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

To clarify the effects of correction of anemia with recombinant human erythropoietin (rHuEPO) on blood coagulation, fibrinolysis and endothelium, these markers were examined in 19 regular hemodialysis patients before and 4, 8, 12 weeks on rHuEPO treatment, and 5 weeks after the end of treatment. Hematocrit significantly increased from 22.8 +/- 2.0 to 31.1 +/- 2.7% at 12 week (p < 0.001). Coagulation and fibrinolysis markers did not show significant changes except for minor and transient alteration of protein C, thrombin-antithrombin III complex and alpha 2-plasmin inhibitor plasmin complex (PIC) throughout the treatment. Endothelin and 6-keto-prostaglandin F1 alpha (PGF1 alpha) significantly increased from 6.1 +/- 4.5 to 14.2 +/- 2.9 pg/ml (p < 0.001) and from 51.9 +/- 14.7 to 66.5 +/- 18.5 pg/ml (p < 0.05) at 12 week, respectively. Human atrial natriuretic peptide (ANP) significantly decreased from 277.9 +/- 88.6 to 179.4 +/- 73.3 pg/ml at 12 week (p < 0.001). Endothelin and PGF1 alpha after 6 month treatment with rHuEPO showed high values as same as those of 12 weeks. These data suggests that rHuEPO therapy did not affect blood coagulation and fibrinolysis, however exerts effects on the endothelium. Changes in endothelial function after rHuEPO may be one of the pathogenetic mechanisms of hypertension and may contribute to a decrease in thrombotic complications.
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PMID:[Changes in endothelial vasoactive substances and blood coagulation and fibrinolysis functions under recombinant human erythropoietin therapy in hemodialysis patients]. 831 81

Short-term effects of ridogrel, a combined thromboxane synthase inhibitor and receptor antagonist, were investigated in 16 patients with uncomplicated essential hypertension. After a 2-week placebo period without antihypertensive medication, patients were admitted to the hospital overnight on two occasions 3 weeks apart. On each occasion, they received two doses of either placebo or ridogrel (300 mg) 12 hours apart according to a double-blind crossover protocol. Renal and systemic thromboxane A2 and prostacyclin biosynthesis were investigated by measuring urinary excretion of thromboxane B2, 6-oxo-prostaglandin F1 alpha, and their respective 2,3-dinor metabolites using gas chromatography/mass spectrometry. Responses of platelets to a thromboxane A2 mimetic and to adenosine diphosphate were studied turbidometrically. Blood pressure was measured automatically at 20-minute intervals. Ridogrel reduced excretion of 2,3-dinor-thromboxane B2 and thromboxane B2 compared with placebo (21 +/- 6 versus 279 +/- 28 and 14 +/- 4 versus 39 +/- 9 ng/g creatinine, respectively; P < .0001 and P < .05). Excretion of 2,3-dinor-6-oxoprostaglandin F1 alpha and 6-oxoprostaglandin F1 alpha was increased by ridogrel compared with placebo (184 +/- 20 versus 146 +/- 11 and 86 +/- 9 versus 58 +/- 6 ng/g creatinine, respectively; P < .05). Ridogrel selectively antagonized platelet aggregation to the thromboxane mimetic (P < .0001). Blood pressure did not differ significantly between ridogrel and placebo treatment periods. Thus, in patients with essential hypertension, acute administration of ridogrel reduces renal and extrarenal thromboxane A2 biosynthesis, increases renal and extrarenal prostacyclin biosynthesis, inhibits thromboxane receptor-activated platelet aggregation, but has no effect on systemic arterial pressure.
Hypertension 1993 Aug
PMID:Thromboxane A2 receptor antagonism and synthase inhibition in essential hypertension. 834 Jan 55

Twenty patients with mild to moderate hypertension took part in this study consisting of a two-week placebo treatment period, followed by treatment with an extended-release calcium channel blocker, felodipine-ER (5 to 20 mg once daily) for 12 weeks. The study evaluated the effects of felodipine-ER on blood pressure, platelet function and rheological properties in hypertension. Felodipine-ER significantly reduced systolic and diastolic blood pressure without changing heart rate. There was a significant decrease in adenosine diphosphate-induced platelet aggregation and platelet intracellular calcium concentration, but no significant change in plasma thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and platelet cyclic 3'5'-adenosine monophosphate concentrations. Adverse effects on biochemical and rheological properties were not found. In conclusion, felodipine-ER is an effective and metabolically safe antihypertensive drug. It reduces platelet aggregability and intracellular free calcium concentration without altering the production of TXB2 and 6-keto-PGF1 alpha.
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PMID:Effect of felodipine-ER on blood pressure, platelet function, and rheological properties in hypertension. 839 93

