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

Blood pressure is not adequately controlled in almost 50% of patients with hypertension who are in receipt of antihypertensive therapy. This multicentre, prospective, open-label trial was designed to determine whether or not once-daily telmisartan 80 mg reduced blood pressure during the last 6 h of the 24-h dosing interval in patients with mild-to-moderate hypertension who were unresponsive to previous antihypertensive therapy. The study comprised 100 patients (47 males, 53 females) who had failed to respond satisfactorily to prior treatment given for a minimum of 3 months. At screening, 24-h ambulatory blood pressure monitoring (ABPM) was conducted after the patient had been treated with the currently prescribed antihypertensive medication. Following 5 weeks of telmisartan 80 mg treatment, ABPM was repeated. Telmisartan significantly reduced mean systolic blood pressure, diastolic blood pressure (DBP) and pulse pressure compared with previous antihypertensive therapy over each time interval (24-h, morning, night-time and the last 6 h of the dosing interval [2.00 a.m.-8.00 a.m.]) analysed. In addition, more than 90% of patients responded successfully (clinic DBP <90 mmHg or a >10 mmHg reduction in clinic DBP) at the end of telmisartan treatment. In conclusion, telmisartan provides effective blood pressure control throughout the 24-h dosing interval in patients with mild-to-moderate hypertension who were unresponsive to previous antihypertensive medication.
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PMID:Effect of telmisartan 80 mg once daily on 24-h blood pressure profile in patients with mild-to-moderate hypertension failing to respond to prior antihypertensive therapy. 1561 53

The objective of this open-label, parallel-group comparative study was to assess the clinical efficacy and safety of once-daily treatment for 8 weeks with telmisartan 80 mg in comparison with atenolol 50 mg on systolic blood pressure (SBP) and diastolic blood pressure (DBP) in patients with mild-to-moderate hypertension (morning supine SBP 141-199 mmHg, DBP 95-114 mmHg). A total of 58 patients were enrolled. The comparability of the two treatment groups was statistically documented at the beginning of the study. Telmisartan was more effective than atenolol, with a decrease in SBP of 21.7 mmHg vs. 11.8 mmHg (p = 0.03) and a non-significant decrease in DBP of 14.7 mmHg vs. 10.1 mmHg. The safety profiles of both drugs were very similar; both drugs were well tolerated. In conclusion, once-daily telmisartan 80 mg is more effective than once-daily atenolol 50 mg in lowering SBP with no negative chronotropism. Furthermore, telmisartan was as well tolerated as atenolol in the treatment of mild-to-moderate essential hypertension in adults.
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PMID:Clinical efficacy and safety of telmisartan 80 mg once daily vs. atenolol 50 mg once daily in patients with mild-to-moderate hypertension. 1561 57

Effects of Micardis (Telmisartan), alone or with low-dose aspirin, on blood pressure and other cardiovascular endpoints are examined in 20 patients with MESOR-hypertension in a crossover, double-blind, randomized study consisting of three stages, each lasting 7 days: I-placebo, II-Micardis, and III-Micardis with low-dose aspirin. Treatment was administered each day at a different circadian stage, upon awakening, and 3, 6, 9, 12, 15 and 18 hr after awakening. During each stage, the following variables were measured at 3-hr intervals during waking: systolic and diastolic blood pressure, heart rate, ejection fraction, intrarenal resistive index, acceleration time, and serum creatinine. Each data series was analyzed by single cosinor. Results were summarized by population-mean least squares spectra. At matched treatment times, the MESOR and circadian amplitude of each variable were compared among the three treatments by paired t-tests. A prominent circadian rhythm characterizes all variables. Micardis was associated not only with a lowering of blood pressure, but also with a reduction of the circadian blood pressure amplitude. The ejection fraction was increased, and the resistive index and acceleration time were decreased, the effect being more pronounced when low-dose aspirin was added to Micardis. Any circadian-stage dependent effect of Micardis, with or without low-dose aspirin, will require monitoring over spans longer than a single day for a given treatment administration time.
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PMID:Chronobiologically explored effects of Telmisartan. 1583 74

