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Angiotensin II Antagonist

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Norman K Hollenberg – One of the best experts on this subject based on the ideXlab platform.

  • effect of Angiotensin II Antagonist eprosartan on hyperglycemia induced activation of intrarenal renin Angiotensin system in healthy humans
    Hypertension, 2000
    Co-Authors: Suzette Y Osei, Deborah A Price, Lori M Laffel, M C Lansang, Norman K Hollenberg
    Abstract:

    Abstract —We have previously reported that hyperglycemia in healthy human subjects increased the renal vasodilator response to the Angiotensin-converting enzyme inhiinhibitor captopril. This observation raised intriguing possibilities relevant to the pathogenesis of nephropathy in patients with diabetes mellitus. To ascertain whether the effect of captopril was indeed mediated by a reduction in Angiotensin II (Ang II) formation, we performed another study in which an Ang II Antagonist, eprosartan, was used in place of captopril. Nine healthy subjects were studied in high sodium balance (ie, sodium intake 200 mmol/d). On the first day, the subjects received 600 mg eprosartan orally, and renal plasma flow (RPF) and glomerular filtfiltratione (GFR) were measured. Glucose was infused intravenously on the second and third study days to increase plasma glucose to a level below the threshold for glycosuria (≈8.8 mmol/L). Eprosartan at a dose of 600 mg or placebo was administered randomly on the second or third study day 1 hour after initiation of glucose infuinfusion. RPF increased (by 76±7 mL · min −1 · 1.73 m −2 , P −1 · 1.73 m −2 , P

  • Renal hemodynamic response to an Angiotensin II Antagonist, eprosartan, in healthy men.
    Hypertension (Dallas Tex. : 1979), 1997
    Co-Authors: D A Price, J M De'oliveira, N D Fisher, Norman K Hollenberg
    Abstract:

    In view of the vasodilator potential of Angiotensin-converting enzyme (ACE) inhibition via prostaglandins and kinins, we asked why renin inhibition induces a larger renal vasodilator response than ACE inhibitors in healthy humans in earlier studies. One possibility was that there was a more complete blockade of the renin system, which could also be achieved by an Angiotensin II Antagonist, eprosartan. We measured the hormonal and renal hemodynamic responses to eprosartan doses, from 10 to 400 mg in 9 healthy young men in balance on a 10-mmol/d sodium intake. The threshold eprosartan dose to influence renal perfusion was

  • renal hemodynamic response to an Angiotensin II Antagonist eprosartan in healthy men
    Hypertension, 1997
    Co-Authors: D A Price, N D Fisher, Jose Mario Deoliveira, Norman K Hollenberg
    Abstract:

    Abstract In view of the vasodilator potential of Angiotensin-converting enzyme (ACE) inhibition via prostaglandins and kinins, we asked why renin inhibition induces a larger renal vasodilator response than ACE inhibitors in healthy humans in earlier studies. One possibility was that there was a more complete blockade of the renin system, which could also be achieved by an Angiotensin II Antagonist, eprosartan. We measured the hormonal and renal hemodynamic responses to eprosartan doses, from 10 to 400 mg in 9 healthy young men in balance on a 10-mmol/d sodium intake. The threshold eprosartan dose to influence renal perfusion was −1 · 1.73 m 2 . When the dose was increased to 400 mg, there was a modest additional increase of 147±57 mL · min −1 · 1.73 m –2 . A highly significant dose-related fall in arterial blood pressure occurred ( r =−.97; P −1 · 1.73 m –2 , was significantly less than that seen with the low salt diet ( P

Shahnaz Shahinfar – One of the best experts on this subject based on the ideXlab platform.

