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)

Pathophysiological characteristics and long-term prognosis were studied retrospectively in 69 malignant hypertensives associated with grade III or IV retinopathy and the diastolic blood pressure greater than 120 mmHg. Thirty three (48%) cases had essential hypertension (EHT) as the underlying disease, 26 (38%) as chronic glomerulonephritis (CGN), and the remaining 10 (14%) as others including chronic pyelonephritis, renovascular hypertension, hydronephrosis, multiple calyceal diverticula, and unknown original disease. The role of the renin-angiotensin system in malignant hypertension was investigated by measuring plasma renin activity (PRA) and determining the blood pressure response to angiotensin (ANG)II antagonist, (Sar1, Ile8) ANG II. Basal PRA was significantly higher in the EHT group than the CGN group, and the ANG II antagonist-induced reduction of blood pressure was only evident in the former group. The regression analysis revealed that PRA was linearly correlated with both mean blood pressure (MBP) and serum creatinine prior to antihypertensive treatment in the EHT group but not in CGN patients, although there was inverse correlation between PRA and serum sodium in both groups. Therefore, the renin-angiotensin system seems to play a significant role in elevating blood pressure and deteriorating renal function in malignant hypertension developed from EHT, while it is less important in that from CGN. The 5-year survival rate was 90% in total 69 patients with malignant hypertension, while the 5-year renal survival rate defined as the probability of surviving without maintenance hemodialysis was 37%, indicating that the treatment with hemodialysis as well as antihypertensive drug therapy contributed to an improvement of prognosis of malignant hypertension. The EHT group showed a poor prognosis for life compared with the CGN group, while in the latter group most patients rapidly developed endstage renal failure. Although the pretreatment serum creatinine levels were matched, the renal function more rapidly deteriorated after development of malignant hypertension in the CGN group than did in the EHT group, indicating renal survival rate to be shorter in the former group. Hence, underlying diseases may affect the long-term prognosis of malignant hypertension. The results obtained from this study suggest that the pathophysiological characteristics of malignant hypertension are different and its long-term prognosis is varied by underlying diseases such as EHT and CGN.
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PMID:[Pathophysiology and prognosis in malignant hypertension: comparison by underlying diseases]. 251 35

To assess the hemodynamic characteristics in malignant hypertension, echocardiography was performed in 18 patients with malignant essential hypertension (MH-I, n = 9) and secondary hypertension (MH-II, n = 9). Patients with benign hypertension with or without left ventricular hypertrophy (n = 8 and 7, respectively), patients with hypertensive heart failure (n = 7) and normotensive volunteers (n = 10) were subjected to controls. Plasma noradrenaline (NA) and renin activity (PRA) were also measured prior to the antihypertensive therapy. There were no significant differences in the durations of hypertension before the malignant phase, and the mean arterial pressure between MH-I and MH-II. Although posterior wall thickness (PWTd) in MH-II was similar to that in MH-I, interventricular septal thickness (IVSTd) was less marked in MH-II. The plasma NA and PRA were markedly increased in both MH-I and MH-II. End-diastolic dimension (Dd) of the left ventricle was within normal range, but end-systolic dimension (Ds) was significantly increased in MH-I, MH-II and hypertensive heart failure. The moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) were observed in both MH-I and MH-II. Marked decreases in EF and mVcf were also observed in patients with hypertensive heart failure. The relationship between systolic blood pressure and Dd/PWTd was shifted toward the right and upper portion of the normal relation in MH-I and MH-II. The present study demonstrated that the hemodynamic characteristics in malignant hypertension are an inappropriate left ventricular hypertrophy due to a marked increase in systolic stress; dilatation of the left ventricle in systole; and a moderate decrease in ventricular systolic function. It is suggested that a decrease in left ventricular systolic function in malignant hypertension might be due in part to a marked increase in the influence of neurohumoral factors on hemodynamics.
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PMID:[Echocardiographic features of left ventricular hypertrophy and contractility in malignant hypertension]. 253 Mar 33

Malignant hypertension developed in an 18-year-old man whose primary hypertension had been diagnosed by chance. Standing blood pressure was 290/170 mmHg. Tests of renal function revealed high blood urea nitrogen and creatinine levels and low levels of both effective renal plasma flow and the glomerular filtration rate. Plasma renin activity and levels of angiotensin II and aldosterone were greatly elevated. Severe concentric left ventricular hypertrophy was noted. The patient received standard antihypertensive treatment with furosemide, propranolol, nifedipine, and prazosin, but his blood pressure did not decrease and there was no improvement in the clinical or biochemical measures. The patient was then given 20 mg of enalapril daily for one year. The inhibition of angiotensin converting enzyme immediately reduced blood pressure. Angiotensin II and aldosterone levels became normal, kidney function and hemodynamics improved, and echocardiograms revealed that the left ventricular hypertrophy had regressed. The results confirm the pathogenetic role of angiotensin II in the development of the malignant phase of hypertension.
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PMID:Treatment of malignant hypertension with an angiotensin converting enzyme inhibitor. 255 Jan 35

