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 influence of shortlasting (less than 1 min) epileptic seizures on the permeability to protein of the blood-brain barrier (BBB) was studied in rats. The protein tracer, horseradish peroxidase (HRP) was used as marker substance. Monitoring arterial blood pressure (BP) and electroencephalogramme (EEG) seizures were induced electrically after HRP was given intravenously. Following a single electroshock seizure slight staining of brain tissue was seen, while after 10 electroshock stimuli followed by sustained seizure activity, this phenomenon was more pronounced. If 10 electroshock stimuli were preceded by transsection of the spinal cord, blood pressure increase was abolished and no tissue staining was seen in spite of epileptic seizure activity recorded on EEG. This means that the acute hypertension and not the seizure activity per se is the mechanism behind the breakdown of the BBB during epileptic seizures. Electron microscopy revealed an increased vesicular transport (pinocytosis) across the endothelial cells, while the vascular structure remained intact.
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PMID:Acute hypertension causing blood-brain barrier breakdown during epileptic seizures. 92 Jan 12

Acute hypertension has been produced in rats by the intravenous infusion of angiotensin amide for 4 hours. Both control and hypertensive animals were injected intravenously prior to sacrifice with either horseradish peroxidase (HRP) or colloidal carbon. Epicardial arteries and blocks of ventricular myocardium containing intramyocardial arteries and arterioles have been processed for electron microscopy. HRP appears to penetrate the endoethelium of epicardial arteries from control animals within vesicles that bypass endothelial junctions and empty into interendoethelial clefts. Peroxidase does not traverse the endothelium of intramural arteries and arterioles of controls over the 10-minute period of observation. There is acceleration of lateral vesicular transport in the endothelium of epicardial arteries after angiotensin infusion and direct permeation of interendothelial clefts of intramural arterial vessels. Medial fragmentation and more extensive necrosis are observed in intramyocardial but not in epicardial arterial vessels. Foci of myocardial damage resembling irreversible ischemic or anoxic injury followed by reflow are described. It is suggested that the increased permeability of epicardial arteries may be due to elevated pressure, while the altered permeability and vascular lesions of intramural arteries and arterioles are more readily attributable to the vasoconstriction produced by angiotension. The vascular and myocardial lesions are also discussed in relation to the regional actions of angiotensin on the coronary circulation and known effects of this vasoactive peptide on myocardium.
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PMID:Effect of angiotensin-induced hypertension on rat coronary arteries and myocardium. 93 12

The selectively-bred substrains of spontaneously hypertensive rats with a greater vulnerability to vascular lesions rapidly developed arterial fat deposition within 1 or 2 weeks as well as a greater hypercholesterolemic response when fed on high fat cholesterol diet including 20% of suet, 5% of cholesterol and 2% of cholic acid. The ring-like arterial fat deposition at the branches of superior mesenteric arteries and cerebrobasal arteries, which was found to be good indices for the deposition of intrarenal or coronary arteries, was not observed in normotensive rats fed on high fat cholesterol diet for 3 months, greatly delayed in SHR under antihypertensive treatment and accelerated by 1% salt loading in drinking water. The horseradish peroxidase infused intravenously 1 to 4 hours before sacrifice leaked in ring-like forms which corresponded to the fat deposit in mesenteric arteries. The incorporation of 3H-proline infused 4 hours before sacrifice was enhanced in the mesenteric arteries with the fat deposition. These results clearly indicated that hypertension was a great contributory factor to rapid arterial fat deposition, which was caused by an increased vascular permeability and enhanced the arterial collagen formation, the initiation process of arterio- or atherosclerosis.
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PMID:Pathogenesis of acute arterial fat deposition in spontaneously hypertensive rats. 115 92

