UMLS:C0020538 - FACTA Search

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

The variation in mechanical stress to which the aortic wall is subjected requires that forces be transmitted between its components by means of relatively strong but compliant attachments. We have used transmission electron microscopy in order to study the cell to stroma contacts (smooth muscle cell-elastic fiber contact) in the tunica media of normotensive and hypertensive aortas of Sprague-Dawley rats. Hypertension was produced with a silver clip positioned around the left renal artery and the vessels were fixed by intravital perfusion at normal and elevated pressure. In ultrathin sections, the density of cell to stroma contacts per 100 microns cell perimeter and per 100 cell profiles were determined using an image analysis computer. In the hypertensive group the density of cell to stroma contacts fell considerably when compared with the control group. This research provides insights into the conditions under which high blood pressure may produce medial injuries and, perhaps, be a factor in the precipitation of dissections.
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PMID:Cell to stroma contacts in the tunica media of the hypertensive rat thoracic aorta. 869 52

The effect of S. rebaudiana extract on renal function was evaluated in normotensive and in experimental renal hypertensive rats (GII) using clearance techniques. Experiments were performed on male Wistar rats weighing 300-330 g (10 animals per group). Goldblatt GII experimental hypertension was induced by placing a silver clip with an internal gap of 0.25 mm around the left renal artery under ether anesthesia. The contralateral kidney was left untouched. Stevia was administered 10-12 weeks after clipping. Oral-administration of Stevia extract, corresponding to 2.67 g dry leaves/day for 30 days, resulted in a significant decrease in mean arterial pressure in both the normo-(N) and hypertensive rats (H) (N rats: 113 +/- 3.0 mmHg in the control (C) group vs 69.5 +/- 4.0 mmHg in the Stevia (S) group; H rats: 155 +/- 3.0 mmHg in C vs 108 +/- 4.0 mmHg in S; P < 0.05). Glomerular filtration rate was constant in the N rats and increased significantly in the H rats after Stevia treatment 16.47 +/- 1.29 vs 14.2 +/- 1.33 ml min-1 kg-1 in the C and S groups, respectively, P < 0.05). Normo- and hypertensive rats presented an increase in renal plasma flow following oral Stevia administration (N rats: 16.4 +/- 3.10 ml min-1 kg-1 in the C group vs 33.3 +/- 3.20 ml min-1 kg-1 in the S group. P < 0.05; H rats: 19.30 +/- 2.45 ml min-1 kg-1 in the C group vs 37.0 +/- 3.93 ml min-1 kg-1 in the S group, P < 0.05). Stevia administration provoked an increase in urinary flow in both N and H animals (1.37 +/- 0.08% vs 2.32 +/- 0.11%, P < 0.05 and 1.47 +/- 0.07% vs 2.96 +/- 0.13%, P < 0.05 in N and H rats, respectively). Sodium excretion increased in N and H animals after Stevia treatment (N rats: 0.61 +/- 0.07% in the C group vs 1.55 +/- 0.20% in the S group, P < 0.05; H rats: 0.70 +/- 0.10% in the C group vs 2.22 +/- 0.45% in the S group, P < 0.05). These results are consistent with impairment of a renal autoregulation mechanism in this hypertensive model after Stevia administration. In conclusion, it was shown that Stevia extract, at doses higher than used for sweetening purposes, is a vasodilator agent in normo- and hypertensive animals.
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PMID:A crude extract of Stevia rebaudiana increases the renal plasma flow of normal and hypertensive rats. 903 21

