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)

First-degree relatives of type 2 diabetic patients with or without a family history of hypertension are at increased risk for cardiovascular diseases. The aim of this study was to verify some possible hemostatic alterations in first-degree relatives of type 2 diabetic, normotensive and hypertensive patients. In 78 non-diabetic, normotensive first-degree relatives of type 2 diabetic patients (47 without a family history of hypertension and 31 with a family history of hypertension) and in 36 normoglycemic, normotensive subjects with no family history of hypertension, we evaluated plasma levels of fasting glucose and insulin, tissue-type plasminogen activator (t-PA), plasminogen activator-inhibitor (PAI-1), D-dimer (DD) and prothrombin fragment 1 + 2 (F1+2). Insulin resistance, calculated by the HOMA model, and plasma levels of t-PA and PAI-1 were significantly higher in relatives of diabetics compared to controls. As far as the thrombin activation indexes are concerned, we detected a significant increase in DD and F1+2 in relatives of diabetics with hypertension compared to other study subjects. In conclusion, our data indicate that familial predisposition may influence the hemostatic system in first-degree relatives of diabetic and/or hypertensive patients.
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PMID:Hemostasis and fibrinolysis factors in first-degree relatives of patients with Type 2 diabetes without hypertension. 1237 26

ACE inhibition reduces plasminogen activator inhibitor-1 (PAI-1), a risk factor for myocardial infarction, whereas the effect of angiotensin receptor antagonism on PAI-1 is uncertain. The present study compares the time course of effects of ACE inhibition and angiotensin type 1 (AT1) receptor antagonism on morning plasma PAI-1 antigen. Blood pressure and endocrine, metabolic, and fibrinolytic variables were measured in 20 insulin-resistant (defined by fasting glucose >8.3 mmol/L, body mass index >28 kg/m2, or fasting serum triglyceride > or =2.8 mmol/L) hypertensive subjects (mean age, 47.9+/-2.1 years) (1) before and after 1 week of hydrochlorothiazide 12.5 mg/d, and (2) before and 1, 3, 4, and 6 weeks after addition of ramipril (escalated to 10 mg/d) or losartan (escalated to 100 mg/d). Hydrochlorothiazide decreased systolic (P=0.011) and diastolic (P=0.019) pressure. Ramipril (from 133.6+/-5.1/94.5+/-2.4 to 127.0+/-3.1/91.4+/-3.3 mm Hg) or losartan (from 137.0+/-3.9/93.1+/-2.9 to 123.7+/-2.6/86.4+/-2.1 mm Hg) further reduced systolic (P=0.009) and diastolic (P=0.037) pressure. The pressure effects of the 2 drugs were similar. Hydrochlorothiazide increased plasma PAI-1 (P=0.013) but not tissue-type plasminogen activator (tPA) (P=0.431) antigen. Addition of either ramipril or losartan significantly decreased plasma PAI-1 antigen (P=0.046). However, the effect of losartan on PAI-1 antigen was not sustained throughout the 6-week treatment period, such that there was a significant drugxtime interaction (P=0.043). tPA antigen decreased during either ramipril or losartan (P=0.032), but tPA activity decreased only during losartan (P=0.018). Short-term interruption of the renin-angiotensin-aldosterone system by either ACE inhibition or AT1 receptor antagonism decreases PAI-1 antigen, but the duration of this effect is greater for ACE inhibition than for AT1 receptor antagonism.
Hypertension 2002 Dec
PMID:ACE inhibition versus angiotensin type 1 receptor antagonism: differential effects on PAI-1 over time. 1246 70

Accumulating data support an association between hypertension and impaired fibrinolytic potential abnormalities in endogenous fibrinolysis. The present study examined whether there was an association between essential hypertension and either a polymorphism in the gene coding for t-PA or the plasma concentration of t-PA antigen. Chinese hypertensive subjects (n = 126) and normotensive controls (n = 102; sex- and age-matched with hypertensives) were recruited from among the outpatients of FuWai Hospital. The distributions of the II, ID, and DD genotypes of the t-PA gene in hypertensive patients (0.15, 0.49, 0.36) were similar to those in control subjects (0.11, 0.51, 0.38; p = 0.626). No significant difference in overall allele frequencies was found between the hypertension and control groups (p = 0.656). The allelic frequencies were in Hardy-Weinberg equilibrium. There was no evidence of an association between the level of t-PA antigen and risk of hypertension. Thus, in this case control study, neither the presence of the insertion allele of the Alu-repeat polymorphism of the t-PA nor the level of t-PA antigen were associated with the risk of essential hypertension.
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PMID:Alu-repeat polymorphism in the gene coding for tissue-type plasminogen activator and the risk of hypertension in a Chinese Han population. 1248 21

