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 distribution of renin in two cases of segmental renal hypoplasia was investigated by immunofluorescence and the peroxidase anti-peroxidase (PAP) method using an anti-human renin antiserum. Renin-containing cells were found only in hypoplasic segments in the vicinity of altered glomeruli and small arteries. Well-preserved renal cortex and areas of chronic atrophic pyelonephritis failed to show any demonstrable site of renin production. Whatever is the mechanism of the disease, the characterization of large numbers of renin-containing cells in the affected kidney support a role for the renin-angiotensin system stimulation in this form of hypertension.
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PMID:Renin localization in segmental renal hypoplasia. Immunohistochemical demonstration in two cases. 701 53

An increase in the weight of the thyroid gland, accompanied by reductions in uptake and release of 1311, serum T3 and reverse T3 concentrations and an increase in serum TSH concentration, occurs during the development of renal hypertension in rats. Renal function, as assessed by BUN, serum and urinary creatinine concentrations, and ability to concentrate urine during dehydration, is depressed. The kidneys of both normotensive and renal hypertensive rats contain a thyroid depressing factor (TDF) which inhibits uptake of 131I both in vivo and in vitro as well as inhibiting the lactoperoxidase enzyme in vitro. The kidneys of renal hypertensive rats contain less, and the serum more, TDF than those of normotensive rats. Whether TDF is produced as a result of hypertension per se or as a result of renal damage accompanying hypertension remains for further study. TDF appears to be a peptide with a molecular weight in the range of 400 to 419 daltons.
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PMID:Renal-thyroid interrelationship in normotensive and hypertensive rats. 707 Feb 20

The effect of induced hypertension on the blood-brain barrier (BBB) change in Mongolian gerbils exposed to various periods of ischemia was studied. Evans blue dye was used to determine the BBB change in animals subjected to different levels of hypertension after 3 h ischemia. Horseradish peroxidase (HRP) was used in electronmicroscopic studies of animals subjected to 30 min, 1, 3 or 6 h ischemia and subsequently exposed for 30 min to varying periods and sequences of normo- and hypertension. Furthermore, HRP-labeled vesicle counts were performed in animals from the 30-min ischemia group. Our findings revealed that hypertension, after blood flow restoration following ischemia, induces and/or accelerates BBB damage by enhancing endothelial vesicular and/or tubulo-channel transport.
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PMID:Effect of hypertension on blood-brain barrier. Change after restoration of blood flow in post-ischemic gerbil brains. An electronmicroscopic study. 721 66

The effects of carotid artery constriction on cerebrovascular ultrastructure and permeability in acute hypertension have been assessed. The right common carotid artery of 26 male Wistar-Kyoto normotensive rats was constricted with a silver wire clip. Forty-eight hours later these animals received an angiotensin amide injection (1 microgram/kg body weight) or infusion for 3--4 hours (0.5 or 1.7 microgram/min/kg body weight) or were subjected to subdiaphragmatic aortic constriction. All animals were injected with horseradish peroxidase (HRP) (20 mg/100 g body weight) and sacrificed after 5--15 minutes. Parietal cortex from both hemispheres was processed for light and electron-microscopic examination. The arterial vessels of the right hemisphere from animals given injections of or infused with angiotensin II exhibited increased permeability to HRP, as manifested by the presence of reaction product in interendothelial cell clefts, in subendothelial space, in endothelial and smooth muscle cell pinocytotic vesicles, and along smooth muscle cell basal laminas. In contrast, no alterations in the permeability of ipsilateral vessels were seen in rats with aortic constriction. Cerebral cortical arterial vessels from the left hemisphere in all groups of animals exhibited segmental dilatation and constriction and abnormal permeability to HRP. The results suggest that angiotensin administration can produce increased permeability of cerebral cortical vessels in the absence of elevated blood pressure.
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PMID:Carotid artery constriction in acute hypertension. 723 64

Our previous studies of cerebrovascular permeability in angiotensin-induced acute hypertension demonstrated that the principal mechanism resulting in increased permeability is enhanced pinocytosis. In order to exclude the possibility that the enhanced pinocytosis was a direct effect of exogenous angiotensin, cerebrovascular permeability alterations were studied in nonpharmacologically induced acute hypertension. Rats receiving horseradish peroxidase (HRP) intravenously, were sacrificed 2 1/2 minutes after the onset of hypertension induced by placing a clip on the abdominal aorta. These animals showed the same pattern of permeability alterations as had been observed previously in animals with angiotensin-induced acute hypertension. Focal segments of penetrating arterioles in the temporal and parietal cortex showed increased permeability to HRP. Permeable vessels showed increased numbers of pinocytotic vesicles and the interendothelial junctions revealed no alterations. Enhanced pinocytosis appears to be the principal mechanism resulting in increased cerebrovascular permeability in this model as well as suggesting that the alterations of cerebrovascular permeability observed previously in angio-tensin-induced acute hypertension occur due to the hypertensive state and are not a direct drug effect of exogenous angiotensin.
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PMID:Cerebrovascular permeability in mechanically induced hypertension. 728 98

