Drugs online research references
Hypertension. 1982 May-Jun;4(3 Pt 2):19-25.
Calcium- and endothelial-mediated vascular smooth muscle relaxation in rabbit aorta.
Singer HA, Peach MJ.
The role of calcium in the relaxations evoked by methacholine and A23187 in intact rabbit aortic rings was investigated. Methacholine (10(-8) to 10(-6) M) and the calcium ionophore A23187 (10(-8) to 10(-6) M) produced dose-dependent relaxations of rings which had been contracted with the alpha-adrenergic agonist phenylephrine. The ability of a ring to relax in this manner was correlated with the presence of endothelium as judged by transmission and scanning electron microscopy. Purposely disrupting the endothelium led to a loss of the relaxation response. In these rings methacholine caused dose-dependent contractions at concentrations greater than 10(-7) M. Deletion of Ca++ from the incubation medium inhibited maximum methacholine-induced relaxations by 67% and A23187-induced relaxations by 92%. The Ca++-channel blockers verapamil (10 microM) and nifedipine (0.5 microM) inhibited maximum methacholine-induced relaxations by 39% and 45%, respectively. The blockers had no effect on the methacholine ED50 (2.5 x 10(-7) M) for relaxation. Verapamil and nifedipine also inhibited maximum A23187-induced relaxations by 43% and 47% with no effect on the ED50 (6 x 19(-8) M) for relaxation. A structurally dissimilar vasodilator, sodium nitroprusside (10(-7) M), had no effect on the A23187-induced relaxation. These data are consistent with a role of Ca++ in regulating either the production or release of endothelial-derived relaxing factor(s).
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6279503&dopt=Abstract
Br J Ophthalmol. 2002 Feb;86(2):227-32.
Systemic vascular endothelial cell dysfunction in normal pressure glaucoma.
Buckley C, Hadoke PW, Henry E, O'Brien C.
Department of Medicine, Royal Infirmary of Edinburgh, UK.
AIM: Vascular risk factors, and particularly vasospasm, are thought to play a part in the pathogenesis of normal pressure glaucoma (NPG). This study aimed to determine whether the function of systemic resistance arteries was altered in patients with NPG. METHODS: Contractile and relaxant function was assessed in arteries dissected from gluteal fat biopsies (11 NPG, 12 control) using small vessel myography. RESULTS: Responses to K(+) and noradrenaline were similar in patients and controls and were unaffected by endothelial removal. In contrast, responses to 5-hydroxytryptamine (5-HT; pD(2); 7.29 (SD 0.16) v 6.66 (0.19); p=0.03) and endothelin-1 (ET-1; pD(2), 9.12 (0.10) v 8.72 (0.13); p=0.03) were enhanced in arteries from patients with NPG. Removal of the endothelium enhanced responses to 5-HT (pD(2), 6.66 (0.19) v. 7.66 (0.08); p=0.003) and ET-1 (pD(2), 8.72 (0.13) v. 9.66 (0.39); p=0.02) in control arteries but not in those from patients. ET-1 mediated contraction in control and patient arteries was reduced in the presence of (10(-5) M) nifedipine. Endothelium dependent and independent relaxation was not impaired in arteries from patients. CONCLUSIONS: This study has identified dysfunction of the systemic vascular endothelial cell in patients with normal pressure glaucoma. The vascular endothelium modulates contractile responses to 5-HT and ET-1 in human subcutaneous resistance arteries but this effect is lost in patients with NPG, indicating a selective defect in agonist mediated release of endothelium derived vasodilators. Selective antagonists of 5-HT and ET-1 may, therefore, help to prevent vasospasm in patients with NPG.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11815352&dopt=Abstract
Am J Physiol. 1999 Jun;276(6 Pt 1):E1067-72.
Mechanism of endothelin-1-(1-31)-induced calcium signaling in human coronary artery smooth muscle cells.
Inui D, Yoshizumi M, Okishima N, Houchi H, Tsuchiya K, Kido H, Tamaki T.
Department of Pharmacology, The University of Tokushima School of Medicine, Tokushima 770-8503, Japan.
We have found that human chymase produces a 31-amino acid endothelin [ET-1-(1-31)] from the 38-amino acid precursor (Big ET-1). We examined the mechanism of synthetic ET-1-(1-31)-induced intracellular Ca2+ signaling in cultured human coronary artery smooth muscle cells. ET-1-(1-31) increased the intracellular free Ca2+ concentration ([Ca2+]i) in a concentration-dependent manner (10(-14)-10(-10) M). This ET-1-(1-31)-induced [Ca2+]i increase was not affected by phosphoramidon, Bowman-Birk inhibitor, and thiorphan. The ET-1-(1-31)-induced [Ca2+]i increase was not influenced by removal of extracellular Ca2+ but was inhibited by thapsigargin. ET-1-(1-31) at 10(-12) M did not cause Ca2+ influx, whereas 10(-7) M ET-1-(1-31) evoked marked Ca2+ influx, which was inhibited by nifedipine. ET-1-(1-31) also increased inositol trisphosphate formation. These results suggest that the ET-1-(1-31)-induced [Ca2+]i increase at relatively low concentrations is attributable to the release of Ca2+ from inositol trisphosphate-sensitive intracellular stores, whereas Ca2+ influx into the cells evoked by high concentration of ET-1-(1-31) probably occurs through voltage-dependent Ca2+ channels. We concluded that the physiological activity of ET-1-(1-31) may be attributable to Ca2+ mobilization from intracellular stores rather than influx of Ca2+ from extracellular space.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10362619&dopt=Abstract
Herbs and Pharmaceuticals Online ||
Hair Million herbal formula for hair loss and hair growth ||
Wellstreet online pharmacy for click-order prescription medications ||
Altace Online Pharmacy ||
Rx Drugs USA, Prescription Drugs Online Pharmacy ||
Insurance plans and information ||
Insurance policies for all purposes ||
Antibiotics and prescription medications online literature ||