day. In 8 patients (group II) hydrochlorothiazide was proposed first and the addition of captopril was necessary in 4 cases. No relationship between pretreatment PRA and the maximum effect of captopril was observed (r = -0.34, NS). No disturbance of upright blood pressure regulation was noted. Adverse reaction consisted of 4 cases of benign and spontaneously regressive skin rash or pruritus.
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PMID:[Effect of captopril in essential hypertension (author's transl)]. 702 49

To investigate the pathogenic role of the sympathetic nervous system and the renin-angiotensin system in essential hypertension, we evaluated plasma catecholamine and PRA levels after glucagon stimulation and during one hour in upright posture after i.v. injection of furosemide. In nine normal and high renin essential hypertensive (NHRH) subjects, i.v. injection of 1000 micrograms of glucagon caused rapid and significant increases in plasma epinephrine(E) concentration. Both the 5 min. level after glucagon injection (314 +/- 30 pg/ml, mean +/- S.E., p less than 0.05) and peak value (358 +/- 87 pg/ml, p less than 0.05) were significantly higher than the basal level(170 +/- 25 pg/ml). Plasma norepinephrine(NE) concentration of the peak value(1065 +/- 231 pg/ml) was significantly higher than the basal(357 +/- 50 pg/ml, p less than 0.02). PRA levels increased in 4 out of 9 patients. In seven patients with low renin essential hypertension(LRH), there was an impaired PRA response to glucagon, E also failed to increase at any time after glucagon injection, but peak value of NE(1212 +/- 274 pg/ml) was significantly higher than the basal level(391 +/- 77 pg/ml, p less than 0.01). NE level of NHRH during one hour in upright posture after i.v. injection of 40 mg of furosemide were higher than LRH. Particularly at 10 min. level, the NE level of NHRH(895 +/- 115 pg/ml) was significantly higher than LRH(523 +/- 91 pg/ml, p less than 0.05). These results suggest that the sympathetic-adrenomedullary function in LRH is diminished, and the renin secreting ability of JG cells is also diminished in LRH. The glucagon stimulation test is useful to assess renin secreting ability of JG cells.
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PMID:[Response of plasma catecholamine and PRA to i.v. injection of glucagon in upright posture after furosemide injection in essential hypertension (author's transl)]. 702 7

Low PRA and active renin (AR) may be accompanied by low inactive renin (IR), indicating impaired renin production, or by normal or elevated IR, suggesting defective conversion to AR. To explore these possibilities, plasma AR and IR (acid activation method) were measured in normal volunteers and in patients with low PRA. All low renin states showed significant low PRA and AR when compared to normals; on the other hand, IR was 11.8 +/- 1.1 ng/ml.h in normals; low in primary aldosteronism (2.1 +/- 0.5 ng/ml.h) and anephric subjects; normal in low renin essential hypertension (7.5 +/- 1.3 ng/ml.h), nondiabetic hyporeninemic hypoaldosteronism (9.4 +/- 1.6 ng/ml.h) and diabetic hyporeninemic hypoaldosteronism (17.3 +/- 2.5 ng/ml.h); and significantly elevated in diabetics with nephropathy (21.0 +/- 1.6 ng/ml.h). The acute iv infusion of 2 liters saline in normal subjects did not decrease IR (11.8 +/- 2.0 vs. 13.0 +/- 1.8 ng/ml.h) despite a reduction in PRA and AR of 50-75%. These data indicate that in cases of primary aldosteronism and in anephric subjects both AR and IR are decreased, suggesting a decrease in total renal synthesis or release, whereas in low renin essential hypertension, nondiabetic hyporeninemic hypoaldosteronism, diabetic hyporeninemic aldosteronism, and diabetics with nephropathy AR is low and IR is normal or high, suggesting the possibility of impaired conversion to AR.
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PMID:Active and inactive renin in low renin states: studies in human plasma. 702 85