This study examined characteristics of paracellular and pinocytotic permeability pathways across the middle cerebral artery endothelium of 12- to 16- month-old spontaneously hypertensive rats (SHR). Interendothelial junctions in SHR, like those of age-matched Wistar-Kyoto controls, were impermeable to lanthanum and horseradish peroxidase (HRP) tracers. Freeze-fracture preparations revealed that interendothelial junctions of chronically hypertensive rats are characterized by a twofold increase over controls in the number of tight junctional strands and the mean apical-basal depth. It is believed that this tight junctional hypertrophy may function to increase adhesive forces between neighboring endothelial cells, and may play a role inthe prevention of hypertension-induced paracellular permeability increases. Morphological and tracer studies of pinocytotic pathways indicated that, it the middle cerebral artery, endothelial vesicular transport activity is not increased during chronic hypertension. No evidence was found to indicate the presence of transendothelial permeability channels across control or hypertensive arterial endothelium. Thus, increased transendothelial permeability, commonly observed in acute hypertension, does not appear to occur during chronic hypertension, at least in the middle cerebral artery. Our findings suggest that the arterial endothelium may undergo structural (tight junctional) adaptation in response to prolonged hypertension.
Hypertension
PMID:Ultrastructural characteristics of endothelial permeability in chronic hypertension. 729 13

A longitudinal study on the development of vascular lesions was carried out in the spontaneously hypertensive rat (SHR) of the Aoki-Okamoto strain. The aorta and intrarenal arterial vessels were examined at different ages, from 5 to 48 weeks, by light and electron microscopy. Endothelial permeability to injected horseradish peroxidase (HRP) was evaluated in 20-week-old animals. Morphologic differences between vessels of SHRs and age-matched normotensive controls (Wistar-Kyoto strain) were first noted at 10 weeks of age and became more pronounced with time. Vascular pathology involved both intima and media. Medial thickening was seen in both aorta and peripheral arteries and, in the latter, was associated with decreased luminal diameters. These medial changes may contribute to the maintenance of the elevated blood pressure. Intimal lesions affected predominantly the aorta and were characterized by an expansion of the subendothelial space with deposition of acid mucopolysaccharides. There was increased accumulation of tracer HRP in the expanded subendothelium, which suggested enhanced permeability and/or retention of the tracer. In animal species susceptible to atherosclerosis, these intimal changes could serve as the structural basis for the higher propensity for atheromatous lesions in hypertensive individuals. In the SHR, despite stabilization of systolic blood pressure at about 20 weeks of age, both intimal and medial lesions continue to progress and become more extensive and severe; this suggests that not only the severity of hypertension but also its duration are significant determinants of the degree of vascular damage.
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PMID:The evolution of vascular changes in the spontaneously hypertensive rat. 735 87

A new approach is described to study the mechanism of protein leakage through the endothelial cells in acute hypertension and after intracarotid infusion of hyperosmolar solutions. The luminarl surface of the cerebrovascular endothelial cells was labeled with choleragenoid-peroxidase before the blood-brain barrier (BBB) dysfunction was induced. Numerous pinocytotic vesicles and some transendothelial channels were formed and showed labeling of parts of their membranes. Our results indicate that the mechanism behind the protein leakage induced by hypertension and by hyperosmolar solutions is the same--ie, transendothelial pinocytosis.
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PMID:Induction of pinocytosis in cerebral vessels by acute hypertension and by hyperosmolar solutions. 740 Nov 97

Our previous studies of angiotension-induced acute hypertension showed increased intracerebral arteriolar permeability associated with markedly enhanced pinocytosis. This study was performed to determine whether similar findings occurred in spontaneous non-pharmacologically induced chronic hypertension. Cerebrovascular permeability to horseradish peroxidase (HRP) was studied over an 82-week period in spontaneously hypertensive rats (SHR) derived from a strain that originated from Japan. In a few animals increased cerebrovascular permeability to HRP was observed, associated with enhanced pinocytosis. Quantitatively, the number of pinocytotic vesicles in permeable arteriolar segments was significantly increased suggesting that enhanced pinocytosis is the principal mechanism of early cerebrovascular changes in SHR. Light microscopy of renal, ocular and cerebral vessels revealed medial hyperplasia affecting renal vessels at 16 weeks and occurring later in ocular and cerebral vessels. Deposition of fibrin in renal vessels was observed from 64 weeks onwards but was not associated with renal failure.
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PMID:Morphological changes in spontaneously hypertensive rats. 743 54

The distribution of endogenous albumin and immunoglobulin G (IgG) has been studied by the immunoperoxidase technique in the superficial glomeruli of both normotensive and hypertensive (acute angiotensin II-induced) Munich-Wistar rats. Endogenous IgG has also been detected in rats immunized with horseradish peroxidase. Labeled antibodies have been applied to sections on a conventional manner as well as by an electrophoretic technique. The immunization of animals with horseradish peroxidase, as well as application of the electrophoretic technique, both result in a greater yield of labeled glomeruli. Albumin is present within the capillary lumina of control animals, penetrates the capillary walls, and extends into the urinary space. Endogenous IgG is mainly confined to lumina of glomerular capillaries, with only small amounts visible in the laminae rarae of the basement membrane. After acute hypertension induced by angiotensin II, there is increased staining of albumin and IgG in the basement membrane and of albumin in the urinary space. There is also penetration of IgG into Bowman's space. Both macromolecules are found in dilated mesangial channels. These modifications of glomerular permselectivity in hypertension are not accompanied by discernible ultrastructural changes in the peripheral capillary wall. It is suggested that the transcapillary passage of albumin and IgG is dependent upon hemodynamic factors and/or subtle changes in the filtering membrane.
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PMID:Glomerular permeability to endogenous proteins in the rat: effects of acute hypertension. 746 38


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