Drugs online research references
Am J Hypertens. 1997 Aug;10(8):913-20.
alpha- and beta-adrenoceptor blockade fail to prevent high sodium diet-induced left ventricular hypertrophy.
Song D, Harmsen E, Leenen FH.
Hypertension Unit, University of Ottawa Heart Institute, Ontario, Canada.
High sodium diet (HS, 8% NaCl) induces left ventricular hypertrophy (LVH) in normotensive rats without an increase in pressure or volume load or in resting cardiac sympathetic activity. HS may affect LV adrenoceptors density or affinity or their postreceptor pathways, thereby causing LVH. We therefore assessed the effects of HS with and without blockade of alpha1- or beta-adrenoceptors by terazosin or nadolol, alone or in combination, on resting hemodynamics, LV and right ventricular (RV) weights, and LV dimensions of male WKY rats. HS increased LV weight by 14% to 17%, and the ratio of LV wall thickness to radius by 18% to 23%. Singly or in combination, the adrenoceptor antagonists did not prevent HS-induced LVH, but instead aggravated it. The increased ratio of LV wall thickness to radius and of LV to RV were attenuated by terazosin or nadolol alone. Neither the resting LV peak-systolic or end-diastolic pressures nor the right atrial pressure was changed by HS, either alone or in combination with the blockers. The failure of chronic alpha1- or beta-blockade to prevent HS-induced LVH suggests that adrenoceptor activation is not important in evoking the LVH. However, the blockers shifted the LVH from a concentric to an eccentric form, suggesting an involvement of additional trophic factors during adrenoceptor blockade.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9270087&dopt=Abstract
Prostate. 1997 Sep 15;33(1):55-9.
Pharmacology of tamsulosin: saturation-binding isotherms and competition analysis using cloned alpha 1-adrenergic receptor subtypes.
Richardson CD, Donatucci CF, Page SO, Wilson KH, Schwinn DA.
Department of Anesthesiology, Duke University, Durham, North Carolina, USA.
BACKGROUND: alpha 1-adrenergic receptors (alpha 1 ARs) are important in the dynamic component of benign prostatic hyperplasia (BPH). Currently, several alpha 1AR antagonists are being used in the treatment of BPH. METHODS: In order to more fully characterize the pharmacology of the alpha 1AR antagonist tamsulosin, we utilized saturation-binding isotherms with [3H] tamsulosin to determine the Kd of this compound at all three cloned alpha 1AR subtypes stably expressed in rat-1 fibroblasts. To confirm these results, we performed competition binding experiments, displacing [125I]HEAT with increasing concentrations of alfuzosin, doxazosin, 5-methyl-urapidil, prazosin, tamsulosin, terazosin, and (+)YM617 (stereoisomer of tamsulosin) in the same clonal cell lines. RESULTS: [3H]tamsulosin binds to cloned alpha 1AR subtypes with a rank order of affinity of alpha 1a = alpha 1d > alpha 1b. Competition experiments confirmed the relative nonselectivity of alfuzosin, doxazosin, and prazosin, but revealed slight alpha 1b = alpha 1d > alpha 1a selectivity for terazosin, and clear alpha 1a = alpha 1d > alpha 1b for (+)YM617 and tamsulosin([-]YM617); alpha 1a > alpha 1d > alpha 1b selectivity for 5-methyl-urapidil was confirmed. CONCLUSIONS: We conclude that tamsulosin displays selectivity for alpha 1a and alpha 1d ARs. This selectivity may contribute to the tamsulosin efficacy reported in several recent clinical studies in patients with BPH.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9294627&dopt=Abstract
Biochem Pharmacol. 1997 Jul 1;54(1):133-41.
Effects of antihypertensive drugs on rat tissue antioxidant enzyme activities and lipid peroxidation levels.
Cabell KS, Ma L, Johnson P.
Department of Chemistry and College of Osteopathic Medicine, Ohio University, Athens 45701, U.S.A.
The effects of three commonly used antihypertensive agents (captopril, hydralazine, and terazosin) on tissue antioxidant enzymes and lipid peroxidation in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY rats) were studied by analysis of antioxidant enzyme specific activities and lipid peroxidation levels in control and drug-treated animals. In the myocardium, changes in some of the enzyme activities between normotensive WKY and hypertensive SHR rats were mitigated by treatment of the SHR rats with an antihypertensive drug. Thus, all three drugs caused significant increases in myocardial Cu/Zn superoxide dismutase (up to 133% of SHR control activity) and decreases in glutathione peroxidase (down to 59% of SHR control activity) to values that were closer to those in untreated WKY rats. Captopril also increased Mn superoxide dismutase activity, and hydralazine and terazosin decreased catalase activity towards untreated WKY values. Hydralazine was the only drug to alter the lipid peroxidation level in the myocardium of SHR rats (a 28% decrease), but in WKY rats all three drugs caused significant decreases in myocardial lipid peroxidation levels. In WKY rats, none of the drugs affected myocardial Mn and Cu/Zn superoxide dismutase activities, although glutathione peroxidase activity was decreased by hydralazine and terazosin treatment and catalase activity was increased by captopril treatment. Enzyme activity changes in liver and skeletal muscle indicated that such changes were often tissue specific. No pattern was found for coordinated changes in antioxidant enzyme expression as a result of the drug treatments, and the changes in antioxidant enzyme specific activities did not correlate generally with changes in lipid peroxidation levels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9296359&dopt=Abstract
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