Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renal lesions of a 5-year-old girl with progressive systemic sclerosis are described. The nephropathy was clinically characterised by moderate proteinuria, microscopic hematuria and transient hypertension. Light microscopy showed membranoproliferative glomerulonephritis of segmental character. On electron microscopy intramesangial, subendothelial and extramembranous glomerular deposits were observed. By immunofluorescence miscrosocpy deposit of IgG, Clq, C4, C3, C5, C8 and C9 in a predominantly subendothelial location were found in all glomeruli. Vascular lesions were of minor degree. Histological and immunohistological findings are compatible with an immune complex disease.
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PMID:Membranoproliferative glomerulonephritis in systemic sclerosis of childhood. 15 Jun 97

Vascular lesions due to neurofibromatosis have been predominantly reported in the renal arteries as cause of arterial hypertension, but they can occur everywhere. The angiography shows a smoothly bordered stenosis at the origin of the artery with an elongated funnel shaped poststenotic deformity. Collateral vessels are often present. Reconstructive arterial surgery is in a high percentage successful. The main differential diagnosis includes fibromuscular dysplasia. Arterial hypertension in a young person with neurofibromatosis should suggest the presence of pheochromocytoma or renovascular disease.
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PMID:[Multiple vascular stenoses in neurofibromatosis (author's transl)]. 40 67

Many different classification systems for Ca2+ antagonists were proposed. They are mostly based on structural aspects or profiles of biological activity. 1,4-dihydropyridines, with Ca2+ channel antagonistic activity, including nifedipine and nitrendipine, are highly effective as antihypertensive agents. Although Ca2+ antagonists have multiple sites of antihypertensive action, their main mechanism of action is inhibition of Ca2+ entry into the vascular smooth muscle cells. Ca2+ channel antagonists bind to specific receptors at Ca2+ channels and stabilize the channels in a mode unavailable for opening. Their effect is enhanced by depolarization of the cell membrane. Currently used pharmacological methods for detection of Ca2+ antagonistic action of drugs include: (1) inhibition of 45Ca2(+)-uptake; (2) displacement of [3H]nitrendipine from isolated membranes, and (3) inhibition of Ca2+ current in single cells or channels. Ca2+ antagonists were reported to prevent hypertension-induced vascular changes and other vascular pathology, probably related to Ca2+ overload. Vascular lesions in Dahl salt-sensitive hypertensive rats and in spontaneously hypertensive rats were prevented by chronic administration of nifedipine or nitrendipine. Hemodynamic effects of Ca2+ antagonists are characterized by reduction in total peripheral vascular resistance, increase in cardiac output, reduction in systemic left ventricular end-diastolic, pulmonary arterial and capillary wedge pressures. Ca2+ antagonists differ in potency, duration of action and their therapeutic ratios. DHPs enhance sympathetic tone and have little or no negative dromotropic action. They are, therefore, safer in combination with beta-adrenoceptor antagonists than either verapamil or diltiazem. In comparison with other Ca2+ antagonists nitrendipine is highly potent as a vasodilator. As a negative inotropic agent, it is, however, less potent than either verapamil or nifedipine. Nitrendipine has, therefore, a better therapeutic ratio than some of the other well-known Ca2+ antagonists. Unlike older vasodilators, e.g. hydralazine and minoxidil, Ca2+ antagonists have diuretic properties which are primarily due to inhibition of tubular reabsorption of salt and water. Under certain experimental conditions, e.g. infusion of angiotensin II, DHPs can increase GFR. Nitrendipine has also renal cytoprotective activity. It protected rats from aminoglycoside-induced nephrotoxicity and antagonized proliferative glomerular changes in nephritic rats.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pharmacological basis for use of calcium antagonists in hypertension. 269 46

