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

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

Eleven open chest, artificially ventilated rats were used to observe and compare the intracellular potential changes induced in the right and left ventricles by an acute right ventricular overload. Graded right ventricular hypertension was produced by external constriction of the main pulmonary artery. Transmembrane potentials were obtained using floating glass microelectrodes filled with 3 mol X litre-1 KCl and connected to a cathode follower through a silverchloride-silver junction. Following right ventricular overload, the level of resting potential was depolarised by 20% on the right ventricle and by 4% on the left (P less than 0.001). The repolarisation was not significantly affected. A significant correlation (P less than 0.01) was observed between the increase of right ventricular pressure and the depolarisation of resting right ventricular potential. The right ventricular distension which occurs in our experimental model thus induces a diastolic depolarisation of right ventricular muscle cells which cannot be neglected in the interpretation of the peripheral ECG changes.
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PMID:Intracellular action potential changes induced in both ventricles of the rat by an acute right ventricular pressure overload. 726 Sep 68

Twelve 3-week-old, Wistar inbred rats were made hypertensive by bilateral constriction of renal arteries with silver clip. At 3-8 weeks after induction of hypertension, nodular lesions of mesenteric arteries were biopsied, and constricting clips were removed. At 5-28 days after removal of the clips, the animals were killed. Systolic blood pressure of the rats was 200mm Hg and over before removal of the clips, and decreased at the time when they were sacrificed. Ultrastructurally, modified smooth muscle cells were seen among the fibrinoid substance during healing process of fibrinoid degeneration in the intima. Fine cytoplasmic processes of these cells contained numerous lysosomes. The fibrinoid substance became reticular and reduced its density. The cytoplasmic processes with lysosomes were seen neither in the biopsied specimens nor in the tissues which showed cellulofibrous intimal thickening. Lysosomal enzymes were considered to increase in the modified smooth muscle cell during healing process of the fibrinoid degeneration. The enzymes were believed to be discharged extracellularly and to digest the fibrinoid substance partially. The partially dissolved substance might be phagocytized by the modified smooth muscle cells to form vacuoles of a medium electron density.
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PMID:Lysosomes in healing process of arterial fibrinoid degeneration in hypertensive rats. 727 Jan 47

1. The time course of changes in baroreceptor reflex sensitivity during the development of renovascular hypertension was studied in male Wistar rats in which the left renal arteries were constricted by silver wire clips of 0.18 mm internal diameter. 2. Groups of animals were studied at 3, 7, 14 and 25 days after induction of renovascular hypertension. Rats of comparable ages were included as controls. There was a significant decrease in mean baroreflex sensitivity from 0.950 +/- 0.157 ms/mmHg (n = 8) in the normal control group to 0.537 +/- 0.105 ms/mmHg (n = 8) in the 3 day hypertensive group (P < 0.05). Baroreflex sensitivity in the 3 day hypertensive rats was independent of the level of arterial pressure achieved in individual animals. 3. These changes in baroreflex sensitivity at 3 days precede the development of left ventricular hypertrophy and, as previously shown in this model, also precede structural vascular adaptation and resetting of the carotid sinus baroreceptor threshold. 4. A further loss of baroreflex sensitivity, which may be structurally based, occurred later. Baroreflex sensitivity in the 14 day hypertensive rats fell to 0.182 +/- 0.039 ms/mmHg (n = 8) compared with the 3 day hypertensive rats (P < 0.01).
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PMID:Baroreflex sensitivity changes during the development of Goldblatt two-kidney one-clip hypertension in rats. 742

The concept has been advanced that malignant hypertension is precipitated in the rat with renal hypertension by a sudden loss of sodium in the urine. In order to test this hypothesis modest degrees of hypertension were produced in Holtzman rats by the application of a silver clip to one renal artery, not touching the opposite kidney. When the systolic blood pressure reached a level between 160 and 180 mm Hg, loss of sodium and water was induced by the administration of furosemide, given either orally over a 7-day period, or by 3 intramuscular injections over a 24-hour period. Sodium and water balance studies, blood pressure determinations, histologic assessment of blood vessels in the nonclipped kidney, and measurement of activity of the juxtaglomerular apparatus were carried out in these 2 groups and appropriate control animals. It was found that in spite of a considerable natriuresis and diuresis in furosemide-treated animals, there was neither a significant increase in the blood pressure nor development of more severe vascular lesions in the nonclipped kidney than in the kidneys of control animals.
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PMID:The failure of furosemide-induced salt and water loss to convert benign to malignant hypertension in the rat. 743 39

It is well established that two-kidney, one clip renovascular hypertension can be rapidly reversed by unclipping. We hypothesized that rapid renal reperfusion and the subsequent fall in blood pressure are mediated in part by nitric oxide, the endothelium-derived relaxing factor. We tested whether the hypotensive response to unclipping could be blocked by nitric oxide synthesis inhibition using a bolus of 10 mg/kg body wt N omega-nitro-L-arginine methyl ester. Rats were made hypertensive by placing a silver clip on the left renal artery. After 4 weeks, they were anesthetized and either not treated (controls) or had nitric oxide synthesis blockade. After 10 minutes, the clip was removed and blood pressure monitored over 60 minutes. Initial pressure in controls was 157 +/- 8 mm Hg, and heart rate was 310 +/- 21 beats per minute. Unclipping resulted in pressure falling to 125 +/- 6 mm Hg within 45 minutes (P < .005). Heart rate was unchanged (312 +/- 9 beats per minute). In contrast, nitric oxide synthesis inhibition increased blood pressure from 149 +/- 6 to 174 +/- 9 mm Hg (P < .001). Unclipping did not change blood pressure, which was 167 +/- 8 mm Hg after 60 minutes (P < .005 versus controls), and heart rate remained unchanged (282 +/- 13 versus 276 +/- 16 beats per minute). We determined the blood flow to the clipped kidneys using radioactive microspheres. Unclipping untreated hypertensive rats resulted in a 10-fold increase in renal blood flow (P < .001), concomitant with a decrease in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Feb
PMID:Nitric oxide synthesis inhibition blocks reversal of two-kidney, one clip renovascular hypertension after unclipping. 784 67

