Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Captopril was used in 21 patients with various forms of stable and malignant hypertension. In symptomatic hypertension the drug had a good antihypertensive effect. When applied in patients with essential hypertension caused by chronic diffuse glomerulonephritis or chronic pyelonephritis captopril neither increased pathological changes in the urine, nor inhibited renal function.
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PMID:[Effect of captopril on the level of arterial pressure and functional state of the kidney in symptomatic (renal) stable and malignant arterial hypertension]. 635 26

In order to investigate the antidiuretic hormone (ADH) in essential hypertension and secondary hypertension, plasma ADH levels were measured in normal subjects, in patients with normal and low essential hypertension, and in other patients with various forms of secondary hypertension. Plasma ADH levels were significantly lower in low renin essential hypertension and higher in malignant hypertension than in normal subjects. The plasma ADH levels tended to be lower in renal hypertension and primary aldosteronism, and higher in renovascular hypertension, but these differences were not statistically significant. From these results, it appeared that ADH might play a role in malignant hypertension, but not in the other hypertensive diseases.
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PMID:Plasma antidiuretic hormone levels in patients with normal and low renin essential hypertension, and secondary hypertension. 636 8

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

Total kininogen (Kgn), kallikrein, and prekallikrein were measured in patients with malignant hypertension (MH), essential hypertension (EH), normotensive control (NC), and hypertension and chronic renal failure (HRF). These components of the kallikrein-kinin system were related to the levels of creatinine and fibrinogen. High molecular weight Kgn and low molecular weight Kgn were also measured in blood samples from a peripheral vein, arterial blood, and suprahepatic vein in NC, EH, and MH. Results showed that total Kgn levels were diminished in MH and this diminution could not be ascribed to decreases in renal function, hematocrit, or fibrinogen levels. Appropriate antihypertensive treatment for over 1 year did not normalize Kgn levels in 10 of 11 patients. High molecular weight Kgn and low molecular weight Kgn were both diminished in MH (0.26 +/- 0.04 nmol bradykinin/ml and 0.93 +/- 0.12 nmol lysyl-bradykinin/ml, respectively) as compared to NC (0.39 +/- 0.07 and 1.92 +/- 0.16) and EH (0.51 +/- 0.07 and 1.65 +/- 0.13). Higher concentrations of high molecular weight Kgn were demonstrated in the suprahepatic vein as compared to arterial blood, demonstrating its synthesis by the liver. However, patients with MH had a diminished capacity to synthetize high molecular weight Kgn. A decrease in synthesis of high molecular weight Kgn may be a partial explanation for low levels of total Kgn. It is suggested that a lack of Kgn may play a role in the pathogenesis of MH.
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PMID:Malignant hypertension: a syndrome accompanied by plasmatic diminution of low and high molecular weight kininogens. 655 4

Many studies have suggested that there is an association between the sodium status, plasma renin and aldosterone profile and essential hypertension. We measured serum, urine and red blood cell (RBC) sodium and potassium, plasma renin and aldosterone levels in normotensive Whites, normotensive Blacks, mildly hypertensive Blacks, severely hypertensive Blacks and Blacks with malignant hypertension. There were no important differences between the groups studied as regarded the serum sodium, serum potassium and urinary sodium excretion values. However, the urinary potassium excretion was significantly lower in normotensive and hypertensive Blacks than in Whites. RBC sodium concentrations showed no significant differences in the mean values across the range of degrees of hypertension in Blacks, although they tended to be higher in the more severely hypertensive groups. Blacks with mild-to-moderate hypertension as well as the severely hypertensive group had significantly lower plasma renin levels than the normotensive group; only in the malignant hypertensives with advanced renal failure did the plasma renin and aldosterone levels rise.
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PMID:Sodium and potassium status, plasma renin and aldosterone profiles in normotensive and hypertensive Johannesburg blacks. 675 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

