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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.
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PMID:Management of hypertensive encephalopathy. 72 Oct 56

Glomerular changes were morphometrically studied in renal biopsies of 27 cases of nephrosclerosis showing clinically benign or malignant hypertension and of 15 cases of mild mesangioproliferative glomerulonephritis with hypertension. In nephrosclerosis, there was a mild increase in mesangial matrix without cell proliferation. The degree of the mesangial changes varied little despite a large variation in blood pressure and showed no significant difference between benign and malignant hypertension. In mild mesangioproliferative nephritis with hypertension, mesangial matrix, as well as the number of mesangial cells, showed an increase of varying degree. A quantitative assessment of the mesangium was proved effective in differentiating the glomerular changes in nephrosclerosis from those in mesangioproliferative nephritis with hypertension.
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PMID:The glomerular mesangium in hypertension: a morphometrical comparison of nephrosclerosis with mesangioproliferative glomerulonephritis on renal biopsies. 81 66

Investigation of the behaviour of the renal juxtaglomerular apparatus in 19 patients with malignant hypertension has shown that in kidneys fixed immediately after operation the juxtaglomerular granulation index is twice as high as in autopsy kidneys. The formation of renin by the epitheloid cells begins with the appearance of osmiophilic substances in the region of the endoplasmic reticulum. The first stages of granule formation are small rhomboid particles in the Golgi cisternes, which aggregate to form bigger round or polymorphic granules in the Golgi area. In pathological conditions the substances synthesized may be set free and become active locally as a result of fibrinoid necrosis of the vascular wall. The rate of production is increased firstly by forcing the production of active agents in the preexistent epitheloid cells, secondly by transformation of the so-called bivalent cells and finally, by cell division. In accelerated hypertension the production of renin also takes place in nephrons whose glomeruli, tubules and macula densa, are damaged. There is a correlation between blood pressure elevation and the juxtaglomerular granulation index.
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PMID:The juxtaglomerular apparatus in malignant hypertension of man. 82 80

Indomethacin inhibits the synthesis of prostaglandin and the release of renin. These effects were studied in normal rabbits and rabbits with two-kidney Goldblatt hypertension (2KGH) and one-kidney Goldblatt hypertension (1KGH) by giving daily intravenous injections of indomethacin (3mg/kg after two initial doses of 9 mg/kg), and in appropriate control rabbits given diluent phosphate buffer without indomethacin. In normal rabbits, indomethacin significantly decreased immunoreactive plasma prostaglandin E-like substance (IPGE) and plasma renin activity (PRA). Indomethacin did not change plasma creatinine (PCr) or mean blood pressure but it decreased renal blood flow (RBF) and glomerular filtration rate (GFR). In 2KGH rabbits, responses depended on the level of renal function and, to a lesser extent, on the level of PRA. In six of10 2KGH rabbits in which hypertension developed without significant changes in PRA, IPGE, PCr, RBF, and GFR, indomethacin produced changes similar to those seen in normals. In the other four rabbits, development of 2KGH was accompanied by increased PRA, increased IPGE, and decreased RBF and GFR, and indomethacin produced renal failure, oliguria, malignant hypertension, and death within 5 days. In 1KGH rabbits, indomethacin decreased IPGE, PRA, and renal function but increased mean blood pressure. These observations suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
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PMID:The effect of indomethacin blockade of prostaglandin synthesis on blood pressure of normal rabbits and rabbits with renovascular hypertension. 83 Apr 37

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.
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PMID:Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension. 84 73

A previously normotensive 24-year-old black man developed malignant hypertension and azotemia. The patient was found to have bladder outlet obstruction due to urethral stricture. Transurethral dilation resulted in brisk improvement in renal function and rapid lowering of blood pressure in association with minimal diuresis. On follow-up one year later, while he was not receiving medications, the blood pressure was 120/70 mm Hg and the creatinine clearance was 150 ml/min. A kidney biopsy specimen showed minimal residual pathologic abnormalities in the renal arteries and arterioles. The renin-angiotensin system was probably involved in the maintenance of the hypertension, in view of the elevated peripheral plasma renin activity on admission. This represents a rare case of hypertension due to urethral stricture. Despite rapid progression to azotemic malignant hypertension, urethral dilation restored the blood pressure and renal function to normal.
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PMID:Reversible malignant hypertension and azotemia due to urethral stricture. 84 54