Different processes of microvascular wound healing under hypertension in comparison to normotension have been suspected. To explore these differences at the site of anastomotic wound repair, we performed microvascular anastomoses of the femoral arteries in 12-week-old, stroke-prone hypertensive rats (SHRSP) whose maximum blood pressure reached 238 mm Hg and in normotensive age-matched Wistar Kyoto (WKY) rats. Morphologic changes under hypertension were examined via light microscopy. The arrangement and number of endothelial cells were examined using the en face silver staining technique. The plasma activity levels of factor XIII were also measured in each group. Transitional healing at the microvascular anastomosis site was evaluated via scanning electron microscopy. The extent of endothelial migration over the exposed media around the needle holes was determined using a computerized graphic analysis system. Histologic cross sections demonstrated a thickened media, with altered shape and arrangement of the smooth muscle cell nuclei in SHRSP arteries compared with WKY arteries. En face silver staining showed small and spindle-shaped endothelial cells with an irregular cell arrangement and distribution in SHRSP arteries relative to WKY arteries. Factor XIII was increased 36% over baseline in SHRSP rats postoperatively; this was significantly higher than the increase in WKY rats (P < 0.05). Although both SHRSP and WKY arteries had similar wound healing responses to microvascular anastomosis, endothelial cell migration over the exposed media was significantly accelerated in the SHRSP rats.
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PMID:Effect of hypertension on arterial structure and wound repair at the microvascular anastomosis site using stroke-prone spontaneously hypertensive rats (SHRSP). 827 29

Some reports have stated that central norepinephrine (NE) depletion inhibited the development of hypertension in the rat. On the other hand, this pharmacological treatment induces changes on the central renin-angiotensin system. The present study was designed to follow the development of 2 kidney-2 clip (2k-2c) renovascular hypertension in rats depleted of central NE and to analyze the central and peripheral renin-angiotensin system. Male Wistar rats (n = 40) were used. Half of the animals was injected, intracisternally, with 6-hydroxydopamine (6-OHDA), the remaining rats only received the vehicle. One week later a silver clip was placed on each renal artery on half of the 6-OHDA treated rats and on half of the vehicle treated animals. A sham operation was performed on the remaining rats. Blood pressure was measured weekly during 7 weeks. Then, blood and cerebrospinal fluid (CSF) samples were obtained. The brain was dissected in several areas. NE and angiotensinogen concentration (AoC) were determined in tissue samples. AoC was evaluated in plasma and CSF; plasma renin activity was also measured. Hypertension development was not prevented by central NE depletion, which was significant in all central areas (p < 0.001). Other significant results showed that renal ischemia and/or NE depletion induced a significant increase in angiotensinogen concentration in the hypothalamus (p < 0.01) and in CSF (p < 0.05). In summary: central NE depletion was not able to modify the development of 2 k - 2 c hypertension. Treatment and renal ischemia induced an increase of central AoC.
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PMID:Effect of central norepinephrine depletion on renovascular hypertension and on the renin system. 837 8

Carotid bodies from 17 human fetuses of gestational age ranging from 10 weeks to full term were examined in histological sections stained by the Bodian silver protargol method to demonstrate nerve axons. At 10 weeks gestation the carotid body was contacted by a single nerve bundle at its apical pole but by the 13th week a second bundle had also reached the proximal pole. Thin, pale nerve axons extended from these bundles and surrounded the carotid body to form a plexus from which several small groups of axons entered its superficial regions. With increase of gestational age beyond this point there was a progressive influx of axons to penetrate the innermost areas of glomic tissue by the 19th week. Nerve endings were not identified until 23 weeks gestation when occasional small boutons, and rarely calyces, were seen to terminate on fetal chief cells. Thus there was by this age a well-developed nerve link between glomus and brain consistent with the view that from this stage of development the carotid bodies are able to function as chemoreceptors. However, results of previous research work in our Department and in the literature lead us to believe that the fully anatomically developed nerve network of the carotid body depends on its cellular and biochemical environment to ensure that it functions efficiently as a chemoreceptor. Thus, reduction of dopamine-turnover or attenuation of chief cells in the carotid bodies is associated with increased chemosensitivity, as in the days following birth and in systemic hypertension in later life.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The development of the nerve network in the fetal human carotid body and its subsequent function in cardiac disease. 840 21

To examine the expression of the GFAP protein in the retina and visual cortex under normal and pathological conditions, hypertension was induced in adult male Sprague-Dawley rats by applying silver clips onto renal arteries and the change in GFAP expression was followed by Western blotting and immunocytochemical staining. One week after operation when the induced hypertension was at the initial stage, GFAP expression in the retina was reduced to half of the sham control. By 4 weeks, when consistent hypertension was developed, a further decrease in the level of GFAP expression in the retina to one third of the sham control was observed. Immunocytochemical staining showed that the number of GFAP-positive cells in the nerve fiber layer of the retina of the hypertensive rat was reduced to less than one third of the sham control. However, similar changes in GFAP expression in the visual cortex of hypertensive rats were not observed. This study represents the first report to date on GFAP expression in the retina and visual cortex and includes discussion of the possible mechanisms through which GFAP expression is mediated.
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PMID:Differential expression of glial fibrillary acidic protein (GFAP) in the retinae and visual cortices of rats with experimental renal hypertension. 855 12


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