1. The alpha 2a/d-adrenoceptor subtype in the rat kidney modulates solute excretion (osmolar clearance). Since the kidney plays a role in chronic regulation of blood pressure, altered renal function may be implicated in the development of hypertension. A second alteration-that of the alpha 2a/d-adrenoceptor subtype gene-has also been correlated with hypertension in rats and man. 2. We hypothesized that as a consequence of the altered alpha 2a/d-adrenoceptor subtype gene previously shown in spontaneously hypertensive (SH) rats, the increase in osmolar clearance following stimulation of the renal alpha 2a/d-subtype would be attenuated in SH rats as compared to normotensive Wistar rats. In contrast, based on the theory that such functional unresponsiveness of the alpha 2a/d-subtype would be genetically determined, we further hypothesized that in one kidney-one clip (1K-1C) rats, the response to stimulation of the renal alpha 2a/d-subtype would be intact as compared to the normotensive Wistar 1K-sham rats. 3. Male rats were unilaterally nephrectomized under ether anaesthesia. In the 1K-1C rats, a silver clip (diameter 0.254 mm) was also placed around the left renal artery. On the experimental day, rats were administered pentobarbitone (50.0 mg kg-1, i.p.). The carotid artery and jugular vein were cannulated for blood pressure monitoring and saline infusion. The ureter was catheterized for urine collection. A 31 gauge needle was advanced into the renal artery for infusion of the alpha 2a/d-selective agonist, guanfacine (vehicle, 1.0, 3.0 and 10.0 nmol kg-1 min-1 in Wistar and SH rats; vehicle and 10.0 nmol kg-1 min-1 in Wistar 1K-sham and 1K-1C rats). 4. In Wistar rats, guanfacine dose-dependently increased urine flow and sodium excretion. An increase in osmolar clearance but not free water clearance was also observed. However, in SH rats guanfacine failed to alter urine flow, sodium excretion, osmolar and free water clearance. In contrast, in both Wistar 1K-sham and 1K-1C rats, guanfacine increased urine flow rate. Again, this response was due solely to an increase in osmolar clearance. At these doses, guanfacine did not alter blood pressure or creatinine clearance during the experiment. 5. In summary, the ability of the alpha 2a/d-adrenoceptor subtype to mediate an increase in osmolar clearance was absent in a genetic model of hypertension, the SH rats. This effect was intact in an acquired model of hypertension (1K-1C rats). This suggested a defective modulation of solute excretion in SH rats which was probably due to alteration of the alpha 2a/d-subtype gene and not secondary to the elevated blood pressure. The altered alpha 2a/d-subtype gene and function may therefore play a causal role in the pathogenesis of hypertension.
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PMID:Renal alpha 2a/d-adrenoceptor subtype function: Wistar as compared to spontaneously hypertensive rats. 922 41

This article provides a brief review of aspects of autonomic and neuroendocrine function studied initially in collaboration with the late Marian Silver. The importance of the sympathetic innervation to the liver in the control of glycogenolysis was established in anaesthetised animals of various species. Otherwise the work has been carried out mainly in conscious animals under strictly physiological conditions and below behavioural threshold. Investigations of the role of the autonomic innervation to the endocrine pancreas in controlling the release of pancreatic hormones, led to the realisation that the parasympathetic innervation mediates responses to glycaemic stimuli while the sympathetic innervation mediates responses to any form of stress. Studies of adrenal medullary function have confirmed that its threshold for many forms of stress is much higher than that of other components of the sympathetic system and revealed the importance of the pattern of electrical stimulation in determining the rates of release of catecholamines, enkephalins, corticotrophin-releasing factor (CRF) and adrendocorticotrophin (ACTH). The splanchnic sympathetic innervation to the adrenal cortex also plays an important role in determining glucocorticoid output by sensitising the cells to ACTH, probably mainly by the release of vasoactive intestinal peptide (VIP) from cortical nerve terminals. Finally studies of feeding in milk-fed calves have shown that suckling is associated with a remarkable hypertension and tachycardia. These cardiovascular effects are due to a selective sympathetic discharge, which does not involve the adrenal medullae, or the release of neuropeptide Y (NPY) and, at least in the calf, can be attributed to activation of adrenoceptors.
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PMID:Aspects of autonomic and neuroendocrine function. 935 12

The homozygous deletion allele of the angiotensin converting enzyme gene (ACE/DD), homozygous threonine allele of the angiotensinogen gene (AGN/TT), and the epsilon4 allele of the apolipoprotein E gene (apoE/epsilon4) are reported to be associated with ischemic heart disease. Cerebrovascular disease (CVD) is another atherosclerotic disease; and the effects of these polymorphisms on CVD have been confusing. In this study, we investigated whether ACE/DD, AGN/TT, and apoE/epsilon4 genotypes are associated with CVD and whether genetic risk is enhanced by the effect of one upon another. We ascertained these genotypes in patients with cerebral infarction (n = 55) and cerebral hemorrhage (n = 38), diagnosed by brain computed tomography. Control subjects for the infarction group and the hemorrhage group were randomly selected from 583 subjects matched for age, gender, and history of hypertension with patients. Frequency of ACE/DD genotype was higher in the patients with infarction than in the controls (chi2 = 6.1, P < .05). The AGN/TT genotype was not associated with either infarction or hemorrhage, but it increased the relative risk for cerebral infarction in the subjects with ACE/DD genotype (chi2 = 8.0, P < .01, odds ratio; 11.7, 95% confidence intervals: 1.4 to 96.0). There was no significant association between apoE/epsilon4 and CVD. These results suggest that ACE/DD predicts cerebral infarction, but not cerebral hemorrhage, and that AGN/TT enhances the risk for cerebral infarction associated with ACE/DD.
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PMID:Polymorphism of angiotensin converting enzyme, angiotensinogen, and apolipoprotein E genes in a Japanese population with cerebrovascular disease. 944 75

