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

The factors responsible for predisposition to progressive organ injury and vascular complications in arterial hypertension are uncertain. Recent evidence shows that leukocytes participate in cardiovascular conditions for which hypertension is a risk factor. Therefore, there is a need to define the properties of circulating leukocytes in hypertensives. There are about twice as many circulating leukocytes in spontaneous hypertensive rats (SHRs) compared with their normotensive controls, the Wistar-Kyoto rats (WKYs). The SHR neutrophils are viscoelastic and similar to neutrophils in WKYs but exhibit lower deformability in short-term elastic deformation. Mature SHRs have elevated levels of spontaneous pseudopod formation. Mild stimulation with N-formyl-Met-Leu-Phe or platelet-activating factor (10(-8) M) results in a significantly enhanced level of neutrophil pseudopod formation in SHRs but not in WKYs. SHRs exhibit higher levels of spontaneous superoxide formation. Alkaline phosphatase content of individual circulating neutrophils in SHRs is on average lower while plasma levels of alkaline phosphatase in the same samples are elevated in the SHRs. Spontaneous degranulation of SHR neutrophils is also detectable with myeloperoxidase measurements. Such activity of circulating leukocytes poses a significant risk for vascular cytotoxicity in the hypertensive rats.
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PMID:Properties of circulating leukocytes in spontaneously hypertensive rats. 870 19

The distribution of substance P in the intermediolateral column of the upper thoracic spinal cord of spontaneously hypertensive (SHR) rats and Wistar-Kyoto (WKY) rats was studied by combined retrograde tracing of choleragen subunit-B horseradish peroxidase (CB-HRP) and immuno-electronmicroscopy. In the T(1)-T(3) segments of the spinal cord, SP-like immunoreactive products were localized in the cell bodies and dendrites of the sympathetic preganglionic neurons as well as in a few pre-axon terminals or axon terminals. In the neuropil of the intermediolateral column (ILN), different synaptic configurations were observed including synaptic contacts between SP-like positive dendrites and negative axon terminals, and between SP-like positive axon terminals and SP-like positive dendrites. Furthermore, a single SP-like positive dendrite was sometimes postsynaptic to several axon terminals, a feature typical of glomerular synapses. The present findings suggest that most of the SP-like immunoreactive elements in the ILN were of intraspinal origin derived mainly from the sympathetic preganglionic neurons in SHR and WKY rats. Since there was no ultrastructural difference in the distribution of SP between the neural elements in the ILN of SHR and WKY rats, the present findings also suggest that SP may not be directly involved in the hyperactivity of the sympathetic nervous system in hypertension.
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PMID:Ultrastructural localization of substance P-like immunoreactivity in the intermediolateral column of spontaneously hypertensive rats and Wistar-Kyoto rats. 886 52

Intracerebroventricular injection of hypertonic saline induces experimental hypertension. To measure [Na] in the vicinity of osmosensitive sites, we continuously measured [Na] in cerebrospinal fluid ([Na]csf) in the lateral ventricle (LV, n = 6), in the third ventricle (V3, n = 6) and in the medial preoptic nucleus (MPO, n = 6) ([Na]MPO) with a Na-sensitive electrode together with mean arterial pressure (MAP) during infusion of hypertonic artificial cerebrospinal fluid (ACSF, [Na] = 1,000 meq/kg H2O) at 5 "mu"l/min for 3 min into the LV in urethane- anaesthetized rats. [Na]csf in the LV began to increase at the beginning of infusion, reaching a peak of 48 +/- 9 meq/kg H2O (mean +/- SE) around the end of infusion, then recovering to the pre-infusion level by 17 min. [Na]csf in V3 changed similarly to that in the LV without any delay, although the peak value was reduced (61% , P < 0.05). In the MPO, in contrast the increase in [Na]MPO was delayed (3 min, P < 0.002) and the peak reduced even further (to 37%, P < 0.01) compared with that in V3. Thereafter, it remained higher than the pre-infusion level until the end of recovery (P < 0.05). MAP began to increase at the onset of infusion (P < 0.05); the maximum increase of 16 +/- 2 mm Hg (n = 18) was reached at the end of infusion, whereafter this level was almost sustained until the end of the 22-min recovery period. To analyse quantitatively the relationship between MAP and [Na]csf, hypertonic ACSF was infused at 2.5 "mu"l/min into the LV. [Na]csf in the LV and MAP increased at half the rates seen with 5 "mu"l/min. These results suggest that the first increase in MAP after hypertonic infusion into the LV is due to the increase in [Na] in the LV and V3, and that the subsequent sustained increase in MAP is related to the delayed increase in [Na] in the periventricular tissues of the V3.
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PMID:Cerebrospinal fluid sodium concentration and osmosensitive sites related to arterial pressure in anaesthetized rats. 892 96

