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

We investigated the alteration of the ACE in different parts of the circulation in 21 patients with essential hypertension, who suffered from angina pectoris attacks. Blood samples were taken during diagnostic cardiac catheterisation. The ACE was fluorimetrically measured and compared to 48 normotensive patients. In 11 patients the Plasma Renin Activity (PRA) was additionally determined by means of bioassay. The ACE was significantly (p less than 0.001) elevated in all investigated regions but a different distribution was not observed. We found a positive correlation between the ACE from the left ventricle and the systolic, mean arterial and diastolic blood pressure. Furthermore, we observed a negative correlation between ACE and PRA. No relationship could be calculated between ACE and electrolytes, creatinine or haemodynamic parameters. Our results indicate that the ACE may contribute to the pathogenesis of so-called essential hypertension.
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PMID:Elevated angiotensin-I-converting enzyme (ACE) in patients with essential hypertension. 628 14

Renin-aldosterone function was studied in 23 patients with low-renin essential hypertension (LREH) under resting and stimulated conditions. Patients were selected on the basis of differential diagnostic tests of renin-angiotensin stimulation and inhibition as well as roentgeno-radiologic findings in order to rule out adrenal lesions. The results were compared with those of patients with primary aldosteronism and with essential hypertension where renin activity can be stimulated under similar sodium balance conditions. Intravenous or prolonged furosemide administration was shown to be the test of choice for the diagnosis of renin suppression. The renin-aldosterone system of LREH patients featured subnormal renin activity and normal aldosterone levels in baseline conditions, and the lack of renin stimulation together with limited aldosterone stimulation following functional tests. The analysis of changes in diuresis, natriuresis and the pattern of Na/K coefficient points to a great diuretic and natriuretic effect of furosemide in patients with LREH.
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PMID:[Low renin variant of hypertension: functional relations of the renin-aldosterone pressor system]. 634 88

We developed new sensitive direct radioimmunoassay for human plasma renin. Renin was purified from Haas' preparation utilizing a pepstatin-C6-Sepharose affinity chromatography. Antiserum, prepared by immunizing rabbits with the purified renin, was used for the direct radioimmunoassay at a final dilution of 1:30,000. The antibody was specific for human renal and plasma renin, but did not cross-react with cathepsin D, trypsin, or renins of mouse, dog, and rat. Radioimmunoassay was performed by the double antibody technique using the delayed tracer addition method. In this method, a standard curve was obtained over a range from 0.2 to 8.0 ng/ml. The values from our assay correlated well with total renin activity measured as the generation rate of angiotensin I after trypsin activation (r = 0.78, p less than 0.01), but correlated weakly with active renin activity. This finding disclosed that both active and inactive renin were detected by this method. In normal participants, plasma renin concentration determined by direct radioimmunoassay was increased by standing and furosemide injection. The plasma renin concentration determined by direct radioimmunoassay of patients with essential hypertension (0.7 to 1.7 ng/ml) was not significantly different from values in normal controls (0.8 to 1.9 ng/ml). The values were higher in patients with renovascular hypertension (1.6 to 2.7 ng/ml), malignant hypertension (2.8 to 3.4 ng/ml) and Bartter's syndrome (1.8 to 2.5 ng/ml), but lower in patients with primary aldosteronism (0.4 to 0.8 ng/ml) than in normal controls. This newly developed radioimmunoassay for human renin was sensitive enough to estimate the levels of renin in plasma of patients with low renin hypertension. It provides a new tool for the understanding of the renin-angiotensin system under various clinical conditions.
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PMID:A new sensitive direct radioimmunoassay for human plasma renin and its clinical application. 638 35

A sensitive direct human renin radio-immunoassay has been developed for clinical use. The antigen source was human renal renin purified from Haas' preparation by pepstatin-C6-sepharose affinity chromatography, this was used to prepare a specific human renin antibody. The radio-immunoassay was performed by the double antibody technique using the delayed tracer addition method. Standard curves were obtained over the range 0.2-8.0 ng/ml. Dilution curves of human renal renin and human plasma were superimposable on the standard curve. Both active and inactive renin were detected by this method, and measurements correlated well with total renin activity after trypsin activation. Intra- and inter-assay coefficients of variance were 4.6% and 5.1%, respectively. Renin concentration was higher in patients with renovascular hypertension (1.97 +/- 0.38 ng/ml, mean +/- s.d., n = 10, P less than 0.01), but lower in primary aldosteronism (0.66 +/- 0.16 ng/ml, n = 13, P less than 0.01) compared with essential hypertension (1.38 +/- 0.34 ng/ml, n = 12). This method provides a new tool for the investigation of the renin-angiotensin system in man.
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PMID:Sensitive direct radio-immunoassay for human renin. 640 Mar 70

