Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the arteries of 17 rejected renal grafts 'activated' smooth muscle cells (ASMC) were discerned from a 'resting' type. Proliferation and fibre production by ASMC resulted in a marked thickening of intima. Each of four normal Wistar rats received 20 mg prednisolone i.v./day for one week and the development of hypertension was therapeutically prevented. Changes similar to those in the graft arteries were found in the rat aortas. We assume that SMC were stimulated by several mechanisms in rejection but also by extremely high dosed corticoids.
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PMID:Corticosteroids and proliferation of smooth muscle cells in arteries of renal transplants. 77 34

To ascertain whether or not vascular lesions lead to renoparenchymal damage through ischemia and to a deterioration of renal function in patients with essential hypertension, correlations among morphometrical findings and renal function were examined in 36 renal biopsies from Japanese patients with a benign nephrosclerosis. The following histological parameters were investigated; glomerular sclerotic index (GS), interstitial volume (IV), measured by the point-counting method, index of arteriolar hyaline change (HC) and intimal thickening (IT), determined by morphometry. Arteries were divided into two groups; those with less than 3 layers of medial smooth muscle cells (SMC less than 3) and those with more than 3 cell layers (SMC greater than or equal to 3). The mean of IT in each size was calculated. IT (SMC less than 3) showed a significant correlation with GS and IV. IT (SMC less than 3), GS and IV significantly correlated with Ccr. On the other hand, IT (SMC greater than or equal to 3) and HC showed no correlation with GS nor Ccr. IT (SMC less than 3) and HC correlated with both blood pressure and the duration of hypertension, and here, IT (SMC greater than or equal to 3) showed no correlation. These data suggest that hyaline change and intimal thickening of small arteries and arterioles (SMC less than 3) are closely related to high blood pressure and that intimal thickening of small arteries rather than hyaline change causes renoparenchymal damage through ischemia and leads to a deterioration of renal function, in those with a benign nephrosclerosis.
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PMID:Morphometrical and functional correlations in benign nephrosclerosis. 342 33

The growth capacity and morphology of cultured human smooth muscle cells obtained from omental arteries from 153 patients were studied. The cells exhibited a very slow growth rate compared to rat or minipig SMC's, but they too developed cultures in a typical hill-and-valley pattern and possessed bundles of myofilaments. Two groups of smooth muscle cell cultures, slowly proliferating ones and rapidly proliferating ones were compared in their relation to donor age, blood pressure, nicotine abuse, diabetes mellitus and carcinoma. In the case of blood pressure and carcinoma significant differences indicated that those smooth muscle cells obtained from patients with high blood pressure or carcinoma revealed lower growth capacities. In the second subculture the proliferation of smooth muscle cells was found to be inversely proportional to donor age (4 to 78 years).
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PMID:Cultivated human arterial smooth muscle cells. The effect of donor age, blood pressure, diabetes and smoking on in vitro cell growth. 668 78

Chronic venous hypertension in rats was provoked by injection of polymethyloxane into the pleural cavity. Hypertrophy of muscular tissue was accompanied by reconstitution of adrenergic nervous structures. In the early stages (up to 40 days), the changes in the latter are reactive in nature: first there occurs a weakening of luminescence, rare-fraction of the network and then "hyperneuria". Pulmonary heart formation was followed by marked hypertrophy of SMC, increased density of adrenergic fibers, convergence of SMC and nerve terminals (synapse formation).
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PMID:[Neurohistochemical and ultrastructural study of the adrenergic innervation of the wall of the rat posterior vena cava during chronic venous hypertension caused by experimental oleothorax]. 731 44