Plasma and kidney renin activity (PRA, KRA) were determined in the spontaneously hypertensive (SHR) rats, the stroke-resistant and -prone substrains (SHRSR, SHRSP) from 5 to 30 weeks of age. Results were compared with those of two normotensive strains, Wistar-Kyoto (WKY) and Donryu (DON) rats. PRA in the SHRSP at 20 and 30 weeks of age were significantly increased when compared to other strains of rats (P < 0.01). In SHRSP rats at these ages, blood pressure exceeded the critical level of 220 mmHg and cerebral lesions were observed in 41% at autopsy. There were no significant differences in PRA among other hypertensive and normotensive strains. KRA in three substrains of the SHR were normal or subnormal as compared to WKY and DON rats. These results indicate that a direct role of the renin-angiotensin system in the SHR and its substrains can be excluded in the initiation and the maintenance of hypertension. However, the activated renin-angiotensin system in SHRSP rats in the course of malignant hypertension at 20 weeks of age and later, could participate in raising blood pressure above the levels of the SHR and SHRSR. Considering out data and others, there are many similarities in renin profile between the SHR and its two substrains, and human essential hypertension in which PRA can be classified as low, normal or high.
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PMID:Variation of plasma and kidney renin activities among substrains of spontaneously hypertensive rats. 699 83

Plasma levels of kininogen, kallikrein, and prekallikrein were determined in patients with malignant hypertension (MH) and compared to normotensive controls (NC) and patients with mild to moderate essential hypertension (EH). Also, a recently described kinin potentiating factor (KPF) was estimated by dividing the value of kininogen determined by trypsin (Kgn-Try) by that of kininogen determined by human urinary kallikrein (Kgn-HuUk). No significant alterations were detected among plasma values of pre-kallikrein and kallikrein of MH as compared to NC. However, Kgn-HuUK values were significantly lower in MH (1.9 +/- 0.3 micron gLBK/ml) as compared to EH and NC (2.7 +/- 0.1 micron gLBK/ml and 3.0 +/- 0.2 micron gLBK/ml respectively, p less than 0.05). Furthermore, KPF values were also low (p less than 0.05) in MH (1.6 +/- 0.3) when compared with similar values obtained in EH and NC (3.0 +/- 0.2 and 2.8 +/- 0.1, respectively). Adequate control of blood pressure levels for 90 days in MH group caused no significant alterations in plasma levels of kininogen and KPF. It is suggested that diminished kininogen levels as well as a decrease in a kinin potentiation KPF that is generated in plasma by trypsin may be involved in the pathogenesis of human malignant hypertension.
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PMID:Malignant hypertension: a syndrome associated with low plasma kininogen and kinin potentiating factor. 702 21

Antihypertensive effect of an orally active angiotensin I-Converting enzyme inhibitor, SQ 14225 (Captopril) was assessed in 18 hypertensive patients, of whom 13 had essential hypertension, 2 had malignant hypertension, 2 had hypertension associated with chronic renal failure, and 1 had renovascular hypertension. Blood pressure decreased markedly not only in patients with high renin levels but also in those with low renin levels. Nevertheless, the magnitude of blood pressure reduction was correlated with the pre-treatment plasma renin activity (r =-0.64, p less than 0.01 systolic, r =- 0.60, p less than 0.05 diastolic). There was a significant correlation between the fall in mean blood pressure and the decrease in plasma aldosterone concentration 3 weeks after treatment (r = 0.64, p less than 0.05). The serum potassium elevated from 4.2 +/- 0.4 to 4.8 +/-0.9 mEq/L (p less than 0.05), and the change correlated inversely with the reduction of plasma aldosterone concentration (r = 0.71, p less than 0.02), while serum sodium slightly decreased from 140-+/- 2 to 138 +/- 3 mEq/L. There was neither finding of orthostatic hypotension nor escape from the antihypertensive effect. These results indicate that chronic inhibition of angiotensin I-converting enzyme with an orally active compound offers an effective and well-tolerated approach to treatment of hypertension.
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PMID:Antihypertensive effect of the oral angiotensin I-converting enzyme inhibitor in long-term treatment of hypertensive patients. 704 Jul 24

1. Human leucocyte ABC antigens were determined by means of a lymphocytotoxicity test in 27 patients with previous essential malignant hypertension and in 500 blood donors. 2. In 18 patients with grade IV retinopathy human leucocyte antigen B15 (HLA B15) was found in 44%, as compared with 23% in the control subjects (P = 0.888). 3. All patients with HLA B15 had a positive family history for hypertension. 4. In 18 patients with grade IV retinopathy HLA B15 was found in eight whereas none of the nine patients with grade III retinopathy had this antigen (P = 0.039). 5. Of the 27 patients, 19 had a positive family history of hypertension and of these eight had HLA B15, whereas none of the eight patients with a negative family history had this antigen (P = 0.068). 6. The findings do not rule out that HLA B15 may be associated with the development of the malignant phase in patients with essential hypertension, but a statistically significant relationship could not be established.
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PMID:Human leucocyte antigens in patients with previous essential malignant hypertension. 744 96


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