  • effect of a reduction in uric acid on renal outcomes during losartan treatment a post hoc analysis of the reduction of endpoints in non insulin dependent diabetes mellitus with the Angiotensin II Antagonist losartan trial
    Hypertension, 2011
    Co-Authors: Yan Miao, Shahnaz Shahinfar, Barry M. Brenner, Mark E. Cooper, Hanshenrik Parving, Stefan Ottenbros, Goos D Laverman, Diederick E Grobbee, Dick De Zeeuw
    Abstract:

    Emerging data show that increased serum uric acid (SUA) concentration is an independent risk factor for end-stage renal disease. Treatment with the antihypertensive drug losartan lowers SUA. Whether reductions in SUA during losartan therapy are associated with renoprotection is unclear. We therefore tested this hypothesis. In a post hoc analysis of 1342 patients with type 2 diabdiabetes mellitus and nephropathy participating in the Reduction of Endpoints in Non-Insulin-Dependent Diabetes Mellitus With the Angiotensin II Antagonist Losartan Trial, we determined the relationship between month 6 change in SUA and renal endpoints, defined as a doubling of serum creatinine or end-stage renal disease. Baseline SUA was 6.7 mg/dL in placebo and losartan-treated subjects. During the first 6 months, losartan lowered SUA by -0.16 mg/dL (95% CI: -0.30 to -0.01; P=0.031) as compared with placebo. The risk of renal events was decreased by 6% (95% CI: 10% to 3%) per 0.5-mg/dL decrement in SUA during the first 6 months. This effect was independent of other risk markers, including estimate glomerular filtfiltratione and albuminuria. Adjustment of the overall treatment effects for SUA attenuated losartan‘s renoprotective effect from 22% (95% CI: 6% to 35%) to 17% (95% CI: 1% to 31%), suggesting that approximately one fifth of losartan‘s renoprotective effect could be attributed to its effect on SUA. Losartan lowers SUA levels compared with placebo treatment in patients with type 2 diabdiabetes mellitus and nephropathy. The degree of reduction in SUA is subsequently associated with the degree in long-term renal risk reduction and explains part of losartan‘s renoprotective effect. These findings support the view that SUA may be a modifiable risk factor for renal disease.

  • increased serum potassium affects renal outcomes a post hoc analysis of the reduction of endpoints in niddm with the Angiotensin II Antagonist losartan renaal trial
    Diabetologia, 2011
    Co-Authors: Yan Miao, Shahnaz Shahinfar, Barry M. Brenner, Mark E. Cooper, H. H. Parving, Diederick E Grobbee, Daniela Dobre, H Lambers J Heerspink, Dick De Zeeuw
    Abstract:

    Aims/hypothesis To assess the effect of an Angiotensin receptor blocker (ARB) on serum potassium and the effect of a serum potassium change on renal outcomes in patients with type 2 diabetes and nephropathy.

  • albuminuria is a target for renoprotective therapy independent from blood pressure in patients with type 2 diabetic nephropathy post hoc analysis from the reduction of endpoints in niddm with the Angiotensin II Antagonist losartan renaal trial
    Journal of The American Society of Nephrology, 2007
    Co-Authors: Wouter B A Eijkelkamp, Shahnaz Shahinfar, Giuseppe Remuzzi, Zhongxin Zhang, William F. Keane, Gilbert W. Gleim, Mark E. Cooper, Hanshenrik Parving, Matthew R Weir
    Abstract:

    Albuminuria reduction could be renoprotective in hypertensive patients with diabetic nephropathy. However, the current use of reninAngiotensin-system intervention is targeted to BP only. Therefore, this study investigated the adequacy of this approach in 1428 patients with hypertension and diabetic nephropathy from the placebo-controlled Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) study. Investigated were the extent of discordance in treatment effects on systolic BP (SBP) and albuminuria and its association with renal outcome in a multivariate Cox model. Among patients with a reduced SBP during treatment, a lack of albuminuria reduction was observed in 37, 26, and 51% (total, losartan, and placebo, respectively) at month 6. SBP or albuminuria reduction was associated with a lower risk for ESRD, whereas combined SBP and albuminuria reduction was associated with the lowest risk for events. Across all categories of SBP change, a progressively lower ESRD hazard ratio was observed with a larger albuminuria reduction. A lower residual level of albuminuria was also associated with lower ESRD risk. In conclusion, changes in albuminuria are not concordant in a substantial proportion of patients when titrated for BP. Meanwhile, the ESRD risk showed a clear dependence on albuminuria reduction. The ESRD risk also showed dependence on the residual level of albuminuria, even in patients who reached the current SBP target. Antihypertensive treatment that is aimed at improving renal outcomes in patients with diabetic nephropathy may therefore require a dual strategy, targeting both SBP and albuminuria reduction.

