Online Pharmacy, Tramadol, Paxil, antibiotics, amoxicillin, zithromax, Rx Online, pharmaceuticals, DHEA, prescription medications, prescription drugs.

Drugs online research references

Rev Esp Cardiol. 2000 Apr;53(4):525-30.
[Effect of losartan on human platelet activation by thromboxane A2]

[Article in Spanish]

Guerra JI, Monton M, Rodriguez-Feo JA, Farre J, Jimenez AM, Nunez A, Gomez J, Rico L, Marcos P, Castilla C, Sanchez De Miguel L, Casado S, Lopez-Farre A.

Laboratorio de Investigacion Cardiovascular e Hipertension. Fundacion Jimenez Diaz. Madrid.

INTRODUCTION AND OBJECTIVES: Previous studies have demonstrated that losartan, an AT-1 receptor antagonist of angiotensin II (Ang II) could block the receptor of thromboxane A2 (TXA2) in the vascular wall. The aim of the present study was to assess the effect of losartan on human platelet activation. MATERIALS AND METHODS: Platelets were obtained from 15 healthy men between the age 26 and 40. Platelet activation was measured by changes in the light transmission of platelet-rich plasma stimulated by a synthetic TXA2 analogue, U46619 (5 x 10(-6) mol/l). RESULTS: The U46619-stimulated platelet aggregation was significantly inhibited by losartan in a dose-response manner. Only a high dose of EXP 3174 (5 10-5 mol/l), the in vivo active metabolite of losartan, was able to attenuate U46619-induced platelet activation. Captopril, an angiotensin I-converting inhibitor failed to modify U46619-induced platelet aggregation. Despite the platelets expressing AT-1 type receptors, of Ang II exogenous Ang II did not modify platelet aggregation induced by U46619. The binding of U46619 to platelets was competitively inhibited by losartan in dose-dependent manner. However, only a high dose of EXP 3174 reduced the binding of U46619. Captopril failed to modify the binding of U46619 to platelets. CONCLUSIONS: Losartan decreased platelet aggregation by a TXA2-dependent mechanism. EXP 3174 showed a lesser potency than losartan to reduce TXA2-platelet activation. Captopril and exogenous angiotensin II had no effect on human platelet activation. These results suggest that losartan reduced TXA2-dependent platelet activation independently of the blockade of AT-1 receptors.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10758030&dopt=Abstract

Am J Cardiol. 2000 Apr 15;85(8):977-80.
Inverse relation between aldosterone and venous capacitance in chronically treated congestive heart failure.

Rietzschel E, Duprez DA, De Buyzere ML, Clement DL.

Department of Cardiology and Angiology, University Hospital, Gent, Belgium.

The purpose of this study was to examine if there is a relation between the aldosterone escape phenomenon and venous capacitance of the upper and lower limbs in patients with long-term congestive heart failure (CHF) receiving chronic treatment with angiotensin-converting enzyme (ACE) inhibitors. The study group consisted of 16 subjects with ischemic CHF in New York Heart Association functional class II (age 59 +/-2 years, ejection fraction 24+/-4%), stabilized under a constant drug regimen comprising furosemide, captopril 50 mg 3 times daily, and digoxin for at least 3 months. Thirteen apparently healthy volunteers, aged 50+/-4 years acted as controls. Forearm and calf venous capacitances were measured simultaneously by venous occlusion plethysmography using mercury-in-silastic strain gauges. The equilibration technique was used to derive venous capacitance from the recorded pressure-volume curves. Active renin, angiotensin II, and aldosterone levels were determined on venous blood samples obtained in the supine position. Angiotensin II (p<0.05) and aldosterone (p<0.01) were statistically significantly higher in patients with CHF under long-term ACE inhibition than in controls (aldosterone escape phenomenon). In CHF, forearm venous capacitance was 2.19+/-0.18 ml/100 ml; calf venous capacitance was 2.83+/-0.27 ml/100 ml. Aldosterone significantly and inversely correlated with venous capacitance in both upper (r = -0.586; p = 0.017) and lower (r = -0.625; p = 0.01) limbs. No correlations were found between forearm or calf venous capacitance and renin or angiotensin II. In patients with heart failure chronically treated with diuretics and full ACE inhibition, venous capacitance is inversely correlated with aldosterone through the mechanism of aldosterone escape, creating the potential for further deterioration of the CHF process.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10760338&dopt=Abstract

Brain Res. 2000 Apr 10;861(2):377-89.
Activation of renal afferent pathways following furosemide treatment. II. Effect Of angiotensin blockade.