The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150-180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p < 0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels.
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PMID:Ultrastructural changes in the blood-brain barrier in rats after treatment with nimodipine and flunarizine. A comparison. 900 89

Cardiovascular diseases remain to be the 4th rank of top ten causes of mortality in Taiwan in recent years. Atherosclerosis and coronary artery disease, which often culminating in the occurrence of myocardial infarction and congestive heart failure, are responsible for the majority of these death. One of the prominent features of atherosclerotic lesion is local accumulation of lipids, mainly in the forms of cholesteryl ester and free cholesterol, either within cells or extracellularly in matrix. Repeated endothelial injury and enhanced lipid infiltration are critical events in the development of atherosclerosis. Plasma lipoproteins may enter the arterial wall through endothelium, either transcellularly via vesicular transport or paracellularly via intercellular junction. Our previous studies have demonstrated that most of the arterial endothelial cells in mitosis are associated with the leakage of fluorescently labeled albumin and low density lipoproteins. Subsequently, such transendothelial leakage of macromolecules is also shown to be associated with endothelial cell death as assessed by immunocytochemical staining for IgG. These findings suggested that transiently leaky junctions occurring during endothelial cell turnover may provide potentially important pathways for increasing transport or leakage of macromolecules, including atherogenic LDL, across the vascular endothelium. Electron microscopic study using horseradish peroxidase as a tracer revealed markedly widening of intercellular junctions around endothelial cells in mitosis providing direct evidence in support of "cell turnover-leaky junction" theory for the localization of atherogenesis. Hypertension, smoking, diabetes, and hyperlipidemia are well-known major risk factors for atherosclerosis and coronary heart disease. In a series of investigations, we examined the hypothesis that hypertension smoking, diabetes, and hyperlipidemia increase the arterial endothelial cell turnover and hence transendothelial macromolecular transport, which may have some implications in increasing lipid entry and thus, accelerating atherogenesis. Animal experiments were performed in adult male spontaneously hypertensive rats (SHR), Wistar-Kyoto (WKY) normotensive rats, and Sprague-Dawley (SD) rats. SHRs were used as hypertensive group with WKY rats as normotensive control. SD rats were given nicotine at a dose of 5 mg/Kg body wt/ day in their drinking water to mimic smoking effect over a period of 6 weeks. Diabetes was induced in SD rats by single intraperitoneal injection of 60 mg/Kg body wt of streptozotocin. The duration of diabetes was 6 weeks. Also, SD rats were fed a diet containing 5% cholesterol for 6 weeks to induce hyperlipidemia. Age-matched rats of comparable number served as control for each experimental group. In en face preparations of thoracic aorta, mitotic endothelial cells were identified by hematoxylin staining, immunoglobulin G-containing dying or dead endothelial cells were detected by an indirect immunoperoxidase method, and endothelial leakage to Evans blue-albumin (EBA) complexes (5 minutes after intravenous injection) was visualized and quantified by fluorescence microscopy. The results showed that SHR, chronic oral nicotine-treated rats, diabetic, rats, and hyperlipidemic rats, when compared to control rats, had higher values for the frequency of endothelial cell death and the number density of EBA leaky foci in the aorta. These findings suggested that hypertension, cigarette smoking, diabetes mellitus, and hyperlipidemia become risk factors in atherogenesis by increasing the rate of arterial endothelial cell turnover and the associated endothelial cell turnover and the to the consequent enhanced entry of atherogenic lipoproteins into the arterial wall and accelerated atherogenesis.
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PMID:Risk factors, endothelial cell turnover and lipid transport in atherogenesis. 903 45