1. Dopamine D2-like receptors were investigated in sections of kidney from male spontaneously hypertensive rats (SHRs) at 6 and 14 weeks of age using radioligand binding assay and autoradiographic techniques with [3H]-spiperone as a ligand. 2. Systolic blood pressure values were slightly higher in 6-week-old SHRs in comparison with age-matched normotensive Wistar-Kyoto (WKY) rats and considerably higher in 14-week-old SHRs in comparison with the other groups investigated. Renal dopamine levels were higher in SHRs aged 6 and 14 weeks in comparison with age-matched WKY rats. Noradrenaline concentrations were similar in 6-week-old SHRs and normotensive WKY rats, and increased slightly in SHRs aged 14 weeks. 3. The density of [3H]-spiperone binding sites was similar in SHRs and WKY rats at 6 weeks of age, and decreased in SHRs at 14 weeks in comparison with age-matched normotensive animals. Light microscope autoradiography revealed the accumulation of silver grains in the tunica adventitia, in the adventitia-media border of intrarenal arteries and within cortical tubules. A few specific silver grains were also developed in the glomerular tuft. No changes in the density and pattern of silver grains were noticeable between SHRs and WKY rats at 6 weeks of age, whereas a reduction in silver grains largely affecting vascular binding sites was observed at 14 weeks of age. 4. Renal denervation considerably decreased the density of [3H]-spiperone binding sites in sections of rat kidney, with an almost complete loss of vascular binding sites. 5. The above findings indicate the occurrence of a decrease of dopamine D2-like receptors in the kidney of SHRs with the progress of hypertension. Dopamine D2-like receptors which are mainly prejunctional are involved in the modulation of sympathetic neurotransmission in the kidney. The loss of these receptors in SHRs may contribute to the pathophysiology of hypertension.
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PMID:Dopamine D2-like receptors in the kidney of spontaneously hypertensive rats: a radioligand binding assay and light microscope autoradiography study. 973 Feb 63

Dense deposit disease (DDD) is a less common form of membranoproliferative glomerulonephritis (MPGN). The disease occurs predominantly in children and young adults and the prognosis is variable. DDD varies considerably in incidence among different populations and has not been reported in Chinese. Herein we reported 2 cases of DDD in young Chinese girls in Taiwan. Although 1 case (case 2) had mild hypertension, both patients had asymptomatic proteinuria and ran a benign course of 8 and 14 years, respectively. The histological features of case 1 resembled membranous glomerulonephritis (MGN) on hematoxylin-eosin stain, but revealed DDD on periodic acid Schiff and chromotrope-2R silver methenamine stains. Whereas case 2 showed focal MPGN on light microscopy, she had a fine granular immunofluorescence pattern resembling MGN. Characteristic intramembranous dense deposits were demonstrated by electron microscopy in the basement membranes of the glomeruli, Bowman's capsules and the renal tubules. Both patients were followed closely, and had stable normal renal function 1 year after renal biopsy.
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PMID:Prolonged asymptomatic dense deposit disease in Chinese. Report of 2 cases in Taiwan. 973 May 78

Hypertensive heart disease caused by renovascular hypertension reflects the response of the heart to an increased afterload and neurohormonal stimulation. We hypothesized that in this condition the composition of the myocardial proteins of rats was altered. To identify yet unknown quantitative and qualitative differences in myocardial proteins in renovascular hypertensive heart disease, we analyzed protein patterns by computer-assisted two-dimensional polyacrylamide large gel electrophoresis. Renovascular hypertension was induced by placing a silver clip on the left renal artery in 9-week-old rat siblings. Sham-operated animals served as controls. Systolic blood pressure (197 +/- 19 mm Hg) and heart/body weight ratios (0.36 +/- 0.04%) were significantly increased in the hypertensive animals. Twenty protein patterns from the left ventricle of five hypertensive and five control rats were compared. The molecular mass and isoelectric point (pI) of proteins spots ranging from 13 to 100 kDa and from 4.5 to 8.5, respectively, were determined using marker proteins. In total, 761 +/- 88 protein spots were resolved in all twenty gels. For the quantitative data analysis a univariate (Mann-Whitney test) as well as a multivariate statistical approach (correspondence analysis) were applied. Only one myocardial protein spot (molecular mass = 41.3 kDa; pI = 6.3) was decreased by more than twofold (p < 0.05) in renovascular hypertension. The vast majority of spots did not indicate a significant alteration of intensity. Left ventricular hypertrophy in early renovascular hypertension induces a form of myocardial hypertrophy that conserves the naturally occurring protein expression pattern.
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PMID:Effects of renovascular hypertension on myocardial protein patterns: analysis by computer-assisted two-dimensional gel electrophoresis. 974 66

