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)

Cationic colloid gold, a polycationic histochemical probe, was used to analyze the distribution of glomerular basement membrane (GBM) polyanions, including heparan sulfate protoglycan in genetic salt-sensitive (SBH/Y) and resistant (SBN/Y) hypertensive rats, with or without high dietary salt intake. GBM morphology, renal function and nitric oxide, as measured by plasma and urine nitrite (NO2) and nitrate (NO3) were also determined. In the salt-sensitive rats the high-salt dietary intake resulted in severe hypertension, proteinuria and decreased glomerular filtration rate. After 1 month of high-salt intake, the average width of the GBM of salt-sensitive rats was higher by 27% than that of salt-resistant rats. The number of GBM anionic sites (lamina rata externa and interna) was much lower in both salt-sensitive and salt-resistant groups after 1 month of salt loading, 8.04+/-0.36 and 7.8+/-0.25 counts/cm, respectively, compared to the respective values of non-salt-loaded animals, 20.58+/-1.08 counts/cm in the SBH/Y (p < 0.001) and 21+/-1.86 counts/cm in the SBN/Y (p < 0.001). A decreased nitric oxide production was found in the salt-sensitive rats before and after salt loading compared with the salt-resistant group. No correlation was found between the nitric oxide changes and the GBM modifications. It is concluded that high-salt intake may be deleterious to the permselectivity of the GBM. It is suggested that salt restriction in hypertension may have a beneficial effect in preventing GBM permselectivity changes and proteinuria.
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PMID:Glomerular basement membrane polyanionic sites and nitric oxide in genetically salt-sensitive and resistant hypertensive rats. 939 26

The activity and protein expression of endothelial nitric oxide synthase (eNOS) and inducible NOS (iNOS) were investigated during the development of hypertension in spontaneously hypertensive rats (SHR). SHR and Wistar-Kyoto rats (WKY) were studied at three different ages: 4, 14 to 17, and 63 weeks of age. After treatment with saline or lipopolysaccharide (LPS, 10 mg/kg IV) for 3 hours, the aortas were removed for measurement of NOS activity and protein expression assay by [3H]-L-citrulline formation method and Western blot analysis, respectively. Plasma levels of nitrite/nitrate (NO2-/NO3-) and tumor necrosis factor-alpha (TNF-alpha) were also determined. At 14 to 17 weeks and 63 weeks, the basal activity and protein expression of eNOS in the aortas were significantly lower in SHR than in WKY. In addition, the aged WKY exhibited lower eNOS activity than that of adult WKY, but this change was not seen in SHR. By comparison, the basal activity and protein expression of iNOS were only observed in SHR of the 14-to-17-week group and in the 63-week group; SHR still exhibited higher activities, and these differences were further exaggerated by treatment with LPS. The basal and LPS-induced NO2-/NO3- and TNF-alpha levels in the plasma were also higher in the SHR except the 4-week group. After treatment with quinapril, the basal and LPS-induced expressions of iNOS in SHR were significantly attenuated. Our results demonstrated that alterations of activity and protein expression of eNOS and iNOS occurred in SHR. In addition, aging may reduce the activity of eNOS in WKY but not in SHR. The decline of eNOS activity and/or expression may contribute to the development of hypertension, whereas the increase of iNOS expression may be a consequence of the pathological state of vessels associated with hypertension in SHR. However, the augmented expression of iNOS in SHR was attenuated by antihypertensive therapy, suggesting that the abnormal expression of iNOS is associated with hypertension.
Hypertension 1998 Feb
PMID:Alterations of nitric oxide synthase expression with aging and hypertension in rats. 946 Dec 35

It has been reported that garlic activates nitric oxide synthase in vitro and that chronic inhibition of nitric oxide (NO) synthesis by N omega-nitro-L-arginine-methyl-ester (L-NAME) induces arterial hypertension in rats. In this work, we studied the effect of oral administration of L-NAME for 4 weeks on control and garlic-fed rats. Basal systolic blood pressure was recorded 4 weeks after garlic supplementation, and on weeks 1, 2, 3, and 4 after L-NAME treatment. At the end of the study, the in vivo NO production was evaluated indirectly by measuring the urinary excretion of the stable end products of NO metabolism, nitrite (NO2-) and nitrate (NO3-). It was found that L-NAME induced arterial hypertension on weeks 1-4 in control rats but not in garlic-fed rats, whose blood pressure remained essentially as the basal values. Also, during this time period, blood pressure remained unchanged in garlic-fed rats without L-NAME treatment. Urinary excretion of NO2-/NO3- decreased in L-NAME-treated rats, increased in garlic-fed rats, and remained unchanged in garlic-fed rats treated with L-NAME. It was concluded that garlic blocks the L-NAME-induced hypertension by antagonizing in vivo the inhibitory effect of L-NAME on NO production.
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PMID:Garlic prevents hypertension induced by chronic inhibition of nitric oxide synthesis. 946 71