Diabetic nephropathy is characterised by hypertension and persistent proteinuria. If ineffectively controlled, a progressive decline in renal function can result in end-stage renal disease. Patients with diabetic nephropathy are also at greatly increased risk of cardiovascular disease. Angiotensin-converting enzyme (ACE) inhibitors display additional renoprotective effects beyond systemic blood pressure lowering, perhaps due to reduction in intraglomerular pressure by inhibition of angiotensin II activity. In type 2 diabetics, ACE inhibitors have variable effects, with some studies showing a reduction in microalbuminuria, prevention of the progression to macroalbuminuria and maintenance of renal function. Randomised studies have demonstrated that angiotensin II receptor blockers (ARBs), as well as controlling systemic blood pressure, delay progression of proteinuria in patients with diabetic nephropathy. Telmisartan has a number of features that may make it particularly suitable for the treatment of diabetic nephropathy. In addition to its long duration of action and almost exclusive faecal excretion, its high lipophilicity should assist in tissue penetration. The Diabetics Exposed to Telmisartan And enalaprIL (DETAIL) study was designed to compare the long-term renal outcome of treatment with telmisartan 40.80 mg versus enalapril 10.20 mg (with titration to the higher dose after 4 weeks) in patients with type 2 diabetes, mild-to-moderate hypertension and albuminuria. The primary endpoint is the change in glomerular filtration rate after 5 years' randomised treatment. Secondary endpoints are annual changes in glomerular filtration rate, serum creatinine and urinary albumin excretion, as well as incidences of end-stage renal disease, cardiovascular events, all-cause mortality and adverse events. The groundbreaking DETAIL study revealed that telmisartan conferred comparable renoprotection to enalapril and was associated with a low incidence of mortality.
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PMID:Preventing renal complications in diabetic patients: the Diabetics Exposed to Telmisartan And enalaprIL (DETAIL) study. 1586 19

The adipose-specific protein adiponectin has been recently discovered to improve insulin sensitivity. Angiotensin type-1 receptor (AT1R) blockers (ARBs) reduce the incidence of type 2 diabetes mellitus by mostly unknown molecular mechanisms. To identify new antidiabetic mechanisms of ARBs, we studied the regulation of adiponectin by angiotensin II (Ang II) and different ARBs in murine 3T3-L1 adipocytes and obese Zucker rats. Adiponectin protein expression was markedly stimulated by Ang II (5 nmol/L), which was inhibited by blockade of the AT2R, and further enhanced by the ARB irbesartan. Irbesartan-mediated adiponectin upregulation started beyond the concentrations needed for AT1R blockade and was also present in the absence of Ang II, implicating an AT1R-independent mechanism of action. Recently, certain ARBs (irbesartan, telmisartan) were identified as ligands of the peroxisome proliferator-activated receptor (PPAR)gamma. Telmisartan also stimulated adiponectin protein expression, whereas the non-PPARgamma-activating ARB eprosartan had no effect. Blockade of PPARgamma activation by the PPARgamma antagonist GW9662 markedly inhibited irbesartan-induced adiponectin expression. Cognate mRNA levels of adiponectin were not affected by ARBs. Kinetic studies using the protein synthesis inhibitor cycloheximide showed that irbesartan prevented the cellular depletion of adiponectin protein. Finally, administration of irbesartan to obese Zucker rats improved insulin sensitivity and attenuated adiponectin serum depletion. The present study demonstrates that AT2R activation and certain ARBs induce adiponectin in adipocytes, which was associated with an improvement of parameters of insulin sensitivity in vivo. ARB-induced adiponectin stimulation is likely to be mediated via PPARgamma activation involving a post-transcriptional mechanism.
Hypertension 2005 Jul
PMID:PPARgamma-activating angiotensin type-1 receptor blockers induce adiponectin. 1593 9

Angiotensin receptor blockers (ARBs) were introduced after clinical trials showed angiotensin-converting enzyme inhibitors (ACEIs) to have extensive clinical benefits in a wide range of diseases. Consequently, it has been more difficult for clinical trials to demonstrate similar, enhanced or additive benefits of ARBs. However, ARBs were introduced with the hypothesis that they were likely a more effective method of interrupting the renin-angiotensin system and would result in enhanced outcomes. Clinical trials in high-risk vascular patients (after myocardial infarction), patients with heart failure and patients with nephropathy show the benefits of ACE inhibition. ARBs likely have similar benefits as ACEIs when used after myocardial infarction, in patients with heart failure and for management of diabetic nephropathy. However, ARBs generally remain a second-line treatment because it has been more difficult to demonstrate that ARBs prevent acute vascular events, such as myocardial infarction, together with the greater clinical trial evidence for ACE inhibition. The primary application of ACEIs over ARBs is reflected in the Canadian clinical guidelines for the management of patients with diabetes, hypertension, heart failure and following myocardial infarction. Until the completion of clinical trials, such as the Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET), that examine whether ARBs have vascular protective properties similar to ACEIs, it is unlikely that the clinical guidelines will change.
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PMID:Have angiotensin receptor blockers lived up to expectations? 1594 Mar 55

The metabolic syndrome leads to cardiovascular disease and type 2 diabetes mellitus, through multiple risks, such as insulin resistance, dyslipidemia, hyperinsulinemia, and hypertension. It also represents a disorder of partial genetic background as mutations of the peroxisome proliferator-activated receptor-gamma (PPAR-g). Thiazolidinedione agonists for the PPAR-g system are effective in control of insulin resistance and diabetes. Telmisartan has a molecular structure that imparts partial agonist properties with the PPAR-g molecule, which results in reductions in glucose and lipid metabolism. Administration of telmisartan to rats on a high-fat, high-carbohydrate diet leads to reductions in glucose, insulin, and triglyceride levels. The results imply that the ARB agent, telmisartan, could treat both the hemodynamic and metabolic aberrations seen in subjects with the metabolic syndrome, such as insulin resistance, glucose intolerance, and hypertension.
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PMID:Angiotensin-receptor blocking agents and the peroxisome proliferator-activated receptor-gamma system. 1606 Oct 40

