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

Locally recurrent, poorly differentiated carcinoma of the prostate was associated with hypokalemic alkalosis, marked hypernatremia, diabetes mellitus of recent onset, and hyperosmolar syndrome. These findings, with mild hypertension, in the absence of clinical features of Cushing's syndrome, suggested an ectopic ACTH syndrome. Plasma ACTH and cortisol levels were markedly elevated, and failed to suppress in response to either low or high-dose dexamethazone administration. The patient's condition deteriorated rapidly. Autopsy findings included carcinoma extensively infiltrating the prostate with extension to the urinary bladder, and metastases confined to the pelvic nodes and soft tissues. The adrenal glands weighed 23 g and showed diffuse hyperplasia. Extract of the prostatic tumor was analyzed for ACTH and showed approximately 40 times normal plasma levels (or about 4,010 pg/g of tissue); ultrastructural features showed secretory granules consistent with ACTH content of the tumor cells. Such cells were positive when stained for ACTH by peroxidase-tagged immunochemical methods. The case fulfills all established criteria for relating excess corticosteroid production and nonpituitary tumors.
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PMID:Ectopic ACTH, prostatic oat cell carcinoma, and marked hypernatremia. 19 43

This review paper deals with the transport of the protein tracer horseradish peroxidase across cerebral vessels under normal and various experimental conditions. Electronmicroscopical investigations have revealed that, under normal conditions, a minor vesicular transfer of intravenously injected peroxidase occurs across the endothelium in segments of arterioles, capillaries and venules, especially in arterioles with a diameter about 15-30 mu. This normally occurring vesicular transport is susceptible to various experimental conditions. Thus the transfer of tracer increases when a hypertonic solution is injected into the internal carotid artery presumably due to vesicular transport. Extensive acute hypertension of short duration also increases the vesicular transfer of peroxidase from blood to brain. Identical observations are obtained when the hypertension is evoked by intravenous injection of phentolamine and by electrically induced seizures. During the postischemic period, one hour after release of the occlusion of an internal carotid artery in the Mongolian gerbil the vesicular transport of peroxidase is increased across the endothelium of cerebral vessels. The explanation may be release of serotonin from blood platelets during the occlusion. The serotonin could then increase the blood pressure locally in the brain resulting in an enhanced permeability. Serotonin, after perfusion through the cerebral ventricular system, is also able to increase the normally occurring vesicular transfer. The most likely mechanism behind this phenomenon seems at the moment to be local hypertension evoked by serotonin-induced vasoconstriction of arterioles. Finally, the enhanced vesicular transport across cerebral endothelium caused by porto-caval anastomosis is mentioned and the possible role of disturbances in the metabolism of amines as responsible for the extravasation is discussed.
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PMID:The blood-brain barrier to horseradish peroxidase under normal and experimental conditions. 33 57

Acute arterial hypertension was produced in male Wistar rats by pressure pulse through the right internal carotid artery. The pressure pulse was induced by infusion of physiological saline as a bolus, at a rate of 0.63 ml per second by syringe pump. Evans blue (Eb) was used to visualize the areas of blood-brain barrier opening. Intravenously injected horseradish peroxidase (HRP) was used to study the ultrastructural basis of permeability changes in cerebral endothelium. Eb outlined circumscribed areas of blood-brain barrier opening. HRP extravasation was found mainly around small arteries. The capillary network was affected to a much lesser extent. Electron microscopy showed that HRP crossed the endothelial cell layer by intercellular routes. Glutaraldehyde fixed brain samples permeated with colloidal lanthanum supported these observations.
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PMID:Opening of tight junctions in cerebral endothelium. II. Effect of pressure-pulse induced acute arterial hypertension. 43 71