Our objective was to evaluate prostanoid release from the placentae of pregnancies complicated by severe intrauterine growth retardation (IUGR) and without hypertension, compared with placentae from normal, uncomplicated term pregnancies. A perifusion system was utilized to study the release of prostanoids 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), thromboxane B2(TxB2), prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) from human placentae from pregnancies complicated by normotensive severe IUGR (n = 9, five at term and four preterm) and normal control pregnancies (n = 6). For each placenta, triplicate chambers of tissue were perifused at a rate of 6 ml/h, and samples were collected from hours 5-10. Prostanoids were measured using specific and sensitive radioimmunoassays. In the IUGR group, the basal placental production of the vasoconstrictor thromboxane was not increased, nor was the ratio of cumulative TxB2 to 6-keto-PGF1 alpha elevated compared with normal term controls. In three term IUGR placentae, the ratio was significantly decreased compared with controls. The basal placental production of the vasoconstrictor PGF2 alpha was likewise not increased compared with controls, nor was the ratio of PGF2 alpha to PGE2 elevated. Two of the placentae in the term IUGR group demonstrated significant elevations of PGE2 and 6-keto-PGF1 alpha. Overall, the IUGR placentae released normal or low normal levels of the prostanoids studied. The pattern of placental prostanoid release over time was similar to that of the normal term placentae. The term and preterm placentae of pregnancies complicated by severe IUGR did not exhibit an excess production of vasoconstrictor prostanoids. Therefore, strategies designed to reduce thromboxane production in severe IUGR without hypertension may be unjustified.
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PMID:Placental prostanoid release in severe intrauterine growth retardation. 857 May 72

To determine whether endothelin-1 (ET-1) contributes to hypertension associated with non-steroidal anti-inflammatory drug (NSAID) usage in healthy, elderly, normotensive individuals a randomised, double-blind, placebo-controlled, crossover trial of indomethacin was undertaken in 41 healthy, elderly individuals with stable normotension or controlled hypertension (blood pressure (BP) < or = 160/90 mm Hg). The main outcome measures were systolic and diastolic BP, heart rate, cardiac output, weight, creatinine clearance, plasma renin activity, aldosterone, endothelin-1 and arginine vasopressin concentrations and 24 h urinary endothelin-1 and 6 keto prostaglandin F1 alpha outputs. Analysis of covariance was used to evaluate the effect of indomethacin on BP and related parameters. Indomethacin treatment for 1 month increased systolic (+/- s.e.m.: 4.1 +/- 2.2 mm Hg; 95% confidence interval 0 to 8.3 mm Hg) and diastolic BP (2.7 +/- 1.1 mm Hg; 0.4 to 4.9 mm Hg) without altering cardiac output (P = 0.59), implying an increase in total peripheral resistance. Indomethacin treatment produced a small increase in weight (1.4 +/- 0.4 kg; 0.6 to 2.2 kg), a small reduction in renal function (creatinine clearance: 6.8 +/- 1.8 mis/min; 3.3 to 10.3 mis/min) but a significant (83%) increase in daily urinary endothelin-1 production (13.1 +/- 3.4 ng/ml; 6.4 to 19.8 ng/ml) without altering plasma ET-1 concentration, suggesting increased renal synthesis. In conclusion, renal paracrine effects of ET-1 may contribute to NSAID-induced blood pressure elevation in humans.
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PMID:Potential mechanisms by which nonsteroidal anti-inflammatory drugs elevate blood pressure: the role of endothelin-1. 873 58

1. The obese fa/fa Zucker rat is a genetic model of obesity and insulin resistance which develops a number of metabolic and endocrine features of non-insulin-dependent diabetes, including hypertension, proteinuria and glomerular sclerosis. 2. We have investigated the urinary excretion of the metabolites of thromboxane (thromboxane B2) and prostacyclin (6-keto prostaglandin F1 alpha), and of endothelin and cyclic GMP as markers for changes in the balance of renal haemodynamic factors in the obese Zucker rat. 3. Obese fa/fa Zucker rats were hypertensive compared with their lean counterparts (161 +/- 3 and 138 +/- 3 mmHg respectively, P < 0.01); obese animals were also markedly proteinuric (16.7 +/- 6.7 versus 1.1 +/- 0.1 mg/ml) and albuminuric (8.3 +/- 2.9 versus 0.4 +/- 0.25 mg/ml) and excreted less creatinine than lean animals (all P < 0.01). Urinary excretion of endothelin was greater in obese rats (123 +/- 24 versus 62 +/- 10 pg/15 h, P < 0.05) as was the level of pre-proendothelin mRNA, but excretion of cyclic GMP was depressed (12.5 +/- 1.6 versus 27.2 +/- 3.1 nmol/ 15 h, P < 0.01). Histological examination of kidneys from obese animals showed evidence of focal glomerulosclerosis and cortical tubular damage. 4. These results show that increased urinary endothelin is associated with proteinuria and early stage nephropathy in this animal model of non-insulin-dependent diabetes mellitus. This finding, coupled with a decreased excretion of cyclic GMP, suggests that these increased renal vasoconstrictor/vasodilator forces might contribute to the renal functional changes in non-insulin-dependent diabetes mellitus.
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PMID:Elevated renal endothelin-I clearance and mRNA levels associated with albuminuria and nephropathy in non-insulin-dependent diabetes mellitus: studies in obese fa/fa Zucker rats. 949 94


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