Low socioeconomic status (SES) and psychological stress are associated with increased risk of coronary heart disease, and both may influence haemostatic responses. Von Willebrand factor (vWF), Factor VIII, plasma viscosity, haematocrit, blood viscosity, tissue plasminogen activator (t-PA) and fibrin D-dimer were measured at rest and following stressful tasks in 238 middle-aged British civil servants. SES was defined by grade of employment. Lower SES was associated with higher resting vWF, Factor VIII and plasma viscosity. Psychological stress stimulated increases in haemostatic and rheological factors. Initial stress responses did not vary with SES, but Factor VIII, plasma viscosity and blood viscosity remained more elevated 45 minutes post-stress in lower SES participants. High blood pressure stress reactivity was also associated with greater haemostatic responses. We conclude that lower SES is characterised by more prolonged elevations in procoagulant responses following psychological stress, and that these processes might contribute to increased cardiac risk.
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PMID:Prolonged elevations in haemostatic and rheological responses following psychological stress in low socioeconomic status men and women. 1254 Sep 57

The endothelium participates in haemostasis, inflammation, blood pressure regulation and other physiological systems. Consequently, endothelial dysfunction has been related to hypertension, thrombosis and atherosclerosis. Both von Willebrand factor (vWF) and tissue-type plasminogen activator (t-PA) are synthesized by the endothelium and their plasma levels increased during endothelium activation or injury. So far, they are well-known markers of endothelial cell function. Many circumstances activate or damage the endothelium, such as viruses, bacterium and inflammation. Circulating vWF and t-PA were studied in 92 unselected human immunodeficiency virus-1 (HIV-1)-infected patients [27 patients with and 65 patients without acquired immunodeficiency syndrome (AIDS)] and correlated with plasma levels of pro-inflammatory cytokines (tumour necrosis factor-alpha, interleukin-6), viral load, CD4 T-cell count and infectious status. HIV-1-infected patients had significantly higher plasma levels of vWF (152 versus 90%), tumour necrosis factor-alpha (31.3 versus 9.0 pg/ml) and interleukin-6 (3.5 versus 1.9 pg/ml) but not t-PA (5.9 versus 4.2 ng/ml) than the control group. These two endothelial markers correlated significantly with viral load and interleukin-6 levels in HIV-1-infected patients. The highest levels of vWF and t-PA were found in patients with AIDS. In conclusion, endothelial cell perturbation is present in HIV infection and may be a consequence of different mechanisms such as viral load, cytokines and advanced diseases.
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PMID:Viral load and disease progression as responsible for endothelial activation and/or injury in human immunodeficiency virus-1-infected patients. 1254 23

A 57-year-old woman with hypertension, mixed mitral valve disease, and atrial fibrillation was admitted to our hospital because of abdominal pain continuing for several hours. On the following day, colonoscopy was performed, and diffuse yellow-white pseudomembranous changes were seen in the right hemicolon, but there were no abnormal findings in the left hemicolon; 24 h after onset, a diagnosis of superior mesenteric arterial embolism was made on the computed tomography (CT) scan findings. Abdominal angiography was performed and showed complete occlusion of the superior mesenteric artery (SMA). Then conservative treatment, using per-catheteric thrombus aspiration, was done, followed by intraarterial injection of tissue type plasminogen activator. After the thrombo-aspiration, the filling deficit of the main artery had disappeared, and the branches on the right side were clearly delineated. After the treatment, the symptoms such as abdominal pain and diarrhea improved accordingly. She was discharged from the hospital 27 days later. Our case suggests that trans-catheter thrombo-aspiration is a possible alternative to open embolectomy for some cases of SMA embolism more than 10 h post-onset.
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PMID:Superior mesenteric arterial embolism: treatment by trans-catheter thrombo-aspiration. 1267 51

The nonapeptide bradykinin (BK) is a Janus-faced hormone, which exerts pathophysiological as well as pronounced beneficial physiological effects, mainly by stimulation of BK B(2) receptors. In various animal models and in humans it has been shown that the stimulation of BK B(2) receptors is not only implicated in the pathogenesis of inflammation, pain and tissue injury but also in powerful cardioprotective mechanisms. Either exogenous administration of BK or locally increased BK concentrations as a consequence of the inhibition of its metabolic breakdown by angiotensin-converting enzyme inhibitors, reveal the significant contribution of BK in powerful cardioprotective mechanisms. These are mainly triggered by the synthesis and release of the vasorelaxant, anti-hypertrophic and anti-atherosclerotic endothelial mediators nitric oxide, prostaglandins and tissue-type plasminogen activator, by ischaemic preconditioning and by an increase in insulin sensitivity. Consequently, BK B(2) receptor agonists may have important clinical value in the treatment and prevention of various cardiovascular disorders such as hypertension, ischaemic heart disease, left ventricular hypertrophy, ventricular remodelling and congestive heart failure as well as diabetic disorders by mimicking the reported beneficial effects of BK. However, none of the currently known potent and selective peptide and non-peptide agonists of BK B(2) receptors--RMP-7 (lobradamil, Cereport; Alkermes), JMV-1116 (Fournier), FR-190997 (Fujisawa) and FR-191413 (Fujisawa)--have been selected for a clinical assessment in cardiovascular indications. One major challenge of this approach is the still unanswered question of whether there is a sufficient safe therapeutic window between potential cardioprotective and pro-inflammatory effects following BK B(2) receptor agonism.
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PMID:The therapeutic potential of bradykinin B2 receptor agonists in the treatment of cardiovascular disease. 1272 Apr 88