Cerebral cortical arterioles in focal neocortical areas develop increased permeability to plasma proteins and protein tracers in experimental hypertensive encephalopathy. The mechanism underlying this increased permeability has been the subject of several studies. In our previous studies of angiotensin-induced acute hypertension, pinocytosis appeared to be the principal mechanism for the increased blood-brain barrier (BBB) permeability observed. In the present study pinocytotic activity was assessed quantitatively to determine whether enhanced pinocytosis was confined to the permeable arteriolar segments of hypertensive animals. In addition, the effect of horseradish peroxidase (HRP) itself on the pinocytotic activity of normal cerebral cortical arteriolar endothelium was determined. In 12 rats following administration of HRP, hypertension was induced by an infusion of angiotensin. The animals were perfusion-fixed 90 s after the onset of the infusion. Control animals received saline only or HRP only. The area of arteriolar endothelium in cross section was determined by a planimeter from overlapping electron micrographs taken at a constant magnification around the circumference of the vessel wall. Results indicate a significant (P less than 0.001) increase in the number of pinocytotic vesicles in the permeable arteriolar segments of hypertensive animals as compared with nonpermeable arteriolar segments of the same animals and comparable segments of normotensive rats. In addition, eight times as many vesicles appear to be transporting tracer in the permeable arteriolar segments of hypertensive animals as compared to the nonpermeable segments of the same animals and normotensive animals. HRP alone did not affect the pinocytotic index, there being no difference (P greater than 0.05) in the number of vesicles in normotensive animals receiving saline only and those receiving HRP only. Our previous observation that disruption of endothelial cells or their tight junctions did not occur was confirmed.
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PMID:Quantitative estimate of pinocytosis in experimental acute hypertension. 45 52

Acute arterial hypertension was induced in male Wistar rats using two experimental techniques: (1) i.v. injection of Aramine and (2) infusion of physiological saline as a bolus via internal carotid artery. Horseradish peroxidase (HRP) was injected i.v. prior to both experimental procedures and subsequently localized in the brain by light and electron microscopy. In the saline infusion (pressure pulse) model, colloidal lanthanum was also applied as a diffusion tracer following fixation of the cerebral endothelium. In the Aramine model, extravsation of HRP correlated with abrupt elevation of blood pressure. In the pressure pulse model HRP extravasation was consistently visualized in the affected hemisphere. Electron microscopy showed consistent labeling of plasmalemmal vesicles by HRP in segments of cerebral endothelium. However, HRP was also clearly visualized in junctional pools suggesting focal opening of endothelial tight junctions as a pathway for extravasation of this tracer in both hypertensive models. Colloidal lanthanum not transported by plasmalemmal vesicles across endothelium after fixation of the brain also bypassed consecutive membrane appositions of endothelial tight junctions indicating existance of interendothelial pathways to macromolecules in acute arterial hypertension.
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PMID:Blood-brain barrier opening to horseradish peroxidase in acute arterial hypertension. 50 90

The morphology and permeability to horseradish peroxidase of the rat aortic intima have been investigated in three experimental models of hypertension having different values of plasma renin content and plasma aldosterone level. During hypertension the aortic endothelium shows three main changes: 1) increased arithmetic mean thickness, with prominent rough endoplasmic reticulum and polyribosomes; 2) the appearance of actin microfilament bundles; and 3) increased permeability to horseradish peroxidase. These changes are not present in all models, do not appear to depend on hypertension per se, and are independent of each other. The subendothelial layer of hypertensive animals shows an increased thickness that appears to be correlated with an increase of endothelial cell volume. Our results suggest that: 1) the aortic intima reacts differently to different types of hypertension, and 2) factors other than hypertension per se play a role in the development of vascular changes observed in animals with elevated blood pressure.
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PMID:Morphologic and functional changes of the aortic intima during experimental hypertension. 57 70

Under normal conditions a slight vesicular transfer of intravenously injected horseradish peroxidase (HRP) occurs across the endothelium of cerebral vessels, especially short segments of arterioles. The vesicular transport can be notably increased by chemically induced acute hypertension. In the present investigation 4 groups of animals received HRP, and the permeability of the cerebral endothelium was studied semimacroscopically, light microscopically and electron microscopically. The rats in group 1 were given 10 electroshocks. This caused a significant rise in the blood pressure (BP). Furthermore, a noticeable extravasation of HRP was observed, especially across the endothelium in cerebral arterioles. From the basement membranes of the vessels reaction product could be followed into the extracellular spaces of the neighbouring neuropil. Group 2 comprises rats that were given 10 electroshocks preceded by transection of the cervical part of the spinal cord. The BP remained at normal level and the permeability was unaltered. The animals in group 3 received only 1 electroshock. Usually, the BP was markedly increased and this was accompanied by enhanced permeability across the vessels of the brain. Group 4 consists of control animals, injected with HRP and treated as groups 1 and 3 with the difference that electrical stimulation was not performed. A general feature was that no endothelial damage was observed and that reaction product was not found between neighbouring endothelial cells from the first luminal to the first abluminal tight junction. Based on the observations it seems reasonable to assume that the increased permeability of tracer that occurs after 10 electroshocks or only one is caused by the acute hypertension evoked by the electrical stimulation; furthermore, the transfer is concluded to be vesicular transport.
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PMID:Increased permeability to horseradish peroxidase across cerebral vessels, evoked by electrically induced seizures in the rat. 63 39