PRA is suppressed in approximately 25% of patients with essential hypertension. To determine if renin suppression precedes the onset of hypertension, PRA and plasma aldosterone were measured before and after treadmill exercise in 129 young adults with relatively high, intermediate, or relatively low blood pressures sustained over 5 yr. PRA and aldosterone responses to exercise were lower (P less than 0.01) in the high blood pressure group. In contrast, plasma renin substrate was lower (P less than 0.01) in the low blood pressure group. Unrelated to blood pressure, PRA, but not aldosterone, was lower in black than in white subjects both before and after exercise. In conclusion, renin suppression precedes the onset of hypertension and may be an appropriate response to higher levels of arterial pressure.
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PMID:Low renin-aldosterone in "prehypertensive" young adults. 703 16

To examine the mechanisms underlying the sensitivity to sodium intake in a subset of patients with essential hypertension, we studied the effects of different sodium intake (10, 100, 200 mEq/day) on blood pressure, the function of the renin-angiotensin-aldosterone system, and on blood levels of catecholamines in 20 patients with essential hypertension and 10 normal subjects. Mean blood pressure (MBP) was not different in hypertensive and normal subjects during low sodium diet. But, with high sodium intake, MBP increased by at least 10% in 12 patients (salt-sensitive), whereas in the remaining 8 patients (salt-resistant) and in normal subjects, MBP did not change significantly. This phenomenon cannot be attributed to differences in sodium retention because the percent change in body weight ad the urinary sodium excretion in the salt-sensitive patients was not different than it was in salt-resistant patients or in normal subjects. The observed difference in blood pressure response to high sodium intake in salt-sensitive patients is also not dependent on an impaired suppressibility of the renin-angiotensin-aldosterone system because there were no significant differences in the basal levels of PRA and aldosterone between the groups, and because the orthostatic increments in PRA were significantly lower in salt sensitive than they were in the salt-resistant patients and in normal subjects. Plasma norepinephrine (NE) levels were not significantly different between normal subjects or hypertensive patients while on low sodium intake. But during high sodium intake, they decreased significantly (P less than 0.05) in normal subjects (from 22 +/- 3.4 to 12 +/- 2.3 ng/dl) and in salt-resistant patients (from 17 +/- 4.5 to 13 +/- 2.4 ng/dl) but not in salt-sensitive patients (from 20 +/- 1.9 to 22 +/- 3.2 ng/dl). Furthermore, the majority of salt-sensitive patients displayed inappropriately high plasma NE in relation to their urine excretion of sodium during high sodium intake. Finally, the increments in plasma NE after 5 min of standing were significantly greater in salt-sensitive patients than they were in salt-resistant patients and normal subjects during both low or high sodium intake. These data indicate that a subset of patients with essential hypertension may have impaired suppressibility of plasma NE during high sodium intake, which suggests hyperactivity of the sympathetic nervous system in these patients. These aberrations may be responsible for the increase in MBP in the salt-sensitive patients during high sodium intake.
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PMID:Abnormal relationship between sodium intake and sympathetic nervous system activity in salt-sensitive patients with essential hypertension. 706 99

Although propranolol administration produces a lowering of PRA, PAC does not decrease in a similar fashion. In the present study the effects of propranolol on the aldosterone MCR were examined. Eight patients with essential hypertension were studied while receiving treatment with a diuretic and again after propranolol (160 to 320 mg/day) was added to the therapeutic regimen. Propranolol therapy was associated with a 25% decrease in PRA (p less than 0.05) and changes in PACs that were variable but not significantly different from diuretic therapy alone. The aldosterone MCR decreased from 1420 +/- 120 to 1120 +/- 90 L/24 hr in response to propranolol (p less than 0.01). The average production rate of aldosterone (MCR X PAC) did not change after propranolol treatment despite a decrease in PRA. There were no changes in plasma concentrations of potassium or in ACTH secretion (as reflected by levels of cortisol) to explain a role for propranolol to sustain aldosterone secretion. Thus propranolol administered to hypertensive patients pretreated with a diuretic can affect circulating levels of aldosterone apart from changes in PRA. Propranolol therapy produces a moderate reduction in aldosterone MCR and appears to augment aldosterone production by a mechanism exclusive of known stimuli.
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PMID:Effects of propranolol on aldosterone plasma concentration and aldosterone metabolic clearance in hypertensive patients. 736 15


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