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

To determine whether the increased thickness seen in media of mesenteric resistance vessels of Wistar-Kyoto rats made hypertensive by a Goldblatt procedure (one-kidney, one clip model) was due to hypertrophy or hyperplasia of smooth muscle cells, the cellular dimensions of these vessels were estimated using a new, unbiased stereological method (the disector). Furthermore, to investigate whether the changes seen could be secondary to the increased blood pressure, morphometric measurements were also made in renal arcuate arteries, which, due to the constricting silver clip, probably had not been exposed to the increased pressure load. Vessels were mounted on a myograph, and their media thickness, lumen diameter, and maximum active wall tension response were measured. In the mesenteric vessels media thickness had increased by 58%, whereas no changes were seen in the renal vessels. Vessels were then fixed, and serial sections were made in the mesenteric vessels. The disector was used to calculate the numerical cell density in each vessel. By combining the myograph measurements and the estimated numerical cell density, the number of cells per segment unit length was calculated (renal hypertensive rats, 6.8 micron-1; sham-operated Wistar-Kyoto rats, 6.3 micron-1; p greater than 0.40) and mean cell volume was determined (renal hypertensive rats, 1541 micron 3; sham-operated Wistar-Kyoto rats, 1256 micron 3; p less than 0.02). No morphometrical changes were found in single sections of the renal arteries. We conclude that the increased media thickness observed in mesenteric resistance vessels of one-kidney, one clip Goldblatt hypertensive rats mainly was caused by smooth muscle cell hypertrophy.
Hypertension 1988 Aug
PMID:Cellular hypertrophy in mesenteric resistance vessels from renal hypertensive rats. 341 May 24

To support our contention that the Wistar-Furth rat is resistant to mineralocorticoid hypertension, we assessed the effects of deoxycorticosterone (DOC) administration or renal artery stenosis on the development of hypertension in the Sprague-Dawley and Wistar-Furth rat strains. Weekly administration of mineralocorticoid in the form of DOC pivalate resulted in rapid, severe hypertensive cardiovascular disease in Sprague-Dawley rats. Within 5 weeks the mean conscious systolic blood pressures in steroid-treated and control rats were 186 +/- 4 and 118 +/- 5 mm Hg, respectively. In contrast, blood pressures of Wistar-Furth rats were only moderately elevated, even after 10 weeks of DOC pivalate administration (136 +/- 2 vs 116 +/- 2 mm Hg for controls). Furthermore, none of the steroid-treated Wistar-Furth animals exhibited cardiovascular lesions. In parallel studies, littermates of these rat strains were subjected to renal artery stenosis and blood pressures were determined weekly in conscious rats. Silver clip constriction of the left renal artery, in the presence of the contralateral kidney, resulted in a rapid, sustained elevation of blood pressure in both Sprague-Dawley and Wistar-Furth rat strains (177 +/- 4 and 176 +/- 5 mm Hg, respectively). Corticosteroid levels were also determined in DOC-treated Sprague-Dawley and Wistar-Furth rats. The regimen employed resulted in a 10-fold increase in DOC levels as compared with controls, and the levels achieved were comparable in both strains. Thus, the Wistar-Furth rat appears to be selectively resistant to mineralocorticoid hypertensive vascular disease and thus affords a model for studying mechanisms of steroid hypertension.
Hypertension 1987 Aug
PMID:Resistance to mineralocorticoid-induced hypertensive vascular disease. 361 Feb 93

Mooren's ulcer is a rare disease of presumed autoimmune aetiology. Some cases run a chronic severe course and fail to respond to local and systemic therapy. We report here such a case with bilateral Mooren's ulcer that failed to respond to local therapy with topical corticosteroids, silver nitrate, and conjunctival resection, as well as systemic immunosuppression with corticosteroids, cyclophosphamide, and azathioprine. Systemic cyclosporin (10 mg/kg/day) resulted in resolution of the corneal ulceration within two weeks of beginning treatment, and the patient has remained in remission after 15 months of therapy. Cyclosporin side effects included hirsutism, hypertension, increased blood levels of urea and creatinine, and abnormalities in liver function tests. All these resolved on reducing the dosage of cyclosporin. The results in this case suggest that cyclosporin is an effective agent in patients with severe sight threatening Mooren's ulcer.
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PMID:Cyclosporin therapy in Mooren's ulcer. 362 Apr 20