1. The preventive effects of exercise and L-arginine intake on hypertension and thrombosis in stroke-prone spontaneously hypertensive rats (SHRSP) were studied. 2. Stroke-prone spontaneously hypertensive rats were divided into three groups: (i) the control, sedentary group; (ii) the exercise group, which was allowed to run voluntarily on running wheels; and (iii) the L-arginine intake group, which was given 2.25% L-arginine solution for 8 weeks from 4 to 12 weeks of age. In the control group, one rat died from stroke and symptoms of stroke were observed in the remaining animals. Similar symptoms were recorded in one rat of the exercise group, but not in the L-arginine group. 3. Blood pressure increased in the control group and this increase was suppressed significantly in the exercise and L-arginine groups. Thrombotic potential in cerebral vessels was the lowest at 4 weeks in all groups and was increased significantly at 12 weeks in the control group, but not in the exercise and L-arginine groups. Plasma concentrations of NO2/NO3 were lower in all animals at 12 weeks compared with those at 4 weeks. This reduction was significantly less marked in the L-arginine group. Cerebral arterioles in control rats at 12 weeks of age were significantly smaller in diameter than those at 4 weeks and these changes were less pronounced in the exercise and L-arginine groups. 4. The results provide clear evidence for the beneficial effects of L-arginine intake and voluntary exercise in mechanisms related to hypertension, thrombosis and stroke.
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PMID:Effects of voluntary exercise and L-arginine on thrombogenesis and microcirculation in stroke-prone spontaneously hypertensive rats. 1022 44

To test the hypothesis that nitric oxide (NO) deficiency occurs in end-stage renal disease (ESRD), NO oxidation products (NO2 + NO3 = NOx) and cGMP were measured in blood, urine, and dialysate effluent of peritoneal dialysis (PD) patients and compared with blood and urine of healthy subjects. All subjects were on a controlled low-nitrate diet (approximately 330 micromol/day). NOx and cGMP outputs were significantly reduced in PD patients (334 +/- 50 micromol/24 h and 55 +/- 13 nmol/24 h, respectively) vs. controls (823 +/- 101 micromol/24 h and 149 +/- 46 nmol/24 h). Plasma arginine was borderline low, plasma citrulline was elevated and plasma levels of the endogenous NO synthase inhibitor asymmetric dimethylarginine were approximately five time higher in PD patients (2.2 +/- 0.3 microM) vs. controls (0.4 +/- 0.1 microM). Although blood pressure (BP) was not different between groups at the time of study, 10 of 11 PD patients were on medication for hypertension. These studies demonstrate that total NO production is low in ESRD, and with appropriate caution, we conclude that this NO deficiency may contribute to the increased BP that occurs in ESRD.
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PMID:Nitric oxide production is low in end-stage renal disease patients on peritoneal dialysis. 1033 62

The relationship between nitric oxide (NO) and blood pressure (BP) in deoxycorticosterone acetate-salt hypertensive rats (DOC) was investigated. Although urinary NO2- + NO3- (NOx) excretion (UNOxV) increased 2 weeks after surgery (2W-DOC), UNOxV decreased 4 weeks after surgery (4W-DOC) compared with that of the control. BP and UNOxV did not change in DOC after treatment with L-arginine (Arg-DOC). Aorta from 4W-DOC and Arg-DOC had significantly decreased relaxation responses to acetylcholine. Deendothelialized aorta from 4W-DOC and Arg-DOC had significantly decreased relaxation responses to lipopolysaccharide. These data suggest that: 1) transient increase of NO synthesis is accompanied by elevation of BP, but long-term elevation of BP decreases NO synthesis in endothelium and smooth muscle cells; 2) L-arginine supplement has no effect on the development of hypertension nor on NO production by endothelium and smooth muscle cells in DOC.
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PMID:[The role of nitric oxide in deoxycorticosterone acetate-salt hypertensive rats]. 1036 18

Clinical effects of recombinant human erythropoietin (rHuEPO) such as thrombosis, convulsions, hyperviscosity, hypertension, and angiogenic effect in culture cells have been described. We studied the rHuEPO effect on endothelial damage markers and endothelial function markers: tissue-type plasminogen activator (t-PA), nitrate (NO3), thrombomodulin (TM), and von Willebrand factor (vWF). Twenty-six peritoneal dialysis patients treated with rHuEPO and 19 controls were included. The study design for rHuEPO patients consisted of four periods: long-term treatment (rHuEPO-1); 2 months of withdrawal (rHuEPO-2); and 4 months on 5000 IU/week rHuEPO subcutaneously, with markers being measured after 2 months (rHuEPO-3) and after 4 months (rHuEPO-4). After 2 months of rHuEPO withdrawal, a decrease in hemoglobin level appeared (11+/-1.8 g/dL to 9.2+/-1.5 g/dL, p < 0.01). After rHuEPO reintroduction, this value reached 10.6+/-1.5 g/dL at two months, and 11.1+/-1.4 g/dL at four months. A significant increase in t-PA ratio was observed from two months without rHuEPO to two months on rHuEPO, returning to previous values after four months. Similarly, TM increased for patients with creatinine clearances (CrC) < 5 mL/min. No changes in the higher-than-normal plasma vWF levels were found during the various periods. A statistically significant lower value was found in controls compared with rHuEPO-4 patients. A statistically significant increase in NO3 levels was observed in the pre-venous occlusion (VO) test immediately after the re-introduction of rHuEPO. This increment returned to prior values four months after rHuEPO was reintroduced. Our results show that rHuEPO treatment causes an increase in some endothelial damage markers (TM, t-PA) and modifies endothelial function markers (t-PA ratio, NO3). These changes might favor thrombosis and atherosclerosis.
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PMID:Effects of recombinant human erythropoietin on functional and injury endothelial markers in peritoneal dialysis patients. 1040 11