Blood pressure in 75 patients with IgA nephropathy (IgA-GN), confirmed by renal biopsy, was related to clinical, immunological and morphological findings. The findings were compared with an age-matched control group of patients with non-IgA-GN. Overall prevalence of hypertension (HT) was similar in IgA-GN and non-IgA-GN (38.7% vs 38.2%). The presence of HT in IgA-GN was related to age, renal function, immunohistological pattern and degree of glomerular sclerosis or vascular lesions respectively. No correlation was found between HT and elevated serum IgA, circulating IgA immune complexes and IgA skin deposits. The current observations underline the value of hypertension for predicting development of renal failure. Vascular lesions are not only strongly correlated with, but may even precede development of, hypertension as confirmed by longitudinal observations.
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PMID:Hypertension in mesangial IgA glomerulonephritis. 399 61

In an unselected series of patients with IgA glomerulonephritis, old age, high blood pressure, and high urinary protein excretion at the time of renal biopsy were found to correlate with impaired renal function, whereas sex, estimated duration of the disease, or high serum IgA levels did not. The following clinical features were favorable prognostic signs: asymptomatic proteinuria, macroscopic hematuria, and isolated microscopic hematuria. The degree of diffuse mesangial alteration and the presence of segmental glomerular lesions correlated clearly with the subsequent clinical outcome. Vascular lesions, i.e. arteriosclerosis and renal vascular deposition of C3, were most often present in patients with severe glomerulopathy. The presence of electron-dense deposits in glomerular capillary walls was also an unfavorable prognostic finding. Renal biopsy findings of interstitial infiltrates of inflammatory cells and IgA distributed along glomerular capillary walls were usually associated with extrarenal manifestations of the disease.
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PMID:Clinicopathologic correlations in a series of 143 patients with IgA glomerulonephritis. 401 21

Placental lesions from 361 singleton full-term pregnancies were studied. These placentas were divided into two major groups: the study group consisting of 146 placentas from mothers with pregnancy-induced hypertension and a normotensive control group, which included 215 placentas from mothers with normal pregnancies. Each group was divided into three subgroups according to the allocation of infant's birthweight in the normal ponderal curve. A statistically significant higher incidence and severity of villous lesions was observed in placentas of mothers with pregnancy-induced hypertension when infants were over the 25th centile of the ponderal curve. Vascular lesions, i.e., absence of physiological changes in spiral arteries of the placental bed, acute atherosis and chronic vasculitis-like lesions were also more frequently observed in the hypertensive group than in controls. These placental lesions have been described in placentas of small for gestational age infants with or without maternal hypertension and in those of preeclamptic women with appropriate for gestational age infants. Since acute atherosis-like lesions have been reported in placentas of pregnant women with systemic lupus erythematosus and in rejected renal transplants, a possible maternal immunological reaction against fetal tissues could be responsible for the pathogenesis of these entities.
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PMID:Chronic villitis of unknown etiology and maternal arterial lesions in preeclamptic pregnancies. 402 72

We report here two cases of isolated angiitis of the central nervous system associated with congophilic angiopathy. The clinical history lasted 9 months in the first patient (65 years old) and 9 years in the second patient (59 years old). It was characterized by progressive intellectual deterioration, increased protein content of the CSF and evidence of focal brain lesions in the CT scan. One patient showed chronic intracranial hypertension. Vascular lesions were limited to the brain and were characterized by granulomatous and necrotizing angiitis of the small leptomeningeal and intracortical vessels. Amyloid deposits were present in large amounts along vascular segments showing vasculitis, in foreign body giant cells, in plaque-like structures surrounding diseased perforating arterioles, along cortical microvessels and in many neuritic plaques. Close proximity and topographic overlap of vasculitis and amyloid changes suggest a possible pathogenetic relationship.
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PMID:Amyloid angiopathy combined with granulomatous angiitis of the central nervous system: report on two patients. 407 38