Renovascular hypertension superimposed on essential hypertension, a condition encountered in the elderly, was studied. An experimental animal model consisting of a two-kidney one-clip Goldblatt preparation in the spontaneous hypertensive (SHR) rat, that would simulate this condition, was designed. A 0.25 mm silver clip was placed on the left renal artery of SHR male rats. The same procedure performed on WKY rats served as control. All experiments were performed on low, normal, and rich sodium diet. Systolic blood pressure (BP) was measured by tail-cuff method. Plasma renin concentration (PRC) was determined before and after clipping of the renal artery. Results were as follows: Mean systolic BP increased significantly in clipped rats fed with normal and rich sodium diets. SHR showed an increase from 144 +/- 3 (mean + s.e.m.) to 168 +/- 3 mmHg, and WKY rats showed an increase from 120 +/- 2 to 139 +/- 5 mmHg. There was a two- to threefold rise in PRC. A low-salt diet given prior to clipping prevented the appearance of renovascular hypertension despite a significant rise in PRC. We concluded that renal artery narrowing plays a significant role in the rise of BP in the basically essential type of hypertension.
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PMID:Renovascular hypertension in spontaneous hypertensive rats: an experimental model of renal artery stenosis superimposed on essential hypertension. 366 6

Voluntary alcohol drinking, using a free-access procedure, was studied in rats three weeks after unilateral renal artery stenosis was produced by applying a 0.20 mm solid silver clip to the left renal artery (Two-Kidney, One-Clip, Hypertension). The group of animals with the arterial clip drank significantly less alcohol and more water than a sham-operated group. The two groups, however, drank similar amounts of a palatable glucose solution, suggesting that they did not differ in taste sensitivity. Blood alcohol levels measured for six hours following a 2.5 g/kg intraperitoneal injection of alcohol indicated that the difference in alcohol consumption between the two groups could not be accounted for in terms of differences in drug disposition or metabolism. These findings provide an example of a previously unknown type of control which originates in the periphery and contributes to the regulation of voluntary alcohol drinking.
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PMID:Renal artery stenosis: an example of how the periphery can modulate voluntary alcohol drinking. 380 49

We have examined the effect of removal of the submandibular gland on one-kidney, one clip (1K1C) hypertension in the rat. Five weeks after application of a silver clip with a 0.20-mm gap, 15 hypertensive rats were sialoadenectomized. This was followed by a decrease in systolic blood pressure (SBP) within 1 day by 22 +/- 4 mmHg (+/- s.e.m.) and in nine rats pressure stabilized within 1 week at 133 +/- 5 (cf. 166 +/- 2 before sialoadenectomy). In the other six rats the initial hypotensive response was followed by a gradual return to hypertensive levels, reaching 178 +/- 4 mmHg 6 weeks later. Sham-sialoadenectomized rats remained hypertensive throughout. When a 0.15-mm gap clip was used in a similar experiment rats became hypertensive after 2 weeks, and sialoadenectomy lowered SBP to normal in half of them, after which pressure tended to return to hypertensive levels in most. No change in SBP was found in sham-operated hypertensive rats. Sialoadenectomy performed at the time of clipping with a 0.15-mm gap clip and unilateral nephrectomy delayed the development of hypertension. Systolic pressure then fell from 153 +/- 14 at 4 weeks to 105 +/- 8 at 12 weeks after operation in five rats, but continued to increase in eight rats from 148 +/- 10 at 4 weeks to 172 +/- 15 at 12 weeks. These experiments thus demonstrate that the submandibular gland may contribute to the onset and maintenance of one-kidney, one clip hypertension in the rat, particularly in less severe stenosis.
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PMID:Antihypertensive effect of sialoadenectomy in one-kidney, one clip hypertension in the rat. 391 Jul 25