We investigated the contribution made by hyperinsulinemia and endothelial dysfunction to the hypertension of rats that had received 10% fructose in their drinking water for 12 weeks. As control animals with endothelial dysfunction, we used streptozotocin-induced diabetic rats. Measurements were made at 12 weeks after the start of fructose feeding or a single streptozotocin injection. Systolic blood pressure was greater in fructose-fed rats than in either streptozotocin-diabetic rats or age-matched controls. By comparison with the age-matched controls, the plasma levels of glucose, triglyceride, high density lipoprotein cholesterol, low density lipoprotein cholesterol and free fatty acids were all significantly raised in both fructose-fed rats and streptozotocin-diabetic rats. The plasma insulin was significantly raised in fructose-fed rats, whereas it was significantly lowered in streptozotocin-diabetic rats. The vasodilatation induced in the perfused kidney by acetylcholine was weaker in both fructose-fed rats and streptozotocin-diabetic rats than in the age-matched controls and these weakened responses were further attenuated by indomethacin. Acetylcholine increased the nitrite and nitrate (NO2- and NO3-) levels in the renal perfusate in age-matched controls. This effect was much weaker in the two experimental groups. These results suggest that endothelial dysfunction in fructose-fed rats and streptozotocin-diabetic rats may be due to a decreased synthesis of nitric oxide at least in the perfused kidney. It is further suggested that hyperinsulinemia is more important than endothelial dysfunction as a cause of hypertension in fructose-fed rats.
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PMID:Insulin resistance and impaired endothelium-dependent renal vasodilatation in fructose-fed hypertensive rats. 1046 86

The protective effect of the extract of Uncariae ramulus et Uncus (URE) against endothelium disorder due to hypertension was investigated. We administered low (150 mg/kg/day) and high (450 mg/kg/day) doses of URE orally to spontaneously hypertensive rats for 8 weeks. Endothelium dependent vasodilatation by acetylcholine increased significantly in the high URE group compared with the control group. Endothelium dependent vasocontraction by xanthine oxidase decreased significantly in the high URE group compared with the control group. Serum NO2-/NO3- were tended to increase in the high URE group. It is suggested that URE may have a protective effect for the endothelium against the influence of hypertension.
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PMID:Effect of Uncariae ramulus et Uncus on endothelium in spontaneously hypertensive rats. 1059 42

Chronic treatment with cyclosporine A (CsA), an immunosuppressive agent, causes hypertension. The effect of CsA on vascular responses was determined in Sprague-Dawley rats and isolated rat aortic rings. Male rats weighing 250 to 300 g were given either CsA (25 mg/kg/day) in olive oil or vehicle by intraperitoneal injection for 7 days. Cyclosporine A administration produced a 42% increase (P<.001) in mean arterial pressure (MAP), which reached a plateau after 3 days. Conversely, the level of both nitrate/nitrite (NO2/NO3), metabolites of nitric oxide (NO), and 3', 5' cyclic guanosine monophosphate (cGMP), which mediates NO action, decreased by 50% (P<.001) and 35% (P<.001), respectively, in the urine. Thoracic aortic rings from rats treated with CsA, and precontracted with endothelin (10(-9) mol/L), showed a 35% increase (P<.001) in tension, whereas acetylcholine-induced (Ach; 10(-9) mol/L) endothelium-dependent relaxation was inhibited 65% (P<.001) compared with untreated rats. This response was similar to that of aortic rings, denuded of endothelium, from untreated rats in which Ach-induced relaxation was completely abolished (P<.001). Ach-induced formation of both NO2/NO3 and cGMP by both denuded and CsA-treated aortic rings was inhibited 95% (P<.001) and 65% P<.001), respectively, compared with intact aortic rings. The effects of CsA were reversed both in vivo and in vitro by pretreatment with L-arginine (L-Arg; 10 mg/kg/day intraperitoneally), the precursor of NO. There were no changes in MAP and tension in rats treated with L-Arg alone. In addition, in the aorta of rats that were treated intraperitoneally with CsA for 7 days, CsA significantly activated protein kinase C (PKC) translocation and decreased NO2/NO3 production. This suggest that PKC mediates, in part, CsA-induced hypertension. In summary, CsA activates PKC, which inhibits endothelial NO formation, with resulting increases in MAP and tension, and this inhibition can be overcome by L-Arg administration.
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PMID:Nitric oxide in cyclosporine A-induced hypertension: role of protein kinase C. 1060 85


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