Whether the serum levels of endothelin, a vasoconstrictive peptide produced in the endothelial cell, increase in preeclamptic patients is still controversial. We performed immunohistochemical studies to observe the changes in endothelin-1 (ET-1) in preeclamptic kidney tissues. The monoclonal anti-human ET-1 antibody (Yamasa, Japan) and anti-von Willebrand factor (vWF, Dako, Denmark), a marker of endothelial cells, were used for the studies by the strepto-avidin-biotin peroxidase method (ABC-POD Kit, Wako, Japan). Twenty-nine patients and 12 normal controls were divided into four groups. The preeclamptic group included 14 patients diagnosed with preeclampsia by clinical symptoms of hypertension, proteinuria, and edema occurring in late pregnancy and as having preeclamptic nephropathy. They underwent renal biopsy 16.7 +/- 1.0 (mean +/- SEM) days after delivery. The nephrotic group comprised 10 normotensive nonpregnant patients with nephrotic-range proteinuria examined through biopsy before treatment (six cases of minimal change, two of focal segmental glomerulosclerosis, one of membranous nephropathy, and one of IgA nephropathy). The pregnant women with preexisting glomerular disease group included five pregnant women with normal renal function who were normotensive and had no increase in the amount of proteinuria throughout pregnancy. They underwent renal biopsy 10.8 +/- 2.9 days after delivery (two cases of membranous nephropathy, one of focal segmental glomerulosclerosis, one of thin basement membrane disease, and one of non-IgA mesangioproliferative glomerulonephritis). The normal kidney group comprised 12 healthy tissue samples taken from nephrectomized kidneys (five cases of renal cell carcinoma, one case of lipofibrosarcoma, and six cases of kidney transplant donors). In these four groups, ET-1 and vWF showed equally positive staining in small arteries. VWF also showed positive staining in arterioles and peritubular capillaries in all groups. Although the glomeruli showed positive staining with ET-1 along the capillary walls in the normal group and the nonpregnant nephrotic group, they showed very weak or negative results in the preeclamptic group. Moreover, gravida with underlying glomerular disease without superimposed preeclampsia also showed negative findings of ET-1 in the glomeruli. The glomeruli in the four groups showed positive findings, with vWF readings the same as in the controls. These results indicate that the production of ET-1 in the glomerular endothelial cells decreases in cases of both preeclampsia and normal pregnancy, and the condition may be caused by pregnancy itself.
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PMID:Immunohistochemical study of endothelin-1 in preeclamptic nephropathy. 904 Dec 9

Hypertension is a known risk factor for the development of atherosclerosis, which is characterized by the abnormal accumulation of low-density lipoprotein and other plasma-borne macromolecules. The goal of this study was to measure accumulation of a plasma-borne macromolecular marker, horseradish peroxidase (HRP; 44 kDa), in the aortic intima and media of chronically hypertensive rats. HRP transport in 2-yr-old spontaneously hypertensive rats (SHR) was compared with that in age-matched Wistar-Kyoto rats (WKY) under conditions in which blood pressures were not significantly different during the 15-min HRP circulation. Intimal accumulation and medial HRP concentration profiles were obtained from methacrylate-embedded sections after reaction with 3,3'-diaminobenzidine and H2O2. Data were analyzed using a mathematical model of macromolecular transport to quantify the permeabilities of endothelium and internal elastic lamina (IEL). Chronic hypertension increased endothelial permeability without a change in IEL permeability. An apparent convective flux of HRP into the intima of SHR raised intimal HRP to a concentration higher than that of HRP in the plasma. Our results suggest that the intimal accumulation of plasma-borne macromolecules from pressure-driven convection is normally minimized by an intact endothelium. Similar changes resulted from acute injury by lipopolysaccharide, suggesting endothelial injury could account for transport changes associated with hypertension. After either chronic or acute endothelial damage, transport of macromolecules into the intima increases, but the IEL continues to retard transport of macromolecules beyond the intima, resulting in increased intimal accumulation.
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PMID:Macromolecular transport in the arterial intima: comparison of chronic and acute injuries. 913 37