A standardized stenosis was induced by applying a silver clip around the left renal artery in male rats. This resulted in arterial hypertension within 10 days (as determined by increase in heart weight). Ornithine decarboxylase (ODC) activity was determined in the right (untouched) kidney, the left kidney, and the adrenal glands 1 day, 10 days, and 3 months after the operation. There was no difference in ODC activity in the right kidney of the operated animals when compared with matched controls. In the left kidney (with artery stenosis), ODC activity decreased to 40% after 1 day. A partial recovery was seen after 10 days (ODC activity 70% of normal), and after 3 months ODC activity had normalized. Removal of the clip 1 day prior to killing induced in the 3-month group a more than two-fold increase in ODC activity in the previously clipped kidney; ODC activity in the contralateral kidney was not affected. Only minor changes in ODC activity occurred in the adrenal glands following the operation. Contents of putrescine and spermidine were increased in the left (stenotic) kidney, and after clip removal, also in the right (untouched) kidney. Our observations thus indicate that alterations in renal blood flow are rapidly followed by changes in ODC activity. Contents of putrescine, spermidine and spermine seemed to a great extent to be independent of the ODC activity.
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PMID:Renal polyamine metabolism in rats with renovascular hypertension. 401 83

Several recent studies have reported the existence of additional plasma proteins in essential hypertensive patients and strains of genetically hypertensive rats. The aim of this work was to look for similar changes in a model of salt induced hypertension, the Dahl salt sensitive (DS) rat, using the sodium dodecyl sulphate (SDS) polyacrylamide gel electrophoresis. No additional proteins were found when different staining techniques were employed (Coomassie, silver). However, during the development of hypertension a characteristic change in the plasma protein pattern of DS rats occurred, which could not be detected in the majority of normotensive control animals. Treatment with nifedipine inhibited both the development of hypertension and this specific change in the plasma proteins, in spite of continuous dietary salt loading. It is postulated that the plasma protein changes reflect a regulatory phenomenon of hypertension.
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PMID:Characteristic changes of plasma proteins in the Dahl hypertensive rat strain (DS) during the development of hypertension. 402 Jan 31

The development of two-kidney, two clip Goldblatt hypertension (2K2C) in the rat seems to be unaffected by chemical sympathectomy with 6-hydroxydopamine (6-HODA) and adrenal demedullation. Since this treatment only partially depletes vascular norepinephrine (NE) content, we evaluated the degree of sympathectomy achieved with the 6-HODA treatment and the structural vascular changes in treated and untreated animals. Litters of male Wistar rats were divided in two groups: 6-HODA-treated (6-HODA) animals (group 1) were injected with 6-HODA since the day of birth until the end of the experiment; control group (CG) animals (group 2) received the vehicle solution. When rats reached about 250 g, a silver clip (0.25 mm width) was placed on both renal arteries in half of them in each group; a sham operation was performed on the rest of the animals. Adrenal demedullation and denervation was performed in all 6-HODA animals. Blood pressure was followed weekly by the tail cuff method for 7 weeks. At the 8th week, Silastic cannulas were placed in the carotid artery and jugular vein in all the animals. Pressor responses to tyramine (0.05 and 0.1 mg), angiotensin (10, 40 and 160 ng), and norepinephrine (NE) (25, 100 and 400 ng) and the hypotensive effect of prazosin (1 mg/kg) were determined in the conscious rats. The pressor effect of carotid occlusion was registered 24 hours later. Animals were sacrificed, and the heart and artery weight as well as the nucleic acids and alkali soluble proteins content in the vascular wall were determined.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Further studies on the development of two-kidney, two clip Goldblatt hypertension in 6-hydroxydopamine-treated rats. 619 76

The effects of simultaneous angiotensin blockade and sodium depletion on the development of one-kidney renovascular hypertension were studied in rats. In sodium-replete rats, systolic blood pressure (SBP) increased from 102 +/- 2 to 153 +/- 11 mmHg by the 12th day after unilateral nephrectomy and subsequent partial occlusion of the renal artery with a 0.22-mm silver clip. When changes in body fluid volume were minimized by sodium restriction in a second group of rats, the increase in SBP from 98 +/- 4 to 149 +/- 7 mmHg after clipping was not different from that in sodium-replete animals. Inhibition of the angiotensin-converting enzyme with SQ 14,225 during sodium restriction prevented the SBP from increasing above 101 +/- 3 mmHg by the 12th day after nephrectomy and clipping. Once SQ 14,225 administration was discontinued, SBP rose significantly to 148 +/- 5 mmHg within 5 days. Because previous studies have shown that neither sodium depletion nor angiotensin blockade alone prevented the development of one-kidney renovascular hypertension, it is concluded that the increase in blood pressure resulting from renal artery constriction and contralateral nephrectomy was prevented only by suppression of both the renin-angiotensin system and body fluid volume.
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PMID:Sodium and angiotensin in the pathogenesis of experimental renovascular hypertension. 626 11


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