F. Bodin – One of the best experts on this subject based on the ideXlab platform.

  • Valsartan, a new Angiotensin II Antagonist for the treatment of essential hypertension: efficacy and safety compared to hydrochlorothiazide.
    European journal of clinical pharmacology, 1997
    Co-Authors: G. Hegner, G. Faust, F. Freytag, Susanne Meilenbrock, J. Sullivan, F. Bodin
    Abstract:

    To compare the antihypertensive efficacy of a new Angiotensin II Antagonist, valsartan, with a reference therapy, hydrochlorothiazide (HCTZ). In this double-blind study, 167 adult out-patients with mild-to-moderate essential hypertension were randomly allocated in equal number to receive valsartan 80 mg or HCTZ 25 mg for 12 weeks. In patients whose blood pressure (BP) remained uncontrolled after 8 weeks of monotherapy, atenolol 50 mg was added to the initial treatment. Patients were assessed at 4, 8 and 12 weeks. The primary efficacy variable was change from baseline in mean sitting diastolic BP (SDBP) at 8 weeks. Secondary variables included change in sitting systolic BP (SSBP) and responder rates (percentage of patients with SDBP < 90 mmHg or drop > or = 10 mmHg compared to baseline) at 8 weeks. Valsartan and HCTZ were both effective at lowering diastolic and systolic blood pressure at all time points. Similar falls were seen in both groups with no significant differences between treatments. For the primary variable (decrease in SDBP) there was no significant difference between treatments. For SSBP there was also no significant difference observed. Responder rates at 8 weeks were 74% for valsartan and 62% for HCTZ (P = 0.10). Both treatments were well tolerated, both as monotherapy, and when combined with atenolol 50 mg per day. The data show valsartan 80 mg to be as effective as HCTZ in the treatment of mild-to-moderate hypertension. The results also show valsartan to be well tolerated when taken alone or in combination with atenolol.

  • valsartan a new Angiotensin II Antagonist for the treatment of essential hypertension a comparative study of the efficacy and safety against amlodipine
    Clinical Pharmacology & Therapeutics, 1996
    Co-Authors: Luigi Corea, Susanne Meilenbrock, Ondina Cardoni, Roberto Fogari, Pierfranco Innocenti, Carlo Porcellati, Michele Provvidenza, John L. Sullivan, F. Bodin
    Abstract:

    Objective To compare the antihypertensive efficacy of a new Angiotensin II Antagonist, valsartan, with a reference therapy, amlodipine. Methods One hundred sixty-eight adult outpatients with mild to moderate hypertension were randomly allocated in double-blind fashion and equal number to receive 80 mg valsartan or 5 mg amlodipine for 12 weeks. After 8 weeks of therapy, in patients whose blood pressure remained uncontrolled, 5 mg amlodipine was added to the initial therapy. Patients were assessed at 4, 8, and 12 weeks. The primary efficacy variable was change from baseline in mean sitting diastolic blood pressure at 8 weeks. Secondary variables included change in sitting systolic blood pressure and responder rates. Results Both valsartan and amlodipine were effective at lowering blood pressure at 4, 8, and 12 weeks. Similar decreases were observed in both groups, with no statistically significant differences between the groups for any variable analyzed. For the primary variable the difference was 0.5 mm Hg in favor of valsartan (p = 0.68; 95% confidence interval, −2.7 to 1.7). Responder rates at 8 weeks were 66.7% for valsartan and 60.2% for amlodipine (p = 0.39). Both treatments were well tolerated. The incidence of drug-related dependent edema was somewhat higher in the amlodipine group, particularly at a dose of 10 mg per day (2.4% for 80 mg valsartan; 3.6% for 5 mg amlodipine; 0% for valsartan plus 5 mg amlodipine; 14.3% for 10 mg amlodipine). Conclusions The data show that valsartan is at least as effective as amlodipine in the treatment of mild to moderate hypertension. The results also show valsartan to be well tolerated and suggest that it is not associated with side effects characteristic of this comparator class, dihydropyridine calcium Antagonists. Clinical Pharmacology & Therapeutics (1996) 60, 341–346; doi:

  • Valsartan, a new Angiotensin II Antagonist for the treatment of essential hypertension: A comparative study of the efficacy and safety against amlodipine
    Clinical pharmacology and therapeutics, 1996
    Co-Authors: Luigi Corea, Susanne Meilenbrock, Ondina Cardoni, Roberto Fogari, Pierfranco Innocenti, Carlo Porcellati, Michele Provvidenza, John L. Sullivan, F. Bodin
    Abstract:

    To compare the antihypertensive efficacy of a new Angiotensin II Antagonist, valsartan, with a reference therapy, amlodipine. One hundred sixty-eight adult outpatients with mild to moderate hypertension were randomly allocated in double-blind fashion and equal number to receive 80 mg valsartan or 5 mg amlodipine for 12 weeks. After 8 weeks of therapy, in patients whose blood pressure remained uncontrolled, 5 mg amlodipine was added to the initial therapy. Patients were assessed at 4, 8, and 12 weeks. The primary efficacy variable was change from baseline in mean sitting diastolic blood pressure at 8 weeks. Secondary variables included change in sitting systolic blood pressure and responder rates. Both valsartan and amlodipine were effective at lowering blood pressure at 4, 8, and 12 weeks. Similar decreases were observed in both groups, with no statistically significant differences between the groups for any variable analyzed. For the primary variable the difference was 0.5 mm Hg in favor of valsartan (p = 0.68; 95% confidence interval, -2.7 to 1.7). Responder rates at 8 weeks were 66.7% for valsartan and 60.2% for amlodipine (p = 0.39). Both treatments were well tolerated. The incidence of drug-related dependent edema was somewhat higher in the amlodipine group, particularly at a dose of 10 mg per day (2.4% for 80 mg valsartan; 3.6% for 5 mg amlodipine; 0% for valsartan plus 5 mg amlodipine; 14.3% for 10 mg amlodipine). The data show that valsartan is at least as effective as amlodipine in the treatment of mild to moderate hypertension. The results also show valsartan to be well tolerated and suggest that it is not associated with side effects characteristic of this comparator class, dihydropyridine calcium Antagonists.

Barry M. Brenner – One of the best experts on this subject based on the ideXlab platform.

  • effect of a reduction in uric acid on renal outcomes during losartan treatment a post hoc analysis of the reduction of endpoints in non insulin dependent diabetes mellitus with the Angiotensin II Antagonist losartan trial
    Hypertension, 2011
    Co-Authors: Yan Miao, Shahnaz Shahinfar, Barry M. Brenner, Mark E. Cooper, Hanshenrik Parving, Stefan Ottenbros, Goos D Laverman, Diederick E Grobbee, Dick De Zeeuw
    Abstract:

    Emerging data show that increased serum uric acid (SUA) concentration is an independent risk factor for end-stage renal disease. Treatment with the antihypertensive drug losartan lowers SUA. Whether reductions in SUA during losartan therapy are associated with renoprotection is unclear. We therefore tested this hypothesis. In a post hoc analysis of 1342 patients with type 2 diabetes mellitus and nephropathy participating in the Reduction of Endpoints in Non-Insulin-Dependent Diabetes Mellitus With the Angiotensin II Antagonist Losartan Trial, we determined the relationship between month 6 change in SUA and renal endpoints, defined as a doubling of serum creatinine or end-stage renal disease. Baseline SUA was 6.7 mg/dL in placebo and losartan-treated subjects. During the first 6 months, losartan lowered SUA by -0.16 mg/dL (95% CI: -0.30 to -0.01; P=0.031) as compared with placebo. The risk of renal events was decreased by 6% (95% CI: 10% to 3%) per 0.5-mg/dL decrement in SUA during the first 6 months. This effect was independent of other risk markers, including estimate glomerular filtration rate and albuminuria. Adjustment of the overall treatment effects for SUA attenuated losartan’s renoprotective effect from 22% (95% CI: 6% to 35%) to 17% (95% CI: 1% to 31%), suggesting that approximately one fifth of losartan’s renoprotective effect could be attributed to its effect on SUA. Losartan lowers SUA levels compared with placebo treatment in patients with type 2 diabetes mellitus and nephropathy. The degree of reduction in SUA is subsequently associated with the degree in long-term renal risk reduction and explains part of losartan’s renoprotective effect. These findings support the view that SUA may be a modifiable risk factor for renal disease.

  • increased serum potassium affects renal outcomes a post hoc analysis of the reduction of endpoints in niddm with the Angiotensin II Antagonist losartan renaal trial
    Diabetologia, 2011
    Co-Authors: Yan Miao, Shahnaz Shahinfar, Barry M. Brenner, Mark E. Cooper, H. H. Parving, Diederick E Grobbee, Daniela Dobre, H Lambers J Heerspink, Dick De Zeeuw
    Abstract:

    Aims/hypothesis To assess the effect of an Angiotensin receptor blocker (ARB) on serum potassium and the effect of a serum potassium change on renal outcomes in patients with type 2 diabetes and nephropathy.

  • Adverse effects of left ventricular hypertrophy in the reduction of endpoints in NIDDM with the Angiotensin II Antagonist losartan (RENAAL) study.
    Diabetologia, 2005
    Co-Authors: G Boner, De Dick Zeeuw, Shahnaz Shahinfar, Tania Z. Dickson, Barry M. Brenner, M. E. Cooper, K Mccarroll, Peter R. Kowey, R S Crow, H. H. Parving
    Abstract:

    We explored the impact of baseline left ventventricular hypertrophy (LVH) and losartan treatment on renal and cardiovascular (CV) events in 1,513 patients from the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial, which studied the effects of losartan on the progression of renal disease and/or death in patients with type 2 diabetes and nephropathy. LVH was assessed using ECG criteria (Cornell product and/or Sokolow-Lyon voltage). The risk of renal or CV events was determined by a proportional hazards model fit with treatment allocation and presence of LVH. Covariates at baseline included age, sex, systolic BP, mean arterial pressure, pulse, proteinuria, serum creatinine, albumin and haemoglobin. A total of 187 subjects (12%) had LVH at baseline. Treatment with losartan resulted in a significant decrease in the Cornell product (-6.2%) and Sokolow-Lyon voltage (-6.3%). LVH was shown to be significantly associated with the primary endpoint, which was a composite of doubling of serum creatinine (DSCR), endstage renal disease (ESRD) or death (hazard ratio [HR]=1.44, p=0.011), as well as with the composite renal endpoint of DSCR/ESRD (HR=1.42, p=0.031) and CV events (HR=1.68, p=0.001). Losartan treatment of patients with LVH decreased the CV as well as renal risk to a level similar to that of patients without LVH. In patients with type 2 diabetes and nephropathy, LVH is associated with significantly increased risk of CV events and the progression of kidney disease. Importantly, in patients with LVH, losartan reduced the CV as well as the renal risk to a level similar to that seen in subjects without LVH.