Three cases of intracerebral hemorrhage are described in which there was fibrinoid degeneration of cerebral arteries and arterioles or miliary aneurysms or both. Fibrous balls are shown to be sclerosed true aneurysms. These changes occurred in the absence of malignant hypertension and perhaps in the absence of any hypertension. A further point of interest was the finding of fibrinoid at the site of apparent aneurysm formation in a small artery on the cerebral surface, a location at which miliary aneurysms are not generally thought to form. The presence of intracerebral hemorrhage in all three cases, and the ready demonstration of similar changes in other cases of intracerebral hemorrhage, suggest but do not prove that the fibrinoid degeneration or aneurysm leads to vessel rupture and to hemorrhage itself. Also unsettled is the question of whether miliary aneurysms form only at sites already displaying fibrinoid change. Our data suggest that pre-existing fibrinoid may not be a prerequisite for miliary aneurysm formation.
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PMID:Miliary aneurysms and "fibrinoid" degeneration of cerebral blood vessels. 85 13

A recently developed 1-day screening procedure for angiotensinogenic ("high-renin") hypertension is based on (A) a fall in blood pressure in response to intravenous infusion of the angiotensin antagonist, saralasin (P-113), and (B) peripheral venous renin assays by radioimmunoassay, in a sodium-depleted state. Out of 700 hypertensive patients screened by these tests, 160 had renal imaging performed with technetium-99m glucoheptonate and iodine-131 Hippuran. The P-113 infusion test proved superior to peripheral venous renin assays for the detection of angiotensinogenic hypertension. Positive infusion tests correlated well with renal vein renin assays. Frequently, however, both these tests were positive with bilateral renal disease and/or malignant hypertension. While renal imaging proved valuable in indicating which patients had a unilateral abnormality, it frequently could not distinguish unilateral renovascular disease from unilateral parenchymal disease unrelated to angiotensinogenic hypertension. Twenty-five patients in this series had arteriographic renal artery stenosis, of whom 3 had false negative P-113 infusion tests, 9 had negative peripheral renin assays, and 3 had no imaging abnormalities. This study indicates that scintigraphy is a useful procedure for the investigation of hypertensive patients when the initial P-113 infusion test is positive, or discordant with other findings. By imaging, angiotensinogenic hypertension due to bilateral renal disease can be distinguished from unilateral renovascular disease, and the site of the ischemic renal tissue can usually be identified.
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PMID:Diagnosis of angiotensinogenic hypertension: the complementary roles of renal scintigraphy and the saralasin infusion test. 87 45

Malignant hypertension occurred in a young man who also was found to have a left renal infarct and higher renal vein renin levels on the left side. His hypertension was controlled with drugs and subsequently treatment with these medications was gradually discontinued over a period of nine months. He remained normotensive when no longer receiving medication, and another intravenous pyelogram demonstrated a persistent cortical defect in the left kidney.
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PMID:Spontaneous remission of accelerated (malignant) hypertension in renal infarction. 87 48

Two cases of scleroderma are presented in which malignant hypertension developed abruptly, accompanied by rapidly progressive renal failure. The malignant hypertension was associated with high plasma renin levels and like other forms of hyperrenninemic hypertension and uremia, was refractory to both antihypertensive medication and extracellular fluid volume control with hemodialysis. Blood pressures became controllable only after bilateral nephrectomy was performed, and in each case resulted in a reversal of a rapidly progressive downhill course. Though both patients had multisystem involvement at the onset of renal failure, the non-renal manifestations of scleroderma have not progressed rapidly. Consequently, when patients with scleroderma develop malignant hypertension and uremia, aggressive therapy with dialysis and nephrectomy may significantly prolong survival.
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PMID:Malignant hypertension and uremia in scleroderma: efficacy of nephrectomy and hemodialysis. 88 14


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