We report a case of a reversible posterior leukoencephalopathy syndrome (RPLS). A 57-year-old male had classical polyarteritis nodosa with mononeuritis multiplex, renal insufficiency, and a high titer of p-ANCA (MPO). He was normotensive. He was treated with high dose methylprednisolone and then with oral prednisolone and cyclophosphamide. Despite the treatment, his renal function rapidly deteriorated and hypertension progressed. He had two generalized seizures; at that time his blood pressure was 200/140 mmHg. CT scan revealed bilaterally symmetric hypodensities in the thalamus, the occipital white matter, and the brainstem. T2-weighted MRI showed increased signal intensities in the temporo-occipital white matter, the thalamus, the posterior limbs of the internal capsules, the external capsules, the midbrain, the pons, and the middle cerebellar peduncles. T1-weighted images showed hypointensities in these areas. Treatment with nifedipine improved his blood pressure; 5 days later he was only moderately disoriented. Follow-up CT demonstrated an ill-defined hypodense area only in the left parietal lobe. To our knowledge, there are only two reported cases of RPLS associated with systemic vasculitides. Interestingly, thalamic lesions are outstanding also in these cases. Under these circumstances, treatment of hypertension is of primary importance, and steroid therapy should not be withdrawn or reduced.
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PMID:[A reversible posterior leukoencephalopathy syndrome in a patient with classical polyarteritis nodosa]. 914 79

Increased renal production of vasodilator mediators like kinins would counteract the vasospasm of pre-eclampsia. This study examines the cellular localisation of tissue kallikrein (TK), the potent kinin forming enzyme within the nephron of patients with early onset pre-eclampsia. Using the peroxidase-antiperoxidase immunoenzyme complex, TK was immunolocalised in the principal cells of the distal connecting tubule and the cortical collecting duct cells of the distal nephron of control tissue. Moderate reactivity was observed in the epithelial cells lining the Bowmans capsule. In early onset pre-eclampsia, TK was additionally localised in the proximal tubule cells, however, the intensity of reactivity was reduced when compared to that of the distal tubule cells. In patients with hypertension of pregnancy, the occurrence of TK in the proximal tubule suggests either gene induction or emiocytosis of TK.
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PMID:Localisation of tissue kallikrein in the kidney of black African women with early onset pre-eclampsia: a pilot study. 922 54

The prostaglandin G2/H2 synthase (cyclooxygenase, COX) is a key regulatory enzyme of prostanoid synthesis pathway. The message-encoding COX isoenzymes (constitutive COX-1 and inducible COX-2) have been described in the rat kidney. However, there is scarce information on the localization of COX-2 in the kidney, although it has been recently reported to be localized in the macula densa. The present study was designed to evaluate the localization of COX-2 in adult rat kidneys. Normal rat kidneys (n=10) were fixed in Bouin and were immunostained with specific antibodies against COX-2 by the peroxidase method. The cellular origin of COX-2 was assessed by the immunostaining of serial consecutive sections with antibodies against Na-K-ATPase, Tamm-Horsfall glycoprotein, H-K-ATPase, kallikrein, and macrophages. COX-2 was consistently observed in a subset of tubular cells located in the cortex and in the outer medulla. The staining of serial sections showed that the COX-2+ cells contained both Na-K-ATPase and Tamm-Horsfall, indicating that they corresponded to thick ascending limb (TAL) cells. They were observed at a considerable distance from the corresponding macula densa, although occasionally they were observed close to glomeruli. The COX-2 staining in the TAL cells was not abolished by dexamethasone treatment (1 to 20 mg/kg), suggesting its constitutive expression in normal kidneys. The presence of COX-2 in TAL (a tubular segment postulated to be devoid of COX-1) may contribute to the handling of ions through local production of prostaglandins.
Hypertension 1997 Sep
PMID:Renal identification of cyclooxygenase-2 in a subset of thick ascending limb cells. 932 6


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