Acute hypertension, experimentally induced by intravenous injection of metaraminol in adult rabbits, rapidly induced a damage of the blood-brain barrier in the cerebral cortex, as visualized by Evans-blue-conjugated albumin and horseradish peroxidase. Extravasation of these two exogenous tracers was demonstrated to occur in arterioles, in capillaries and, rarely, in venules. Peroxidase passed the endothelial cell into the nervous tissue in either or three different ways, i.e. through channels, often sigmoidshaped, in the cytoplasm, and transendothelial pinocytosis. The third pathway could, although rarely, be demonstrated between adjacent endothelial cells after cleavage of junctional complexes. The tracer peroxidase was further spread along the blood vessel within the basement membrane and in the extracellular space of the brain. Damaged endothelial cells with diffuse cytoplasmic peroxidase activity and large vesicles were occasionally observed within the areas with blood-brain barrier injury. There were also signs of increased pinocytotic activity in endothelial cells outside the barrier damaged cortical areas. Nerve cells and neuroglial cells could show either a diffuse cytoplasmic peroxidase activity or a vesicular location of the tracer, or sometimes both. The observations are discussed in relation to previous studies on the mechanism of transendothelial passage of protein tracers at blood-brain barrier damage.
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PMID:Ultrastructural studies on cerebrovascular permeability in acute hypertension. 118 1

Cerebrovascular permeability in stroke-prone spontaneously hypertensive rats (SHR) at various ages was histologically studied using horseradish peroxidase as a tracer and such was related to the cerebrovascular lesions in the animals. An increase in permeability was demonstrated in the brain of SHR, particularly in those animals with an extremely high blood pressure. Increased cerebrovascular permeability occurred in some animals without any organic vascular change or severe parenchymal changes, although edema was present. Histologically, the SHR brain with an increase in permeability showed mild focal edema, rarefaction of tissue and necrosis with cyst formation. Thus a transitional progress was evident. Localization of the increase in permeability corresponded well with the predilection sites of cerebrovascular lesions in SHR. Constrictions and dilatations of intracerebral arterioles and small arteries were also demonstrated by the peroxidase method, and the dilated arterial walls did reveal a darker staining. From these results it is strongly suggested that certain cerebrovascular lesions, especially necrosis with cyst formation in SHR are sequelae of the increased cerebrovascular permeability caused by a chronic hypertensive state.
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PMID:Changes in vascular permeability in stroke-prone spontaneously hypertensive rats studied with peroxidase as a tracer. 119 27

One week after hypertension was produced in male Wistar rats (150 g body weight) by a complete aortic ligature placed between renal arteries, electron microscopic studies showed a striking increase of cytoplasmic microfilaments in the endothelial cells of the aortic segment above coarctation (mean blood pressure 160 mm Hg). These microfilaments measured 40-70 A in diameter and were located particularly close to the endothelial clefts. In "en face" preparation of aortic endothelial cells treated with antiactin autoantibodies (AAA) followed by antihuman IgG, the cells above the ligature of hypertensive animals were intensely fluorescent compared with those of the aortic portion below the ligature or that of controls. The fluorescence was abolished after incubating the AAA-containing sera with thrombosthenin-A, suggesting the presence of actin. There was also an increase transport of horseradish peroxidase and ferritin through the endothelial cell layer. While endothelial cells so modified may play a role in permeability regulation, they may also be related to such mechanisms as electronic coupling and synchronized contraction of aortic cells during hypertension.
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PMID:Contractile apparatus in aortic endothelium of hypertensive rat. 120 6

There is evidence that the blood-brain barrier (BBB) is breached following traumatic brain injury (TBI), allowing the unregulated entry of circulating neuroactive substances into the central nervous system. As the traumatic episode is typically associated with an acute hypertensive event, which in itself may alter BBB status, the effects of the blockade of TBI-associated hypertension on injury-associated behavioral and cerebrospinal fluid (CSF) neurochemical changes were assessed in rats. Animals were injected with either saline or hexamethonium 15 min prior to a moderate fluid percussion injury while under light methoxyflurane anesthesia. This dose of hexamethonium was demonstrated to block the hypertensive response to TBI. Pretreatment with hexamethonium prevented neither acute nor more enduring behavioral deficits observed after TBI. Hexamethonium did not prevent TBI-associated increases in CSF acetylcholine (ACh) content in separate group of rats sampled 12 min following TBI. Furthermore, histological inspection indicated that hexamethonium did not prevent TBI-induced disruption of the BBB, as assessed by intravascular horseradish peroxidase (HRP). Thus, blockade of the hypertensive response to TBI does not afford behavioral protection nor does it prevent changes in the BBB or CSF ACh content following TBI. TBI is in itself sufficient to modify behavior, neurochemistry and BBB function in the absence of hypertension.
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PMID:Blockade of acute hypertensive response does not prevent changes in behavior or in CSF acetylcholine (ACH) content following traumatic brain injury (TBI). 138 Dec 63

