No abstract available.
Antihypertensive Agents ; Hypertension ; Blood Pressure ; Myocardial Ischemia ; telmisartan ; Ramipril ; Risk Factors

BACKGROUND: There is a scarcity of studies on the effects of government-mediated access pricing (GMAP) as another price regulation approach on drug availability.

OBJECTIVES: This study was done to compare changes in percent availability in drug stores from 2009 to 2011 of innovator drugs, competitor drugs and cheap generic drugs containing drug molecules affected by GMAP policies in the Philippines.

METHODS: Data from a random survey of 600 drug stores stratified by location and retail type, undertaken separately in 2009 and 2011 by IMS Health Philippines, were analyzed. Percent availability of the innovator brand, a competitor, and cheapest generic version for 11 selected drug molecules in said drug stores were compared for 2009 and 2011.

RESULTS: Of the 11 innovator drugs, 3 had significant reductions in percent availability in drugstores ranging from 9.7% to 39.0%. Among competitor drugs, 3 had reductions ranging from 37.4% to 81.7%. The availability of cheap generic versions of drug molecules in drug stores immensely increased in 2011 except for telmisartan.

CONCLUSION: GMAP could have adversely affected availability in drug stores of both innovator and competitor drugs. Cheaper generic drugs have become more available in the Philippines.

.telmisartan ; Mesh Scope Note For Drugs, Generic : Drugs Whose Drug Name Is Not Protected By A Trademark. They May Be Manufactured By Several Companies. ; Drugs, Generic ; Philippines ; Benzoates ; Benzimidazoles ; Pharmacies ; Costs And Cost Analysis ; Government ; Surveys And Questionnaires

OBJECTIVE: To compare the nephrotoxicity of high- and low-osmolar contrast media (HOCM and LOCM), and to determine the protective role of fosinopril or telmisartan and its possible mechanism. METHODS: Forty eight healthy SD rats were randomly divided into 6 groups: a normal control group, a glycerol control group, a low-osmolar contrast media (LOCM) group, a high-osmolar contrast media (HOCM) group, a fosinopril group, and a telmisartan group. Glycerine for inducing kidney damage was given to all rats except the normal control group. Twenty-four hours after the injection of glycerine, the mixed fosinopril suspension (10mg/kg) or telmisartan (5mg/kg) was poured into the stomach in the preventive group. Serum creatinine (SCr) and plasma angiotensin II (AngII) levels were detected by an automatical biochemical analyzer and radioimmunoassay; caspase-3 activity and claudin-1 expression of the renal tissue were detected by fluorometric method and immunohistochemical method. The renal injury was assessed by hematoxylin and eosin (HE) staining and terminal deoxynucleotide mediated nick and labeling (TUNEL) staining, respectively. RESULTS: In diatrizoate-injected rats, SCr and AngII levels were increased (P<0.05). Expression of claudin-1 protein and caspase-3 activity in the renal tissue was upregulated. The histologic changes and percentage of apoptotic cells were milder in the LOCM rats than those in the HOCM rats. In the group pretreated with fosinopril or telmisartan, no increase in the levels of SCr and AngII was discovered. The expression of claudin-1 protein and caspase-3 activity was significantly lower than that in the HOCM group. The renal injuries induced by diatrizoate were alleviated. CONCLUSION Both HOCM and LOCM could cause cellular apoptosis in the kidney.LOCM was less toxic to rat kidney than HOCM. Nephrotoxicity induced by HOCM might be related to caspase-3, claudin-1 and AngII. Fosinopril or telmisartan may protect the renal tissue from nephrotoxicity induced by diatrizoate.
Angiotensin II ; blood ; Animals ; Apoptosis ; drug effects ; Benzimidazoles ; pharmacology ; Benzoates ; pharmacology ; Caspase 3 ; metabolism ; Claudin-1 ; metabolism ; Contrast Media ; administration & dosage ; toxicity ; Creatinine ; blood ; Female ; Fosinopril ; pharmacology ; Kidney ; drug effects ; metabolism ; pathology ; Male ; Protective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Telmisartan

OBJECTIVE: To explore the effect of telmisartan on the expression of metadherin in the kidney of mice with unilateral ureter obstruction. METHODS: Eighteen male C57 mice were randomized into sham-operated group, model group and telmisartan treatment group. In the latter two groups, renal interstitial fibrosis as the result of unilateral ureter obstruction (UUO) was induced by unilateral ureteral ligation with or without telmisartan intervention. Renal pathological changes of the mice were assessed using Masson staining, and immunohistochemistry and Western blotting were used to detect the expression of extracellular matrix proteins and metadherin in the kidney of the mice. In the experiment, cultured mouse renal tubular epithelial cells (mTECs) were stimulated with transforming growth factor-β1 (TGF-β1) and transfected with a siRNA targeting metadherin, and the changes in the expressions of extracellular matrix proteins and metadherin were detected using Western blotting. RESULTS: The expressions of extracellular matrix proteins and metadherin increased significantly in the kidney of mice with UUO ( < 0.05). Intervention with telmisartan significantly lowered the expressions of extracellular matrix proteins and metadherin and alleviated the pathology of renal fibrosis in mice with UUO ( < 0.05). In cultured mTECs, siRNA-mediated knockdown of metadherin obviously reversed TGF-β1-induced increase in the expressions of extracellular matrix proteins and metadherin. CONCLUSIONS Telmisartan can suppress the production of extracellular matrix proteins and the expression of metadhein to attenuate UUO-induced renal fibrosis in mice.
Angiotensin II Type 1 Receptor Blockers ; Animals ; Antihypertensive Agents ; Extracellular Matrix Proteins ; metabolism ; Fibrosis ; Kidney ; drug effects ; metabolism ; pathology ; Male ; Membrane Proteins ; genetics ; metabolism ; Mice ; Mice, Inbred C57BL ; RNA, Small Interfering ; Random Allocation ; Telmisartan ; pharmacology ; Transforming Growth Factor beta1 ; pharmacology ; Ureteral Obstruction ; complications ; metabolism