Fitch GK, Weiss ML.

Department of Natural and Allied Health Sciences and Mathematics, Avila College, Kansas City, MO 64145, USA.

The goal here and in the accompanying paper was to evaluate the two pathways used by the kidney to provide information to the central nervous system (CNS); e.g., the indirect, hormonal route via activation of the renin-angiotensin system and the direct pathway via activation of sympathetic afferents in the caudal thoracic spinal cord. Here, three experiments were designed to evaluate the actions of angiotensin elicited by subcutaneous injection of furosemide on neural activation of the CNS. The number of neurons immunocytochemically staining for the protein product (Fos) of the c-fos gene was used as an index of neuronal activation. In the first experiment, furosemide injection was preceded by treatment with a dose of Captopril, CAP, (an angiotensin-converting enzyme (ACE) inhibitor) that blocks the peripheral but not the central formation of angiotensin II. In the second experiment, furosemide injection was preceded by treatment with a higher dose of CAP; this dosage blocks the peripheral and central formation of angiotensin II. In the third experiment, furosemide injection was preceded by treatment with Losartan, a competitive receptor antagonist of type I angiotensin II receptors at a dose that would block central and peripheral angiotensin receptors. Control animals in each experiment received injections of vehicle (sterile isotonic saline) instead of furosemide. In each experiment, rats were sacrificed 1.75 h following furosemide or saline injection by transcardial perfusion and tissues were immunocytochemically processed for demonstration of Fos antigen. Rats receiving furosemide plus the low CAP dose showed more Fos-positive cells than control rats in the subfornical organ (SFO), organum vasculosum lamina terminalis (OVLT), supraoptic nucleus (SON), magnocellular region of the paraventricular nucleus, nucleus of the solitary tract (NTS), and caudal thoracic/rostral lumbar spinal cord dorsal horn. Rats receiving furosemide plus Losartan or furosemide plus the higher CAP dose did not show increased Fos immunoreactivity in any of the abovementioned structures relative to their respective control animals. We conclude that the receptor-mediated action of angiotensin II is in some way involved in the activation of the pathway that occurs in the SFO, OVLT, SON, and magnocellular region of the paraventricular nucleus (PVN) in response to furosemide treatment. It is possible that the furosemide-induced activation in the SON and PVN is not due to direct actions of angiotensin II on angiotensin receptors in those structures, but instead occurs synaptically as a result of inputs from the SFO and OVLT, which have themselves been activated directly by angiotensin II. In the accompanying paper, furosemide-induced activation in the NTS and caudal thoracic spinal cord is abolished by prior bilateral renal denervation, meaning that these neurons are likely part of a renal afferent pathway. Here, these structures did not elaborate Fos in animals injected with furosemide plus the high CAP dose or furosemide plus Losartan. Thus, the present results also suggest that the central blockade of the formation of angiotensin II or blockade of the actions of angiotensin II prevents in some way the activation of the renal afferent pathway mediated by the renal nerves (the direct pathway) in response to the actions of furosemide. Therefore, these results suggest that central angiotensin II is somehow involved in "priming" or increasing the sensitivity of the direct renal afferent pathway. Taken together with the accompanying paper, our results indicate that interruption of the direct pathway via renal denervation did not interfere with the elaboration of Fos in the lamina terminalis; in contrast, modification of the humoral renal afferent pathway can affect the sensitivity of the direct pathway. These results may have important implications for pathophysiological changes associated with fluid balance disorders including renal hypertension.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10760499&dopt=Abstract

online pharmacies || Hair Million herbal formula for hair loss and hair growth || Amoxicillin || Tramadol || Paxil || Rx Drugs USA, Prescription Drugs Online Pharmacy || Zithromax || online pharmacy || Antibiotics and prescription medications online literature || Antibiotics