Kidney biopsy specimens obtained from a group of individuals with chronic glomerulonephritis (CGN) have been processed for light and electron microscopic immunolocalization of total immunoglobulins (Igs). In a few cases, acid phosphatase (ACPase), a lysosomal enzyme marker, was ultrastructurally visualized. In the glomeruli, horseradish peroxidase-stained Igs were revealed in capillary lumina, urinary spaces and in transit through occasional loci of the glomerular basal membranes while ACPase-containing lysosomes resided both within and outside the cells. In the proximal tubules, Igs were traced in the endocytic vesicles and vacuoles, the latter also being positive for ACPase. Statistically significant relationships have been revealed between the number of IGs-labeled proximal tubules and some clinical or pathomorphological stigmata of CGN, in particular, proteinuria and arterial hypertension levels, marked interstitial sclerosis, etc. The data obtained are discussed in regard to the mechanisms of increased macromolecular filtration and the different proteinuria selectivity levels as well as the development of interstitial sclerosis as a result of the elevated reabsorption and incomplete lysosomal degradation of Igs in CGN.
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PMID:[Immunoglobulin filtration and reabsorption as possible factors in the pathogenesis of chronic glomerulonephritis. Clinical, immunomorphological and histoenzymological research]. 144 Mar 30

There are many unanswered questions about chronic glaucoma which cannot be investigated in the available animal models. The present experiments were designed to develop a rabbit model of chronic intraocular hypertension with characteristics similar to human chronic glaucoma by ligating vortex veins or by making single or multiple intraocular injections of 0.5% or 1% alpha-chymotrypsin, 20% chondroitin sulphate, 2% hydroxypropyl methylcellulose, 2% sodium carboxymethylcellulose or 1% or 2% methylcellulose. Evaluation was based on the clinical findings, intraocular pressure and the retrograde axoplasmic transport function of the optic nerve using a horseradish peroxidase histochemical technique. Most methods either failed to produce moderate chronic intraocular hypertension or were associated with other complications. However, a reliable and relatively long period (eight weeks) of intraocular hypertension was developed by a series of four intra-anterior chamber injections of 1% or 2% methylcellulose. This model has been proved suitable for the study of structural and functional damage to the retina and optic nerve caused by chronic glaucoma.
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PMID:Development of experimental chronic intraocular hypertension in the rabbit. 144 75

The dendritic complexity of peripheral autonomic neurons is positively matched with the size of the target they innervate, apparently by trophic interactions with the target (D. Purves, W. D. Snider, and J. T. Voyvodic. Nature Lond. 336: 123-128, 1988). We have asked whether the vascular hypertrophy associated with hypertension is accompanied by dendritic hypertrophy of sympathetic ganglion cells. To do this, we examined the morphology of stellate ganglion cells in the spontaneously hypertensive rat (SHR), its normotensive control Wistar-Kyoto rat (WKY), and two new strains derived from the SHR that independently express the hypertensive phenotype of the SHR (WKHT) and the behavioral hyperactivity present in the SHR (WKHA). Cells were examined by intracellular staining with horseradish peroxidase in in vitro preparations of the ganglia. Carotid arterial wall size was also examined. Significant hypertrophy of both the carotid arterial wall and stellate ganglion cell dendrites was observed in the two hypertensive strains (SHR and WKHT) but not in either of the normotensive strains (WKY and WKHA). This increased total dendritic length of stellate ganglion cells associated with hypertension provides a greater target area for preganglionic innervation that may result in hyperinnervation of these cells.
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PMID:Hypertrophy of stellate ganglion cells in hypertensive, but not hyperactive, rats. 192 45


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