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Clin Exp Pharmacol Physiol. 1992 Jun;19(6):425-31.
Cardiac effects of local angiotensin-converting enzyme inhibition in hypertensive patients.

Nakashima Y, Nii T, Tashiro E, Ikeda M, Arakawa K.

Department of Internal Medicine, Fukuoka University, School of Medicine, Japan.

1. The direct cardiac effects of angiotensin-converting enzyme (ACE) inhibitor in 22 hypertensive patients were investigated. Radionuclide ventriculography and echocardiography were performed to measure left ventricular function before and 60 min after administration of a subdepressor dose of captopril. 2. Since the response to ACE inhibitor is not uniform, patients were classified into 12 patients without significant blood pressure change following captopril (group I) and 10 patients with reduction of blood pressure (group II). 3. Clinical and baseline haemodynamic characteristics were similar for the two groups. 4. Ejection fraction (EF) increased without changes of heart rate and end-diastolic dimension after ACE inhibitor in group I as well as group II. The change of EF was not different for the two groups. No correlation was found between changes in EF and blood pressure in group I patients. 5. This study indicates that ACE inhibitor might directly influence left ventricular function independent of systemic haemodynamic changes.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1606744&dopt=Abstract

J Control Release. 2000 May 15;66(2-3):271-80.
Controlled release of a water-soluble drug, captopril, by a combination of hydrophilic and hydrophobic cyclodextrin derivatives.

Ikeda Y, Kimura K, Hirayama F, Arima H, Uekama K.

Wakunaga Pharmaceutical Co., 1624 Shimokotachi, Kodacho, Takata-gun, Hiroshima, Japan.

Parent beta-cyclodextrin (beta-CyD) and 2-hydroxypropyl-beta-CyD (HP-beta-CyD) form 1:1 solid complexes with an orally active angiotensin-converting enzyme inhibitor, captopril, while hydrophobic perbutanoyl-beta-CyD (TB-beta-CyD) forms a solid dispersion or solid solution with the drug. The binary system of captopril/HP-beta-CyD or captopril/TB-beta-CyD and the ternary system of captopril/TB-beta-CyD/HP-beta-CyD in different molar ratios were prepared by the kneading method, and the release behavior of the drug was investigated. The release rate of captopril from the binary HP-beta-CyD system was rather fast, whereas that from the binary TB-beta-CyD system was comparatively slower, the retarding effect being dependent on the amounts of TB-beta-CyD. The release rate from the ternary captopril/TB-beta-CyD/HP-beta-CyD system was slowed down by the addition of small amounts of HP-beta-CyD, whereas the rate became faster as the molar ratio of HP-beta-CyD further increased (>.25 molar ratio). Both water penetration studies and microscopic observation suggested that the retarding effect is attributable to a gel formation of HP-beta-CyD in the TB-beta-CyD hydrophobic matrix. It was difficult to prolong plasma levels of captopril by administering orally either the binary HP-beta-CyD or TB-beta-CyD system in dogs. On the other hand, the ternary captopril/TB-beta-CyD/HP-beta-CyD system (molar ratio of 1:0.5:0.5) gave a plasma profile comparable to that of a commercially available sustained release preparation (Captoril R). Therefore, a combination of HP-beta-CyD and TB-beta-CyD is useful for the controlled release of water-soluble drugs such as captopril.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10742586&dopt=Abstract

Clin Exp Pharmacol Physiol. 2000 Mar;27(3):191-6.
Role of brain angiotensin II in the somatosensory induced antinatriuresis in the anaesthetized rat.

Huang C, Johns EJ.

Department of Physiology, The Medical School, Birmingham, United Kingdom.

1. The present study set out to explore the importance of angiotensin (Ang)II in the brain in allowing the somatosensory system to cause a reflex renal nerve-mediated reduction in renal sodium and water excretion. 2. In chloralose-urethane-anaesthetized rats receiving saline i.c.v. (2 microL + 1 microL/h), the administration of capsaicin (0.5 mg, s.c.) increased blood pressure by 14% (P < 0.001) and, while renal perfusion pressure was regulated at an unchanged level, neither renal blood flow (RBF) nor glomerular filtration rate was changed. However, urine flow and absolute and fractional sodium excretion was reduced between 29 and 38% (P<0.05-0.01). All variables had returned to control levels 30 min later. 3. The administration of captopril (40 microg + 20 microg/h i.c.v.) decreased blood pressure and sodium excretion by 6 and 17%, respectively (both P < 0.05). Under these conditions, capsaicin s.c. increased blood pressure by 9% (P<0.05); however, with renal perfusion pressure regulated at a constant level, neither renal haemodynamics nor water nor sodium excretion were changed. 4. A final group of animals received AngII (100 ng + 50 ng/h) concomitantly with captopril i.c.v., which increased blood pressure, RBF and urine flow, absolute and fractional sodium excretions by 8 (P < 0.05), 22 (P < 0.001 ) and 52-149% (P < 0.05-0.01), respectively. Capsaicin given s.c. under these conditions increased blood pressure by 6% (P < 0.05) and, while renal perfusion pressure was maintained at an unchanged value and renal haemodynamics remained constant, urine flow and absolute and fractional sodium excretion were reduced by 35-38% (all P < 0.05). 5. These data show that for the somatosensory system to induce a reflex increase in renal sympathetic nerve activity sufficient to cause an antinatriuresis and antidiuresis, the presence of AngII is necessary in the brain. How AngII exerts this facilitatory action within the central nervous system remains to be investigated.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10744346&dopt=Abstract

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