The study included evaluation of respiratory function, bronchial conductivity, gas homeostasis, and 24-hour profile of blood pressure (BP) in 15 male patients with chronic obstructive lung disease and I-II stage arterial hypertension prior to and after 2 weeks of therapy with telmisartan. The drug, administered in a dose of 80 mg/day, significantly increased 1 sec forced expiratory volume, peak expiratory flow rate, decreased effective bronchial resistance and CO2 partial pressure in arterial blood. Telmisartan also significantly reduced mean systolic BP (SBP) (p < 0.003) and diastolic BP (DBP) (p < 0.001) during day hours, SBD (p < 0.01) and pulse BP (p < 0.05) during night hours, significantly reduced SBP load (p < 0.02) and DBP load (p < 0.003) during day hours, and SBP load during night hours (p < 0.02).
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PMID:[Efficacy of telmisartan in chronic obstructive lung disease wtih arterial hypertension]. 1611 30

Epidemiological studies have established that left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular and cerebrovascular morbidity and mortality. In turn, hypertension is a well-established risk factor for LVH. Ambulatory blood pressure monitoring has shown that 24-h mean ambulatory blood pressure is a particularly powerful predictor of LVH, being superior to casual clinic blood pressure measurements. The magnitude of the rise in blood pressure in the early morning correlates with the extent of LVH. Prospective studies have shown the advantageous effects of antihypertensive therapy on LVH in terms of regression of left ventricular mass (LVM) and subsequent reduction in overt cardiovascular disease. Meta-analysis has identified differences in the ability of different classes of anti-hypertensive agents to bring about regression of LVH, with agents that target the renin angiotensin system (RAS) appearing superior to other agents, such as beta-blockers and diuretics. The distinct pharmacological features of telmisartan suggest that it may be a suitable agent for managing hypertensive patients because it provides sustained control of blood pressure and appears to be very effective in reversing cardiac remodelling. Pre-clinical evaluation has demonstrated that telmisartan suppresses angiotensin II-induced collagen production and secretion by cultured fibroblasts, and reduces left ventricular weight in different animal models. Several clinical studies have demonstrated that, as well as reducing blood pressure (including 24-h mean ambulatory values), telmisartan brings about LVM regression in patients with hypertension, and improves left ventricular and left atrial function. Comparative studies have shown telmisartan's superiority compared with both hydrochlorothiazide and carvedilol in regressing LVM, the additional activity probably being explained by the sustained blood pressure control and the non-haemodynamic effects of targeting the RAS. The ultimate proof of the clinical value of telmisartan will be provided by the outcome trials ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial/Telmisartan Randomized AssessmeNt Study in aCE iNtolerant subjects with cardiovascular Disease (ONTARGET/TRANSCEND) currently being conducted in high-risk patients.
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PMID:Pre-clinical and clinical experience of telmisartan in cardiac remodelling. 1622 96

In this open-label, non-comparative study, the anti-hypertensive efficacy and effect on left ventricular hypertrophy (LVH) of 24 weeks' treatment with once-daily telmisartan 40-80 mg was evaluated in 24 patients with mild-to-moderate hypertension and LVH. Patients were titrated to the higher dose of study drug at week 4 if they did not achieve blood pressure normalization (i.e. systolic blood pressure [SBP]/diastolic blood pressure [DBP] remained > or = 140/90 mmHg). The anti-hypertensive action of telmisartan was assessed using clinic cuff measurements and 24-h ambulatory blood pressure monitoring, and left ventricular mass index (LVMI) was determined by two-dimensional echocardiography at baseline and after 24 weeks of therapy. Telmisartan significantly reduced mean 24-h, daytime and night-time SBP and DBP compared with baseline after 12 and 24 weeks of therapy. Target blood pressure levels, defined as SBP/DBP < 140/90 mm Hg, were achieved in 16 (69.6%) patients at the end of the treatment period. After 24 weeks of telmisartan treatment, LVMI decreased from 151.6 +/- 5.4 to 135.1 +/- 5.9 g/m2. In conclusion, anti-hypertensive treatment with telmisartan for 24 weeks produced significant reductions in blood pressure and regression of LVH, as assessed by LVMI, in patients with hypertension and LVH.
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PMID:Angiotensin II receptor blocker telmisartan: effect on blood pressure profile and left ventricular hypertrophy in patients with arterial hypertension. 1622 97


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