In atherosclerosis numerous qualitative and quantitative changes in connective tissue metabolism parameters in serum and aorta occur. In atherosclerosis there is an enhanced activity of local renin-angiotensin systems. It leads to overexpression of ANG II, both in serum and arterial wall. ANG II stimulates SMC to over-synthesize the collagens type I and III. Hyper-cholesterolemia is a form of metabolic injury which can both induce phenotypic change of SMC and activate RA system in arterial wall. ACEI lower the accumulation of collagens type I and III, and enhance elastin content in arterial wall in experimental hypertension. The aim of this study was to assess the influence of captopril, enalapril and quinapril on connective tissue metabolism of the aorta in experimental hyper-cholesterolemia. 64 male New Zealand rabbits were used. Animals were fed with standard fodder, special diet (1% cholesterol content) or special diet + tested ACEI. Two doses of ACE inhibitors were used: 1st--equivalent to doses applied to human subjects (in mg/kg of body weight), 2nd--dose 10 times higher. The animals were divided into 8 equal groups: K--standard fodder, B--special diet, C1, C2--special diet + captopril in doses 2.5 and 25 mg/kg/24 hours, respectively, E1, E2--special diet + enalapril in doses 0.75 and 7.5 mg/kg/24 hours, respectively, Q1 i Q2--special diet + quinapril in doses 0.75 and 7.5 mg/kg per day, respectively. The experiment lasted for 6 months. After 24 weeks the animals were sacrificed and aortae were excised for collagens assay. The statistical analysis was performed using ANOVA, followed by LSD test; p < 0.05 was considered statistically significant. The aorta collagens content of cholesterol-fed rabbits significantly increased. The tested ACEI (captopril, enalapril in both doses and quinapril in lower dose) had a preventive effect against the increase of aorta collagen content.
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PMID:[The influence of angiotensin-converting enzyme inhibitors on collagen content of the aorta wall in experimental hypercholesterolemia]. 1080 May 84

The aim of this study was to evaluate the proliferative behavior of vascular smooth muscle cells in primary culture (pC-SMC) and the endothelial nitric oxide synthase (eNOS) activity in the endothelial lining of the aorta of fructose-fed rats (FFR). This is an experimental model of syndrome X, a cluster of cardiovascular risk factors including hyperinsulinemia, insulin resistance, and hypertension that has been suggested to be of pathophysiologic importance for the development of atherosclerosis. Male Wistar rats were used: Control (n = 12) and FFR (n = 12). After receiving fructose in drinking water (10% w/v) during 8 weeks, biochemical parameters, systolic blood pressure (SBP) and relative heart weight (RHW) were determined. The proliferative effect of 10% fetal calf serum (FCS) was examined in aortic pC-SMC by [3H]thymidine incorporation and by cell counting. Ca2+/calmodulin-dependent NOS activity was estimated in aortic endothelial lining and in heart tissue homogenates by conversion of [3H]arginine into [3H]citrulline. Fructose-fed rats showed hyperinsulinemia (P = .0263), altered glucose tolerance test (P < .001), higher SBP (P < .0001), and RHW (P = .0145), compared to control rats. These animals also showed an increase of 10% FCS-induced [3H]thymidine incorporation (P < .0001) and cell number of aortic pC-SMC (P = .0049) and decreased eNOS activity in both aortic endothelium (P = .0147) and cardiac tissue (P < .0001). These data support the hypothesis that syndrome X is associated to changes in SMC proliferation and endothelial dysfunction, which could be involved in the onset or progression of the atherogenic process.
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PMID:Aortic smooth muscle cell proliferation and endothelial nitric oxide synthase activity in fructose-fed rats. 1172 13

Prostaglandin D(2) (PGD(2)) and its metabolites bind to the intracellular PPARs to regulate vasoactive substances involved in vascular remodeling through regulation of mRNAs transcription as well as through receptor-mediated mechanisms. PGD(2) decreases inducible NO, PAI-1, endothelin, and VCAM expression through inhibition to NF kappa B, STAT, or AP-1 transcription factors, which are regulated by cytokines/immune system. Moreover, transfer of L-PGDS (PGD(2) synthase) into the intracellular space of EC or SMC increases intracellular PGD(2), thereby decreasing these substances. PGD(2) attenuates in vivo organ injury mediated by cytokines and the immune system. The pretreatment with PGD(2) attenuates the liver damage and hemodynamic collapse following LPS. Dahl salt-sensitive rats, with decreased PGD(2) in the outer medulla of the kidney, are prone to hypertensive kidney injury. Serum L-PGDS level is increased in renal dysfunction through a decrease in glomerular filtration. L-PGDS in urine may be derived from a failure of tubular reabsorption or from in situ synthesis. Urinary L-PGDS excretion markedly increases in the early stage of kidney injury, and urinary L-PGDS is a useful predictor of the forthcoming renal injury. Indeed, urinary L-PGDS precedes clinically overt proteinuria or other parameters indicating renal dysfunction in hypertension, primary renal diseases, and diabetes in humans. PGD(2)/L-PGDS system is a Cinderella of vascular biology.
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PMID:[PGD(2)/L-PGDS system in hypertension and renal injury]. 1469 55