The renin-aldosterone system contributes to the regulation of arterial pressure and to the maintenance of sodium and potassium balance. Alterations in plasma potassium concentration have opposite and independent effects on renin secretion by the kidney and on aldosterone secretion by the adrenal gland. Renin secretion tends to be inhibited by hyperkalemia and stimulated by potassium depletion. In contrast, increases of plasma potassium directly stimulate aldosterone secretion. This effect of potassium on aldosterone serves as a protective mechanism against the development of hyperkalemia. Conversely, hypokalemia inhibits aldosterone production. Small changes in plasma potassium have a greater effect on aldosterone than on renin secretion. In patients with essential hypertension, diuretic induced alterations in serum potassium concentrations may affect both renin and aldosterone secretion. We have observed that therapy with a thiazide diuretic results in a reduction of serum potassium and a greater increase in renin activity than therapy with the potassium-retaining diuretic, spironolactone, despite comparable natriuretic responses with both drugs. Conversely spironolactone therapy is associated with a greater increase in aldosterone production. The greater effect of thiazides on renin activity and the greater effect of spironolactone on aldosterone production may be related to the thiazide induced reduction of serum potassium and the spironolactone induced increases of serum potassium.
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PMID:[Effects of potassium on renin and aldosterone]. 642 66

A body of evidence indicates that all hypertensive phenomena ranging from mild disorders to fulminant malignant hypertension can be profitably analyzed by assessing the relative contribution of two final determinants of the arterial blood pressure--the degree of arteriolar vasoconstriction and size of the volume filling the arterial tree. The latter function is largely determined by the state of sodium balance. Renin-sodium profiling and separate testing with specific pharmacologic probes are the basic tools for quantifying these factors in individual patients. This bidimensional analysis of blood pressure phenomena has considerable practical value for identifying and treating curable renovascular and adrenocortical forms. Beyond this, the analysis provides pathophysiologic information of practical value for characterizing and treating individual patients in the whole spectrum of human hypertensive diseases including essential hypertension. This new analytical scaffold also identifies key physiologic questions for future research. About 90 percent of the circulating renin occurs in an inactive form as a possible prorenin, which could be an important regulatory point for renin release. In response to stimuli prorenin rises and falls with active renin. Beta blockade may lower active renin by blocking the conversion process. At the physiological level the activation and/or release of renin appears to be primarily determined by sodium-volume changes perceived by a distal tubular mechanism.
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PMID:The renin system for understanding human hypertension: evidence for blood pressure control by a bipolar vasoconstriction-volume mechanism. Prorenin as a determinant of renin secretion. 675 98

Acute hemodynamic changes induced by Betaxolol (B.) were studied in 10 patients (7 men, 3 women, mean age: 36 years), with uncomplicated essential hypertension. The brachial artery was cannulated with a short Teflon catheter and Swan-Ganz catheter was introduced into the pulmonary artery. Brachial (BAP) and Pulmonary arterial pressures (PAP), cardiac output (dye dilution) were recorded before (To) and after intravenous infusion of B. (0.2 mg/kg) during 5 minutes (T1), followed by the infusion of B. at a rate of 0.4 mg/kg during 15 minutes (T2). Cardiac index (C.I.), Stroke index (S.I.), Systemic Vascular (SVR) and Pulmonary Vascular Resistances (PVR), Left Ventricular Stroke Work Index (LVSWI) were calculated. C.I. declined significantly. This resulted from a significant decrease of heart rate, since S.I. was unsignificantly changed. BAP (systolic and mean) decreased significantly, since unsignificant changes of PAP were noted. SVR and PVR were significantly increased and LVSWI was significantly decreased. Plasmatic Renin Activity was unsignificantly decreased.
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PMID:[Acute hemodynamic effects of betaxolol in uncomplicated arterial hypertension in young persons]. 681 Aug 22