The anatomical-pathological findings of 15 woolly monkeys were comparable with those described in man with essential benign or malignant hypertension. Kidneys revealed arterio- and arteriolosclerosis or an onion peel-like proliferation, in some cases necrotizing endarteritis. Obesity due to restricted physical activity, unnatural feeding, and psychical and physical stress could have contributed to the development of this condition. Further, high vulnerability of the genus woolly monkey is postulated. Thus, essential hypertension of woolly monkeys appears to be a multifactorial disease.
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PMID:The woolly monkey (Lagothrix lagothricha): a possible model for human hypertension research. 258 76

Three types of antihuman atrial natriuretic peptide antiserum were obtained. From the study of cross-reactivity to human atrial natriuretic peptide fragments, it was suggested that antisera-1, -2, and -3 are mostly specific to 1-28, 5-25, and the ring structure, respectively. The estimated values of this hormone were significantly lower in the order of antisera-1, -2, and -3. Moreover, high performance liquid chromatographic study showed that various types of fragments of atrial natriuretic peptide exist in human plasma. These findings suggested that the highly specific antiserum to 1-28 human atrial natriuretic peptide such as antiserum-1 should be used to estimate the 1-28 human atrial natriuretic peptide levels in human plasma. From the study by using antiserum-1, it was concluded that the plasma human atrial natriuretic peptide increased in essential hypertensives, and in patients with primary aldosteronism, chronic renal failure, and malignant hypertension. Regarding the pathophysiological significance of increased plasma atrial natriuretic peptide, it is unlikely that this plays an important role in the etiology of essential hypertension or other hypertensive diseases, because the plasma level of this hormone is elevated in these patients. The increase of plasma atrial natriuretic peptide level in these patients should be considered to be a secondary or compensatory reaction to high blood pressure.
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PMID:Plasma levels of human atrial natriuretic peptide in patients with hypertensive diseases. 296 24

Heavy proteinuria in patients with essential hypertension raises the question of underlying primary renal disease. While malignant hypertension may be associated with proteinuria in the nephrotic range, it is generally held that protein excretion in benign nephrosclerosis is almost invariably less than 0.5-1.0 g/24 h. We report 18 patients with biopsy-proven hypertensive nephropathy and heavy proteinuria, of which only 6 had malignant hypertension. In the remaining 12 patients with benign nephrosclerosis, protein excretion reached up to 6.5 g/24 h, and nephrotic range proteinuria was present in 3 patients. All patients with heavy proteinuria suffered from long-standing moderate or severe, poorly controlled hypertension and were azotemic. We suggest that hypertensive nephrosclerosis be included in the differential diagnosis of massive proteinuria accompanying azotemia in poorly controlled hypertensives.
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PMID:Marked proteinuria in hypertensive nephrosclerosis. 316 Feb 40

Novel approaches to managing refractory arterial hypertension (AH) have been tested in 130 patients aged 28 to 59 years with severe or malignant hypertension. Hemosorption was performed in 70 patients in whom AH was caused by chronic diffuse glomerulonephritis (49 cases) or chronic pyelonephritis (21 cases) accompanied by the appearance of chronic renal failure. In all patients, blood pressure after hemosorption decreased by 15% to 16% on the average, resulting in progressively improved renal function and a nearly 2.0-fold reduction in plasma aldosterone concentration (PAC), and allowing the doses of antihypertensive drugs to be reduced. Plasmapheresis was performed in 31 patients with refractory severe or malignant AH due to essential hypertension or parenchymatous diseases of the kidneys. After two to four plasmapheresis sessions with up to 2 L of plasma exchanged, blood pressure dropped by 24% compared to baseline while the doses of antihypertensive drugs were diminished and some were discontinued completely in several cases. Analysis of the sensitivity to antihypertensive drugs after plasmapheresis using the rosette technique revealed a significant decrease in the number of rosette-forming cells. The level of angiotensin II and urinary excretion of aldosterone-18-glucuronide declined progressively by nearly 50% after plasmapheresis, correlating with the antihypertensive effect of plasmapheresis. In 32 patients with severe AH complicated by refractory cardiac failure, isolated ultrafiltration was used. After one to eight sessions and the removal of 1.0 L to 35.8 L of fluid, the signs of cardiac failure diminished, the blood pressure level responded to drug therapy, and the PAC level decreased significantly. Although the mechanisms of the antihypertensive actions of hemosorption, plasmapheresis, and isolated ultracentrifugation are still not completely elucidated, these data suggest that hemosorption may act by removing nitrogenous residues from the body and reducing PAC, plasmapheresis by deblocking receptors for antihypertensive drugs and reducing the concentration of angiotensin II and the synthesis of aldosterone in the body, and isolated ultrafiltration by eliminating hyperhydration and edema of the parenchymatous organs.
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PMID:Extracorporeal methods in the management of severe and malignant arterial hypertension. 324 17