This study aimed to characterize the vasorelaxing effects of ANP, BNP and CNP in isolated renal resistance arteries (RRA) from wild-type mice and mice with either systemic (GC-A -/-) or smooth muscle-restricted deletion of GC-A (SMC GC-A KO). In RRA from wild-type (GC-A +/+) mice natriuretic peptides (NP) induced concentration-dependent vasorelaxations with the rank order of potency ANP>BNP>CNP. In RAA obtained from mice with systemic or smooth muscle-restricted deletion of GC-A, the effects of ANP and BNP were abolished. In contrast, CNP induced concentration-dependent vasorelaxations of GC-A -/- and SMC GC-A KO RRA. However, the efficacy of CNP for vasorelaxation was markedly diminished compared with wild-type RRA. Such changes in CNP responsiveness did not affect large arteries as the aorta and they were not due to vascular changes secondary to chronic arterial hypertension in GC-A -/- mice. Unaltered vasorelaxing effects of acetylcholine and sodium nitroprusside demonstrated unaltered function of downstream targets regulated by cGMP in vascular smooth muscle. An increased expression of the clearance receptor (NPR-C) or diminished expression of GC-B were not found to account for the differences in CNP responsiveness. In conclusion, observations in isolated aortic rings do not necessarily allow conclusions concerning the physiology of natriuretic peptides in the smaller resistance size arteries. Changes at the GC-B receptor level are likely to explain the diminished responsiveness of GC-A-deficient RRA to CNP.
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PMID:Diverging vasorelaxing effects of C-type natriuretic peptide in renal resistance arteries and aortas of GC-A-deficient mice. 1509 94

Pulmonary vascular medial hypertrophy due to enhanced pulmonary artery smooth muscle cell (PASMC) proliferation and/or decreased PASMC apoptosis is a primary cause of increased pulmonary vascular resistance and arterial pressure in patients with pulmonary arterial hypertension. While many factors can contribute to this form of vascular remodeling, it is generally agreed upon that altered transmembrane ion flux via ion channels is involved. While much focus has centered on the role of cations and cation channels in controlling PASMC contraction and proliferation, anion efflux via Cl- channels has recently gained interest for its role in SMC proliferation, differentiation, migration, contraction, and angiogenesis. In this issue, Dai et al. report that the putative volume-sensitive ClC-3 channel is upregulated in PASMC from monocrotaline-induced pulmonary hypertensive rats and in inflammatory cytokine-treated canine PASMC. They also provide evidence that ClC-3 upregulation may protect against oxidative stress-induced PASMC necrosis, thereby improving PASMC survival and promoting medial hypertrophy.
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PMID:ClC-3: more than just a volume-sensitive Cl- channel. 1572 96

The nature of the primary defect responsible for triggering and maintaining pulmonary artery smooth muscle (PA-SMC) proliferation in pulmonary artery hypertension (PH) is poorly understood but may be either an inherent characteristic of PA-SMCs or a secondary response to an external abnormality, such as up-regulation of growth factors. In previous studies, we found that cultured PA-SMCs from patients with idiopathic PH (iPH) had an abnormally strong proliferative response to serotonin or serum (which contains high levels of serotonin). This abnormal response is due to overexpression of the serotonin transporter (5-HTT) which mediates the mitogenic action of serotonin. That 5-HTT plays a key role in pulmonary vascular remodeling is supported by experimental studies showing that transgenic animals overexpressing 5-HTT in smooth muscle (at a level close to that seen in PH) spontaneously develop pulmonary vascular remodeling and PH. Conversely, mice with targeted S-HTT gene disruption are protected against hypoxic PH, and selective 5-HTT inhibitors reverse or prevent experimental PH. In patients with chronic lung disease, a close association has been found between a 5-HTT gene polymorphism and the severity of pulmonary hypertension. Agents capable of selectively inhibiting 5-HTT-mediated PA-SMC proliferation deserve to be investigated as potential treatments for pulmonary hypertension.
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PMID:The serotonin pathway in pulmonary hypertension. 1687 24


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