Disease relevance of Hypertension, Malignant

• These results suggest that (1) PRA is normal in normotensive diabetics, (2) upright PRA in diabetics with hypertension but no nephropathy is similar to that in essential hypertension, and (3) patients with diabetes, hypertension, and nephropathy have "low renin hypertension," explaining the virtual absence of malignant hypertension in this group [1].
• Twelve scleroderma patients with hypertension, seven of whom had malignant hypertension and renal failure of scleroderma renal crisis, were treated with captopril [2].
• We report the rapid development of severe nephrotic syndrome, malignant hypertension, and microangiopathic hemolytic anemia during the first trimester of pregnancy in a 29-yr-old woman with IDDM of 18 yr duration [3].
• Diazoxide and hydralazine are chiefly used to treat severe hypertensive emergencies, primary pulmonary and malignant hypertension and in severe preeclampsia [4].
• Our experimental studies on renovascular malignant hypertension indicate that endogenous vasoconstrictor agents produce choroidal ischemia and AION [5].

High impact information on Hypertension, Malignant

• In the patients with malignant hypertension, vasopressin levels were elevated (13 +/- 2 pg per milliliter. [+/- S.E.M.]) but did not correlate with arterial pressure; however, in normal volunteers, blood pressure did not rise when vasopressin was increased beyond these levels through infusion of the peptide [6].
• Blood pressure in acute and chronic vasopressin excess: studies of malignant hypertension and the syndrome of inappropriate antidiuretic hormone secretion [6].
• Minoxidil treatment of malignant hypertension. Recovery of renal function [7].
• This data suggest that ET-1 is an independent stimulator of aldosterone secretion and we are speculating that it might be important in those situations, like in malignant hypertension, where endothelial damage might result in increased ET-1 production [8].
• Phlebotomy for erythropoietin-associated malignant hypertension [9].

Chemical compound and disease context of Hypertension, Malignant

• Closed-loop systems have been used to control postoperative fluid infusion, reduce malignant hypertension to a reasonable range through nitroprusside infusions, and control continuous insulin infusions-in effect, an artificial pancreas [10].
• Acute and chronic treatment of severe and malignant hypertension with the oral angiotensin-converting enzyme inhibitor captopril [11].
• We conclude that captopril, alone or in combination with other drugs, is effective in both the acute and long-term management of severe and malignant hypertension [11].
• The evolution of malignant hypertension was studied under metabolic balance conditions in 11 uninephrectomized rats given deoxycorticosterone acetate and 1% NaCl as drinking water [12].
• The failure of furosemide-induced salt and water loss to convert benign to malignant hypertension in the rat [13].

Biological context of Hypertension, Malignant

• We studied the changes in mean arterial pressure (MAP), cardiac index (CI), pulmonary wedge pressure (PWP), and in plasma volume (PV) induced by a single oral dose of captopril (150 mg) in 11 patients with malignant hypertension [14].
• In conclusion, malignant hypertension is associated with abnormal endothelial damage (elevated von Willebrand factor), platelet activation (soluble P-selectin), and fibrinogen levels, which may be related to the pathogenesis of this condition, as well as the development of complications [15].
• To examine the pathogenetic role of platelet-derived growth factor (PDGF) in hypertensive kidney damage, we studied the gene expression of PDGF A-chain and B-chain in an animal model of malignant hypertension [16].

Anatomical context of Hypertension, Malignant

• These animal models provide pathological, pharmacological, and genetic evidence supporting the hypothesis that intra-renal generation of angiotensin 2 and exposure of the microcirculation to elevated blood pressure co-operate in causing tissue damage in malignant hypertension [17].
• Inhibition of nitric oxide synthase by L-arginine analogues such as N omega-nitro-L-arginine methyl ester (L-NAME) in spontaneously hypertensive rats (SHR) is associated with malignant hypertension and enhanced expression of the endothelin-1 gene in some blood vessels [18].
• OBJECTIVE: To determine whether cellular cation concentrations and cell membrane ATPase activity are altered in patients with malignant hypertension [19].
• Cerebrospinal fluid lactate and pyruvate concentrations in patients with malignant hypertension [20].
• Thus, the enhanced local generation of Ang II in the adrenal gland may contribute to the increased release of aldosterone in SHRSP with malignant hypertension [21].

Gene context of Hypertension, Malignant

• 4. These data support the hypothesis of a role of endothelin-1 in blood pressure elevation in this hypertensive model with malignant hypertension [22].
• Our results raise the possibility of renoprotective effects of ETA/B receptor blockers in certain forms of malignant hypertension [23].
• These results demonstrate the existence of autoantibodies against a functional extracellular domain of human AT1 receptors in patients with malignant hypertension, and suggest that these autoantibodies might be involved in the pathogenesis of malignant hypertension [24].
• These results demonstrate that ANG II-induced PLD activation is regulated by PKCzeta and suggest a crucial role of PKCzeta-dependent PLD2 in VSMC functions such as adhesion, spreading, and hypertrophy, which are associated with the pathogenesis of atherosclerosis and malignant hypertension [25].
• 1. The response of arterial blood pressure, plasma renin activity and plasma aldosterone concentration to inhibition of angiotensin I converting enzyme (kininase II) with captopril has been studied in patients with severe, treatment-resistant, malignant hypertension [26].

Analytical, diagnostic and therapeutic context of Hypertension, Malignant

• Systolic blood pressure was measured by tail-cuff plethysmography during treatment; tissue and plasma angiotensin converting enzyme levels and renal histological changes were assessed at the end of the treatment period or upon development of malignant hypertension [27].
• Filtration fraction decreased in the malignant hypertension and CRF groups [28].
• Focal lesions in the renal artery caused by fibromuscular dysplasia (FMD) are susceptible to spontaneous intramural dissection, and carry a serious risk of malignant hypertension and loss of renal function [29].
• The relationship between plasma renin activity (PRA), angiotensin II (AT II) and renin substrate concentration (PRS) were studied in a patient with left renal artery occlusion and malignant hypertension before and after left-side nephrectomy [30].

References