Effects of captopril on arterial pressure (AP) and renal function were investigated in patients with non-malignant "benign" or malignant phase essential hypertension (EH group), or with chronic renal failure (CRF group). After captopril administration, AP and renal vascular resistance (RVR) decreased significantly, and renal blood flow (RBF) and plasma renin activity (PRA) increased in both groups. Glomerular filtration rate (GFR) increased in the EH group, but was unchanged in CRF. Filtration fraction decreased in the malignant hypertension and CRF groups. Significant correlations were found between baseline PRA and baseline RVR, and the captopril-induced decrease in mean AP, decrease in RVR, increase in RBF, and increase in GFR in the EH group, while these associations were not observed in CRF. These results indicate that the high AP, RVR, suppressed RBF and GFR in the EH group were closely related to activity of the renin-angiotensin system, but not so the low RBF and GFR in CRF. Small doses of captopril may improve impaired renal function in EH, and may not cause deterioration in the CRF group.
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PMID:Renal haemodynamics and comparative effects of captopril in patients with benign- or malignant-essential hypertension, or with chronic renal failure. 330 Oct 82

This article has reviewed the involvement of the kidney as a target organ of essential hypertension. Since Bright first made the association of renal disease and hypertension in 1836, the nature of this relationship has been debated. Although there is evidence implicating abnormalities of renal function in the pathogenesis of essential hypertension, hypertension frequently precedes histologic evidence of alterations in renal structure. Nephrosclerosis, or hardening of the kidney, is the term used to describe the histologic changes occurring in the kidney as the result of hypertension. It can be though of as an acceleration of the normal aging process of the renal vasculature. Glomerular and tubular changes have been traditionally thought to be ischemic in origin. Experimental evidence supports the notion that, as renal function is lost, intraglomerular hypertension develops and may be responsible for additional nephron loss in hypertension. This idea may have therapeutic implications for hypertensive patients with renal insufficiency in that agents that reduce both systemic and intraglomerular pressure may be preferable. Hemodynamically, early hypertension is often characterized by normal peripheral and renal vascular resistance and an increased cardiac output. In established hypertension, cardiac output is usually normal, and peripheral and renal vascular resistances are increased. Renal blood flow is reduced, glomerular filtration rate is maintained, and the filtration fraction rises. In the absence of an accelerated malignant phase, renal failure is uncommon in essential hypertension. Males and blacks are most sensitive to the vascular damage of essential hypertension. Essential hypertension remains an important cause of end-stage renal disease, especially in blacks. Atherosclerotic obstruction of the renal arteries may be a more common cause of renal failure in patients with essential hypertension than has been previously recognized. There are few sensitive markers of early renal involvement in essential hypertension. Several studies of sensitive markers are promising and may detect patients who are prone to renal injury and deserve more aggressive treatment. Malignant hypertension is characterized pathologically by vascular changes of proliferative endarteritis and fibrinoid necrosis. Fortunately, its frequency is decreasing because of early identification and effective treatment of essential hypertension. Effective treatment of severe and malignant hypertension clearly leads to stabilization (and occasionally improvement) of renal function.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal parenchymal involvement in essential hypertension. 330 6

A long-term prognosis was studied in 69 patients with malignant hypertension, followed for an average of 56 months. Overall survival rate was 90% for a 5-year period, although the prognosis was different between two major underlying diseases, namely the 5-year survival was 79% for 33 essential hypertension (EHT) and 100% for 26 chronic glomerulonephritis (CGN); the difference is significant (p less than 0.01). In contrast, the 5-year rate for renal survival, defined as the probability of surviving without hemodialysis, was 37% in all cases. However, there was significant difference in the renal survival between EHT (60% for a 5-year period) and CGN (4% for a 18-month period). Multivariate analyses of the Cox's proportional hazards model revealed that the long-term change in renal function was different between the two groups, namely more rapid deterioration in the CGN group. These results indicate that a long-term prognosis of malignant hypertension is influenced by the underlying diseases and hemodialysis besides antihypertensive treatment may increase survival in malignant hypertension associated with severely damaged renal function.
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PMID:Long-term prognosis of malignant hypertension; difference between underlying diseases such as essential hypertension and chronic glomerulonephritis. 335 95


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