Blood pressure, cardiac output, plasma volume, renin, and aldosterone were measured in 13 patients with essential hypertension on placebo and after 1, 4, and 12 wk on hydrochlorothiazide 100 mg daily. In 9 patients the same variables were also measured after 24 and 36 wk. Hydrochlorothiazide lowered mean arterial pressure (p less than 0.01). Cardiac output was reduced after 4 and 12 wk of treatment, followed by a return to placebo levels. Stroke volume changed in the same way but heart rate and total peripheral resistance did not differ from placebo values. Plasma volume was reduced after 1 and 24 wk. Renin was permanently elevated (p less than 0.01), but aldosterone rose only during the first 12 wk of treatment. A comparison between responders (greater than 10% fall in mean arterial pressure) and nonresponders (less than 10% fall) revealed different hemodynamic patterns. In responders the initial fall in cardiac output was followed by a return to pretreatment levels, whereas in nonresponders it was permanently reduced. Consequently, total peripheral resistance was lowered only in responders. Nonresponders tended to show a greater degree of plasma volume depletion and greater stimulation of renin and aldosterone, which probably contributed to elevated peripheral resistance. It is concluded that changes in cardiac output are unlikely to be of decisive importance in the ultimate reduction of peripheral resistance in responders to thiazide therapy.
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PMID:Hemodynamic changes during long-term thiazide treatment of essential hypertension in responders and nonresponders. 698 24

Eight patients with essential hypertension were treated with chlorothizide 250 mg daily for 4 weeks with 500 mg daily for further 8 weeks. Both systolic and diastolic blood pressures (BP) decreased significantly during the lower dosage (p < 0.05). Only the diastolic BP continued decrease during the higher dosage regimen of chlorothiazide (p < 0.05). Plasma renin activity (PRA) and plasma aldosterone (PA) did not increase during the lower dosage of chlorothiazide. During 4 weeks on the dosage of 500 mg of chlorothiazide daily, PRA increased by 79 per cent (p < 0.001) and PA by 66 per cent (p < 0.001) from the level of the lower dosage. During the next 4 weeks, no changes in PRA or PA were seen. The result shows the strong compensatory activation renin-aldosterone system on the usual chlorothiazide therapy. In spite of a decrease in BP, the lower dosage was not accompanied with any significant compensation. Renin-aldosterone system during diuretic therapy not only causes the so-called false tolerance to antihypertensive effect, but also potentiates the loss of potassium. This can best be avoided by using the minimal effective dosage of the diuretic drug.
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PMID:The renin-aldosterone system in low-dose chlorothiazide treatment of hypertensive subjects. 699 21

The acute responsiveness of plasma catecholamine, renin (PRA), and aldosterone levels to exogenous norepinephrine was studied under placebo conditions and following renin (PRA), and aldosterone levels to exogenous norepinephrine was studied under placebo conditions and following renin-angiotensin activation by diuretic pretreatment in 25 normal subjects and 34 patients with borderline-to-moderate essential hypertension. Norepinephrine infusion caused increases in plasma norepinephrine (PNE) that correlated with the infused norepinephrine dose (p < 0.001); this relationship was similar in normal and hypertensive subjects and unaltered by diuretic therapy. Plasma epinephrine and dopamine levels were unchanged during norepinephrine infusion. Norepinephrine infusion at pressor doses stimulated PRA (p < 0.01). The PRA responses correlated with the dose of infused norepinephrine (p < 0.0025), and norepinephrine-stimulated PRA correlated with basal PRA (p < 0.001). These norepinephrine-PRA relationships were unaltered by diuretic treatment and similar in normal and hypertensive subjects. In both groups, norepinephrine also caused a similar increase in plasma aldosterone (p < 0.05) under placebo conditions, but not following diuretic therapy. These findings demonstrate that an acute increase in the blood levels of the adrenergic neurotransmittor, norepinephrine, causes mild but distinct stimulation of plasma renin and aldosterone levels. Renin release in response to exogenous norepinephrine is not enhanced following renin-angiotensin activation by diuretic pretreatment. The responsiveness of the renin-angiotensin-aldosterone system to an acute norepinephrine input seems to be intact in essential hypertension.
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PMID:Effects of short-term norepinephrine infusion on plasma catecholamines, renin, and aldosterone in normal and hypertensive man. 699 68


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