There is growing evidence that stress contributes to cardiovascular disease. Chronic stress contributes to the atherosclerotic process through increased allostatic load, which is mediated by the neuroendocrine and immune systems (sympathetic nervous system and hypothalamus-pituitary adrenal axis) and related chronic risk factors (insulin resistance syndrome, hypertension, diabetes, and hyperlipidemia). In addition, acute stress can trigger cardiovascular events predominantly through sympathetic nervous activation and potentiation of acute risk factors (blood pressure increase, endothelial cell dysfunction, increased blood viscosity, and platelet and hemostatic activation). Earthquakes provide a good example of naturally occurring acute and chronic stress, and in this review we focus mainly on the effects of the Hanshin-Awaji earthquake on the cardiovascular system. The Hanshin-Awaji earthquake resulted in a 3-fold increase of myocardial infarctions in people living close to the epicenter, particularly in women, with most of the increase occurring in nighttime-onset events. There was also a near doubling in the frequency of strokes. These effects may be mediated by changes in hemostatic factors, as demonstrated by an increase of D-dimer, von Willebrand factor, and tissue-type plasminogen activator (tPA) antigen. Blood pressure also increased after the earthquake, and was prolonged for several weeks in patients with microalbuminuria.
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PMID:Disasters and the heart: a review of the effects of earthquake-induced stress on cardiovascular disease. 1288 26

Prior studies have reported significant gender differences in the procedural outcomes after elective percutaneous transluminal coronary angioplasty (PTCA). Many of these differences have been explained by the presence of more comorbidities and worse clinical characteristics such as older age, unstable angina, congestive heart failure, diabetes mellitus, and hypertension in women than in men. Moreover, women have a smaller vessel diameter, more coronary tortuosity and different plaque composition compared to men that can lead to a higher dissection rate and a greater number of procedural complications. Although early data on PTCA suggested worse immediate results in women than in men, more recent data suggest that this difference is less marked. The introduction of stents with a low profile and a higher tractability and pushability has allowed the extensive application of these devices even in small and tortuous vessels improving the outcome of PTCA. This improvement has been higher in women than in men leading to the equalization of the immediate outcome in the two sexes, even if the baseline characteristics remain worse in women. In particular, mortality and the need for urgent surgical revascularization have become extremely low without any differences between sexes. However, some authors have still found a higher incidence of complications in the first period after the procedure due to stent thrombosis in the stenting era. For this reason, meticulous antiplatelet treatment should be prescribed and drugs such as glycoprotein IIb/IIIa inhibitors may also be considered advisable to reduce the excess risk in the female population particularly in women with prothrombotic risk factors such as diabetes. At 6 and 12 months similar rates of death, late myocardial infarction, and repeated revascularization have been shown in the two sexes. Coronary stenting and the use of glycoprotein IIb/IIIa inhibitors have also improved the immediate results in patients with acute myocardial infarction (AMI) undergoing primary PTCA. Studies comparing the outcome differences between women and men with AMI and treated with primary PTCA are limited but all suggest that women benefit more than men from this procedure. The in-hospital mortality in patients with AMI is significantly higher in the female than in the male population with a higher incidence of intracranial hemorrhage in women among tissue-type plasminogen activator-treated patients. Vice versa, women and men have a similar or a slightly higher in-hospital mortality after primary PTCA without intracranial bleeding complications. For this reason, an earlier diagnosis of AMI, an earlier hospital admission and an earlier primary PTCA should be the aims of management in order to improve the outcome in women with AMI and to equalize the procedural results in the two sexes.
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PMID:Gender differences in the outcome of interventional cardiac procedures. 1456 77

Remodeling of blood vessels underlies the pathogenesis of major cardiovascular disorders, including atherosclerosis, restenosis, and hypertension. Because remodeling of arteries is highly dependent on degradation of the extracellular matrix, which enables cells to migrate and proliferate, there is intense interest in the regulation and the roles of matrix metalloproteinases (MMPs) and the plasminogen activator-plasmin (PA-P) systems in vessel remodeling. Factors that promote vessel remodeling have been shown to be important in upregulating the activities of both proteolytic systems and include chronic changes in hemodynamics, vessel injury, cytokines involved in inflammation, and elevations in reactive oxygen species. The two proteolytic systems utilize common transcription factors to activate their respective genes and are frequently coexpressed in remodeling and atherosclerotic arteries. In this review, we discuss the effects of activating the MMP and PA-P systems on processes involved in vascular remodeling, factors regulating their expression and activation, their roles in restenosis, and the development and progression of atherosclerosis, as well as the ability of currently available inhibitors to prevent unfavorable remodeling and atherosclerosis.
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PMID:Metalloproteinases and plasminogen activators in vessel remodeling. 1459 65


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