Foam cell lesions were found in cholesterol-fed rabbits with induced hypertension, particularly in intimal cushions at branching sites, where permeability to horseradish peroxidase was enhanced. Permeability to horseradish peroxidase was enhanced at the edge of intimal cushions without foam cell accumulation. This finding suggests that permeability is increased before foam cell infiltration. No foam cell lesions were observed in the intima of cerebral arteries distant from branching sites, but insudation of plasma constituents here caused endothelial cells to separate from the subendothelial matrices. Foam cell lesions were absent from the cerebral arteries in normotensive cholesterol-fed rabbits.
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PMID:Hypertension-induced cerebral atherosclerosis in the cholesterol-fed rabbit. 67 15

Multiple focal cortical areas of increased vascular permeability to tracer substances occur in experimental hypertensive encephalopathy. In this study, rats with angiotensin-induced acute hypertension were used to determine whether increased permeability was associated with focal cerebral edema and if so, the tissue component involved. In addition, the mechanism of increased permeability and the types of vessels involved were investigated using horseradish peroxidase as a tracer. Quantitative morphometric studies 8 minutes after the onset of hypertension demonstrated significant perivascular glial swelling around arterioles, venules, and capillaries; the swelling was confirmed to the permeable areas and absent in the nonpermeable areas of the same animals. Ninety seconds after the onset of hypertension, horseradish peroxidase reaction product was present in focal superficial segments of the walls of penetrating arterioles but rarely in venular and capillary walls. At this time period endothelial cells showed prominent pinocytotic uptake of tracer. Eight minutes after the onset of hypertension, reaction product was again found in arteriolar walls and had extravasated into the surrounding extracellular space of the neuropil as well. Extravasation also occurred through capillary and venular walls but was less frequent. At this time interval endothelial pinocytotic activity was still prominent. There was no mechanical damage of vessel walls in the form of endothelial discontinuities or disruption of interendothelial spaces. Tracer was not found in interendothelial jundtions in continuity from lumen to base. The principle mechanism of increased permeability was enhanced pinocytosis, which occurred rapidly, being demonstrable 90 seconds after the onset of hypertension; it was observed principally in permeable arteriolar segments.
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PMID:Cerebral cortical changes in acute experimental hypertension: An ultrastructural study. 83 31

Acute hypertension in rats was produced by intravenous infusion of metaraminol bitartrate (Aramine). The permeability to intravenously injected horseradish peroxidase (HRP) was increased across the cerebral arterioles, capillaries and venules. From the basement membranes of the vessel walls the protein tracer moved into the extracellular spaces of the adjacent neuropil. No endothelial cell damage was observed. The tight junctions between endothelial cells were intact and prevented intercellular movement of peroxidase. Many HRP-labeled vesicles within the endothelial cells or connected with the luminal or abluminal surface, occurred in segments of the microvasculature. Otherwise the endothelium was unchanged. Diffuse uptake of HRP into the cytoplasm of neurons and glial cells was not observed. The alphablocker phentolamine (Regitin) was given to a group of rats simultaneously to Aramine. The increase in blood pressure was thus prevented; furthermore, the permeability remained as under normal conditions. The Aramine, Regitin and HRP did not significantly influence the pH, PO2 and pCO2 of the arterial blood. It is concluded that acute hypertension increases the vesicular transport of HRP across the endothelium of cerebral arterioles, venules and capillaries that normally occurs to a small extent only after intravenous injection of the tracer.
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PMID:Increased vesicular transfer of horseradish peroxidase across cerebral endothelium, evoked by acute hypertension. 84 78


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