Drugs online research references
Eur J Pharmacol. 2001 Apr 13;417(3):223-30.
Neurovascular interactions between aldose reductase and angiotensin-converting enzyme inhibition in diabetic rats.
Cotter MA, Mirrlees DJ, Cameron NE.
Department of Biomedical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill Aberdeen, AB25 2ZD, Scotland, UK.
Increased polyol pathway flux has been linked to nerve complications in diabetic rats, which are attenuated by aldose reductase inhibitors, defective nitric oxide-mediated vasodilation being a particular target. Diabetes also elevates the endothelial angiotensin system, increasing vasa nervorum vasoconstriction. The aim was to assess whether promotion of vasodilation by treatment with the aldose reductase inhibitor, ZD5522 (3',5'-dimethyl-4'-nitromethylsulphonyl-2-(2-tolyl)acetanilide), coupled with reduced vasoconstriction using the angiotensin-converting enzyme inhibitor, lisinopril, interacted positively to improve neurovascular function. After 8 weeks of streptozotocin-induced diabetes, sciatic nerve blood flow and motor conduction velocity were 51% and 21% reduced, respectively. Two weeks of lisinopril treatment dose-dependently corrected the conduction deficit (ED(50) approximately 0.9 mg kg(-1)). Low-dose lisinopril (0.3 mg kg(-1)) or ZD5522 (0.25 mg kg(-1)) had modest corrective (10-20%) effects on nerve conduction and perfusion. However, when combined, blood flow and conduction velocity reached the nondiabetic range. The ZD5522 dose used gave a approximately 45% nerve sorbitol reduction but had no significant effect on fructose content; lisinopril co-treatment did not alter ZD5522 action on polyols. Thus, there was a marked neurovascular synergistic interaction between angiotensin-converting enzyme and aldose reductase inhibition in diabetic rats. This points to a potential therapeutic benefit, which requires evaluation in clinical trials.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11334854&dopt=Abstract
Pharmacoepidemiol Drug Saf. 2000 Dec;9(7):557-63.
A pharmacodynamic assessment of the impact of antihypertensive non-adherence on blood pressure control.
Choo PW, Rand CS, Inui TS, Lee ML, Ma CC, Platt R.
Channing Laboratory, Department of Medicine, Brigham and Women's' Hospital, Boston, MA, USA.
OBJECTIVES: To evaluate if antihypertensive regimens that conform to present FDA guidelines by maintaining > or = 50% of their peak effect at the end of the dosing interval protect patients during sporadic lapses in adherence. METHODS: 169 patients on monotherapy for high blood pressure underwent electronic adherence monitoring for 3 months. Blood pressures were measured during non-study office visits and were retrieved from automated medical records. Questionnaires were used to obtain other covariate information. The ratio of the dosing interval to the half-life of drug activity (I') was used to capture conformity with FDA guidelines. Data analysis focused on the interaction between I' and the impact on blood pressure of delayed dosing. RESULTS: The average (+/- standard deviation) blood pressure during the study was 139.0(+/- 12.0)/85.0(+/- 6.9) mm Hg. Lisinopril followed by sustained-release verapamil, atenolol, and hydrochlorothiazide were the most frequently prescribed agents. The majority of regimens (99%) conformed to FDA dosing guidelines. Of the patients 23% missed a dose before their blood pressure check. Non-adherence, however, did not have a direct impact on blood pressure, and no interaction with I' of was detected. CONCLUSIONS: Among patients with relatively mild hypertension on single-drug therapy, regimens that conform to current FDA dosing guidelines may prevent losses of blood pressure control during episodic lapses of adherence. These findings should be replicated in other patient populations with standardized blood pressure measurement to confirm their validity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11338913&dopt=Abstract
Jpn Circ J. 2001 May;65(5):395-8.
Effect of angiotensin-converting enzyme inhibition on sympathetic tone in patients with mild to moderate heart failure.
Inoko M, Fujita M, Nakae I, Tamaki S, Watanuki M, Hashimoto T, Konishi T.
Division of Emergency Medicine, Kyoto University Hospital, Japan.
Sixteen patients with mild to moderate heart failure were examined to investigate whether sympathetic deactivation plays a role in the improvement in the failing heart by chronic angiotensin converting enzyme (ACE) inhibition. Measurements, including echocardiography, blood examinations, neurohumoral samplings (atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), norepinephrine), and spectral heart rate variability analysis by Holter electrocardiography, were carried out before and 6 months after the administration of lisinopril (5-10 mg/day). Quality of life assessment was accomplished by the Specific Activity Scale (SAS) questionnaire. Treatment with lisinopril for 6 months resulted in a significant reduction in systolic blood pressure. The left ventricular diastolic dimension significantly decreased and fractional shortening significantly increased on echocardiography. Of the 16 patients, 8 had improvement in their symptoms as measured by the SAS. Lisinopril did not significantly reduce the plasma norepinephrine concentration, but there was a significant reduction in the plasma ANP and BNP concentrations. In the heart rate power spectral analysis, total spectral power, high-frequency components and low/high frequency ratios did not change significantly with lisinopril. The mechanism by which ACE inhibitors improve mild to moderate heart failure is not by suppressing sympathetic activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11348042&dopt=Abstract
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