Drugs online research references
J Hypertens. 1995 Jul;13(7):763-9.
Expression of cardiac angiotensin II AT1 receptor genes in rat hearts is regulated by steroids but not by angiotensin II.
Della Bruna R, Ries S, Himmelstoss C, Kurtz A.
Physiologisches Institut, Universitat Regensburg, Germany.
OBJECTIVE: To examine the regulation by angiotensin II and by steroids of the expression of the angiotensin II AT1a and AT1b receptor genes in rat hearts. METHODS: Endogenous levels of angiotensin II in the rats were increased either by unilateral 0.2-mm renal artery clips or by subcutaneous infusions of frusemide (12 mg/day) and by low-sodium diet. To inhibit endogenous angiotensin II actions the rats received the AT1 receptor antagonist losartan (40 mg/kg per day) or the angiotensin converting enzyme inhibitor ramipril (8 mg/kg per day). Circulating levels of glucocorticoids were elevated by subcutaneous injections of dexamethasone (400 micrograms/kg per day) and levels of mineralocorticoids were increased by subcutaneous injections of deoxycorticosterone acetate (2 mg/kg per day). AT1a and AT1b messenger RNA (mRNA) levels were semiquantified by reverse-transcriptase polymerase chain reaction and related to actin mRNA. RESULTS: The AT1a mRNA:AT1b mRNA ratio in the hearts of untreated rats was 10:1. Unilateral renal artery clipping led to a 30% decrease in AT1a mRNA, whereas treatment with frusemide, losartan or ramipril had no effect on the AT1a or AT1b mRNA levels. Rats fed a low-sodium diet showed a 37% increase in AT1a gene expression. Dexamethasone increased AT1a mRNA by 100% and AT1b mRNA by 300%, whereas deoxycorticosterone acetate treatment decreased AT1a mRNA levels to 30% of the control values. CONCLUSIONS: The present results suggest that the expression of the predominant cardiac AT1a receptor gene is not feedback-regulated by endogenous angiotensin II, whereas steroid hormones appear to be effective regulators, because glucocorticoids stimulate AT1 receptor gene expression and mineralocorticoids inhibit it.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7594440&dopt=Abstract
Hepatogastroenterology. 2000 May-Jun;47(33):795-806.
Effects of angiotensin-converting enzyme inhibitors and sclerotherapy on portal hemodynamics in patients with portal hypertension.
Nasr AA, el-Hak NG, Settein ME, Khafagy MA, Tadros MT.
Internal Medicine Department, Faculty of Medicine, Mansoura University, Egypt.
BACKGROUND/AIMS: Since pharmacotherapy of portal hypertension has always been a subject of wide interest, we decided to study the effects of different angiotensin-converting enzyme inhibitors and endoscopic sclerotherapy on portal hemodynamics in patients with portal hypertension and bleeding esophageal varices. METHODOLOGY: The study included 72 patients with portal hypertension divided into 6 equal groups. Endoscopic sclerotherapy was done to all patients every 2 weeks for 3 months. In addition, the first 5 groups of patients were maintained on angiotensin-converting enzyme inhibitors for 3 months as follows: group I on perindopril, II on ramipril, III on fosinopril, IV on lisinopril and V on captopril. Portal hemodynamics were determined before and after therapy (using an ultrasonic duplex system). New Doppler portal indices were derived and portal vein kinetic pressure was estimated for the first time by using data derived from the ultrasonic duplex system. RESULTS: 1) Short-term endoscopic sclerotherapy alone resulted in significant elevation of portal vein kinetic pressure, wall stress index and flow volume (P < 0.01) and non-significant increase in the total portal circulation resistance index (P > 0.05) and significantly decreased portal vein compliance and distensibility indices (P < 0.05); 2) Angiotensin-converting enzyme inhibitors reduced the maximum and average portal velocities, the portal flow volume, total portal circulation resistance index and increased portal vein compliance and distensibility indices, hence they reduced the portal vein kinetic pressure significantly in group IV (P < 0.05 for the flow volume and P < 0.01 for other indices); 3) The only side effect encountered was allergic cough (in 8.33% of patients). No effects were noticed on the pulse, systolic, diastolic or mean blood pressures or Child-Pugh Score of liver disease. CONCLUSIONS: 1) Angiotensin-converting enzyme inhibitors when added to endoscopic sclerotherapy can ameliorate the effects of the latter on portal hemodynamics in patients with portal hypertension; 2) Portal vein kinetic pressure, total portal circulation resistance index, portal vein wall stress index, compliance and distensibility indices are new Doppler portal indices that proved to be of value in the follow-up of patients with portal hypertension under sclerotherapy alone or in conjunction with pharmacotherapy; 3) Angiotensin-converting enzyme inhibitors are safe drugs that can be used for portal decompression with endoscopic sclerotherapy. Their use as sole portal anti-hypertensive agents still awaits further studies.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10919035&dopt=Abstract
Farmaco. 2000 Mar;55(3):233-8.
The voltammetric study and determination of ramipril in dosage forms and biological fluids.
al-Majed AA, Belal F, Abadi A, al-Obaid AM.
Department of Pharmaceutical Chemistry, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
The voltammetric behavior of ramipril was studied using cyclic voltammetry, direct current polarography (DCt), differential pulse polarography (DPP) and alternating current polarography (ACt). Ramipril developed well-defined cathodic waves in Britton-Robinson buffers over the pH range 6-12. The waves were characterized as being diffusion-controlled, irreversible and partially affected by adsorption phenomenon. The diffusion-current constant (Id) was 1.24 +/- 0.02. The current-concentration plots were rectilinear over the range 10-50, 4-40 and 0.16-12 micrograms/ml in the DCt, DPP and ACt modes, respectively, with a minimum detectability (S/N = 2) of 0.02 microgram/ml (4.8 x 10(-8) M) using the latter mode. The proposed method was successfully applied to the determination of ramipril in commercial tablets. Hydrochlorothiazide, which is frequently co-formulated with ramipril, did not interfere with the assay. Furthermore, the proposed method was applied to the determination of ramipril in urine and plasma adopting the ACt technique. The percentage recoveries were 97.12 +/- 0.56 and 94.97 +/- 0.62%, respectively. A pathway for the electrode reaction was proposed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10919088&dopt=Abstract
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