H. A. Schmid – One of the best experts on this subject based on the ideXlab platform.

  • Effects of Angiotensin II and its blockers Sar^1-lle^8-Angiotensin II and DuP 753 on drinking in ducks in relation to properties of subfornical organ neurons
    Journal of Comparative Physiology B, 1996
    Co-Authors: Eckhart Simon, H. A. Schmid
    Abstract:

    Properties of systemically applied Angiotensin II in stimulating water intake of normally hydrated ducks were studied and the results compared with properties of Angiotensin II-responsive neurons of the subfornical organ which are considered as targets for circulating Angiotensin, II acting as a dipsogen. Following intravenous infusion of hypertonic saline (2000 mosmol·kg^-1 at 0.3 ml·min^-1 for 1 h), intravenous infusion of 0.3 ml·min^-1 isotonic saline with Angiotensin II (200 ng·min^-1), starting 1 h later, stimulated drinking in each case at an Angiotensin II plasma level of about 1400 pg·ml^-1. Without hypertonic priming, the same Angiotensin II infusion did not stimulate drinking in each experiment; however, if effective, repeated infusions of ANGII induced stable dipsogenic responses. Angiotensin II infusions did not alter plasma levels of antidiuretic hormone. Sar^1-Ile^8-Angiotensin II, a non-selective Angiotensin II Antagonist, acted weakly as a partial agonagonist when injused at a dose 200-fold higher than Angiotensin II and effectively blocked the dipsogenic action of Angiotensin II; this corresponds to the inhibition of Angiotensin II-induced excitation by Sar^1-Ile^8-Angiotensin II observed in duck subfornical organ neurons. DuP 753 (losartan), an Angiotensin II Antagonist specifically blocking AT_1 receptors in mammals, had equivocal effects on Angiotensin II-induced drinking in ducks at rates 50- and 200-fold higher than Angiotensin II, which corresponds to the weak inhibitory action of this compound on Angiotensin II-induced neuronal excitation in the duck SFO. Blood pressure was only marginally elevated by the applied Angiotensin II dose and Sar^1-Ile^8-Angiotensin II had no effect.

  • Effects of Angiotensin II and its blockers Sar1-lle8-Angiotensin II and DuP 753 on drinking in ducks in relation to properties of subfornical organ neurons
    Journal of comparative physiology. B Biochemical systemic and environmental physiology, 1996
    Co-Authors: Eckhart Simon, H. A. Schmid
    Abstract:

    Properties of systemically applied Angiotensin II in stimulating water intake of normally hydrated ducks were studied and the results compared with properties of Angiotensin II-responsive neurons of the subfornical organ which are considered as targets for circulating Angiotensin, II acting as a dipsogen. Following intravenous infusion of hypertonic saline (2000 mosmol·kg-1 at 0.3 ml·min-1 for 1 h), intravenous infusion of 0.3 ml·min-1 isotonic saline with Angiotensin II (200 ng·min-1), starting 1 h later, stimulated drinking in each case at an Angiotensin II plasma level of about 1400 pg·ml-1. Without hypertonic priming, the same Angiotensin II infusion did not stimulate drinking in each experiment; however, if effective, repeated infusions of ANGII induced stable dipsogenic responses. Angiotensin II infusions did not alter plasma levels of antidiuretic hormone. Sar1-Ile8-Angiotensin II, a non-selective Angiotensin II Antagonist, acted weakly as a partial agonagonist when injused at a dose 200-fold higher than Angiotensin II and effectively blocked the dipsogenic action of Angiotensin II; this corresponds to the inhibition of Angiotensin II-induced excitation by Sar1-Ile8-Angiotensin II observed in duck subfornical organ neurons. DuP 753 (losartan), an Angiotensin II Antagonist specifically blocking AT1 receptors in mammals, had equivocal effects on Angiotensin II-induced drinking in ducks at rates 50- and 200-fold higher than Angiotensin II, which corresponds to the weak inhibitory action of this compound on Angiotensin II-induced neuronal excitation in the duck SFO. Blood pressure was only marginally elevated by the applied Angiotensin II dose and Sar1-Ile8-Angiotensin II had no effect.