In renovascular hypertensive rats, low doses of angiotensin converting enzyme (ACE) inhibitors have been found to prevent myocardial hypertrophy independent of blood pressure level. This finding would suggest humoral rather than mechanical control of myocyte growth. The aim of this study was to examine the effect of nonantihypertensive doses of ACE inhibitor on myocardial hypertrophy and necrosis in hypertensive rats. Renovascular hypertension (RHT) was induced in four-week-old Wistar rats. Twenty-eight animals were treated for four weeks with three doses of ramipril (0.01, 0.1 or 1. 0 mg/kg/day, which are unable to lower blood pressure. Fourteen animals were not treated (RHT group). A sham operated, age/sex-matched group was used as control (n = 10). Myocardial histology was analysed in 3 microm thick sections of the ventricle stained with either haematoxylin-eosin, reticulin silver stain or Masson's trichrome. There was a significant correlation between systolic blood pressure and left ventricular to body weight ratio in both sets of animals: untreated plus controls and ramipril-treated rats. ACE inhibition prevented myocyte and perivascular necrosis and fibrosis in a dose-dependent manner. We conclude that myocardial hypertrophy in rats with renovascular hypertension is directly related to arterial pressure, and that this relationship is not affected by nonantihypertensive doses of ACE inhibitor. Myocardial necrosis/fibrosis and coronary artery damage induced by angiotensin II are prevented by ACE inhibitor in a dose-dependent manner, despite the presence of arterial hypertension.
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PMID:The effect of non-antihypertensive doses of angiotensin converting enzyme inhibitor on myocardial necrosis and hypertrophy in young rats with renovascular hypertension. 1046 64

The contralateral kidney of 2-kidney, 1-clip hypertensive (2K1C) rats is unable to escape the renal vasoconstrictive and sodium-retaining effects of increased circulating angiotensin II levels. Evidence is accumulating that renal function is relatively preserved by enhanced influence of NO in the contralateral kidney. In this study, we investigated (1) whether the high NO dependency of renal hemodynamics in the contralateral kidney is due to increased availability of NO or increased sensitivity to NO and (2) whether elevated NO activity dampens the actions of angiotensin II to enhance tubuloglomerular feedback (TGF) responses in the nonclipped kidney of 2K1C rats. To estimate whether the available NO is increased, the NO clamp technique was applied in rats that underwent sham operation (n=6) and in the contralateral kidney of 2K1C Sprague-Dawley rats (3 weeks old; 0.25-mm silver clip; n=6). During systemic infusion of nitro-L-arginine (L-NNA; 50 microg/kg. min(-1)), sodium nitroprusside (SNP) was infused in the renal artery and the rate was adjusted so that renal vascular resistance (RVR) was restored to baseline levels. In sham rats, RVR increased during L-NNA treatment from 17.2+/-2.0 to 33.0+/-3.6 U (P<0.01) and was restored to baseline values during SNP infusion (17.1+/-2.3 U); 9. 2+/-1.8 nmol/min of SNP was needed to restore RVR to baseline values. In 2K1C rats, RVR increased during L-NNA treatment from 16.7+/-1.1 to 53.4+/-3.5 U (P<0.01). This increase of RVR was significantly larger than in sham rats. RVR was restored to baseline values during SNP infusion (17.4+/-0.9 U); 26.0+/-4.3 nmol/min of SNP was needed to restore RVR to baseline values (P<0.05 versus sham). Furthermore, maximum TGF responses were assessed before and during late proximal tubular infusion of L-NNA in the kidneys of sham rats and the nonclipped kidneys of 2K1C rats. Control maximum TGF responses were 4.7+/-0.7 and 5.1+/-0.4 mm Hg in sham and 2K1C rats, respectively. During intraluminal L-NNA infusion, maximum TGF responses were 15. 4+/-0.9 mm Hg in sham rats and 22.2+/-2.5 mm Hg in 2K1C rats (P<0.05 versus sham). Finally, urinary NO(2)+NO(3) excretion in the nonclipped kidney was significantly higher than in the clipped kidney (P<0.05). In conclusion, (1) as assessed using the NO clamp, ambient intrarenal NO levels are increased in the contralateral kidney of 2K1C rats and (2) the NO dependency of the TGF system is enhanced. These experiments indicate that adaptations in NO activity lead to relatively low TGF responsiveness, which will offset the simultaneous sodium-retaining actions of angiotensin II on proximal tubular reabsorption and TGF responsiveness.
Hypertension 1999 Oct
PMID:Increased availability of nitric oxide leads to enhanced nitric oxide dependency of tubuloglomerular feedback in the contralateral kidney of rats with 2-kidney, 1-clip Goldblatt hypertension. 1052 46

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