Vascular lesions in addition to pheochromocytoma are now recognized as causes of hypertension associated with neurofibromatosis. We have analyzed hospital charts of 106 pediatric patients with neurofibromatosis, eight of whom were noted to have been hypertensive on at least one occasion. Of these eight patients, five had vascular lesions involving the renal vasculature, one had obstructive uropathy and two had transient hypertension associated with traction and pain. Approximately 5% of pediatric patients with neurofibromatosis have vascular lesions causing hypertension.
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PMID:Renovascular hypertension in pediatric patients with neurofibromatosis. 641 42

A new congenic rat strain, the Dahl salt-sensitive/NIH-corpulent (DSS/N-cp) rat, has been developed to study the role of obesity and type of dietary carbohydrate in the development of hypertension and its complications. Three groups (n = 6) of young male obese and lean DSS/N-cp rats were fed diets containing either 54% sucrose, 18% sucrose plus 36% starch, or 54% starch, with 0.1% dietary sodium for 12 weeks. Regardless of the diet, obese and lean rats showed mildly elevated systolic blood pressure (SBP), being significantly higher in obese than in lean rats (SBP 156 +/- 5 mm Hg v 141 +/- 3 mm Hg, P < .05). However, SBP was not different between the three diet groups. Levels of serum insulin, triglyceride, and cholesterol as well as urinary protein excretion were significantly higher in obese than in lean rats. Obese rats fed the sucrose diets as compared to the starch diet, had higher serum insulin and lipid levels, but had lower body weights and higher serum creatinine levels. Histopathologic examination of tissues from different organs revealed a vasculopathy seen almost exclusively in obese rats fed the sucrose diets. Vascular lesions were characterized by subintimal fibrin deposition, fibrinoid necrosis, and cell proliferation with "onion skinning" in small arteries and arterioles of kidneys, intestine, pancreas, and testes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development and characteristics of a new strain of obese hyperinsulinemic and hyperlipidemic Dahl salt-sensitive rat. The Dahl salt-sensitive/NIH-corpulent rat. 766 22

We studied the effect of excessive salt intake on vascular lesion development in hypertensive transgenic mice that overproduce angiotensin II, ie, Tsukuba hypertensive mice (THM). At 6 weeks of age, THM and C57BL/6J (controls) were given either 1% sodium chloride ("salt-loaded") drinking water or tap water for 30 days. Salt-loaded THM, but not controls, suffered frequent thoracic or abdominal cavity hemorrhage. THM mortality after 7 days of salt loading was 23%; after 30 days of salt loading, it rose to 67%. Hemorrhaging occurred due to the development of aortic aneurysm and rupture at the aortic arch and aorta near the renal arteries. Vascular lesions progressed with structural degeneration of the aortic media. Electronmicroscopic analysis revealed that intact THM already exhibited vascular remodeling consisting of vascular smooth muscle cells (VSMCs) with developed organelles and an increased extracellular matrix. Salt-loaded THM suffered aggravated vascular hypertrophy and vascular structure destruction by plasma material invasion, necrosis of VSMCs possessing extremely swollen cytoplasm and abundant organelles, and interlamellar bleeding, resulting in aortic aneurysm and eventual rupture. Interestingly, blood pressure levels and heart rates in salt-loaded THM did not differ significantly from those of controls; plasma renin activity between drinking regimens was also comparable between the two groups. Drinking volume and the concentration of atrial natriuretic peptide (ANP) in plasma, however, were significantly higher in salt-loaded THM than in intact THM. In addition to aneurysm localization, the findings regarding drinking volume and plasma ANP suggest that aortic aneurysm and rupture in salt-loaded THM occurred as the result of an unknown mechanical stress, other than blood pressure, on the aortic wall. High salt ingestion is involved in the development of thoracic and abdominal aortic aneurysm in the presence of hypertension in the activated renin-angiotensin system. THM should therefore serve as a useful animal model for studying the pathogenesis of aortic aneurysm accompanied by hypertension.
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PMID:Salt-sensitive aortic aneurysm and rupture in hypertensive transgenic mice that overproduce angiotensin II. 975 50


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