Drugs online research references
J Pharmacol Exp Ther. 1994 Dec;271(3):1223-7.
Inhibition by nickel of endothelin-1-induced tension and associated 45Ca movements in rabbit aorta.
Shetty SS, DelGrande D.
Research Department, Ciba-Geigy Corporation, Summit, New Jersey.
Contractions induced by 10 nM endothelin-1 (ET) in the rabbit aortic media intimal layer were inhibited by prior exposure to 100 microM Ni++ (33.1%) or to a Ca(++)-free buffer (80.2%) but were unaffected by pretreatment with 0.1 microM nifedipine. Contractions elicited by phenylephrine (1 nM-100 microM) or K+ (10-50 mM) were not inhibited by 100 microM Ni++ but those induced by ET in tissues submaximally precontracted with 20 mM K+ were selectively antagonized by the divalent cation. The mechanism for the inhibitory action of Ni++ was ascertained by an examination of the effects of the cation on ET-induced alterations in the cellular distribution and mobilization of Ca++. Efflux of 45Ca from the muscle into a solution without added Ca++ was not altered by ET. Total or cellular 45Ca uptake (uptake after exposure to La and low temperature), at either low- or high-affinity sites in resting muscles was also not affected by the peptide. However, low-affinity cellular 45Ca retention in muscles depolarized with high K+ levels (160 mM) was significantly enhanced (45.1%) by ET. Ni++ did not alter 45Ca retention in control and K(+)-treated muscles but it blocked the additional incremental 45Ca uptake associated with ET (in the presence of high K+). Thus, Ni++ produced a selective blockade of an ET-activated Ca++ influx pathway, distinct from the dihydropyridine-sensitive L-type Ca++ channels, in rabbit aortic smooth muscle. This action by Ni++ apparently inhibits subsequent contractile responses of the muscle to ET.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7996430&dopt=Abstract
Circ Res. 1989 Aug;65(2):265-71.
Ionic requirements of the endothelin response in aorta and portal vein.
Borges R, Carter DV, von Grafenstein H, Halliday J, Knight DE.
Division of Biomedical Sciences, King's College, University of London, England.
The vasoconstrictor responses of isolated rat portal vein and aorta to synthetically prepared endothelin are investigated. Both preparations respond to 10(-9) M levels of the peptide although the aortic response is more sustained than that of the portal vein. Endothelin-evoked contractions, unlike those evoked by scorpion alpha-toxins (which are homologous to endothelin) or by veratridine, are insensitive to tetrodotoxin or to the removal of sodium ions from the tissue-bathing medium. Contractile responses to endothelin may still be observed in high-potassium depolarizing medium and are not dependent on the presence of extracellular chloride; however, the responses are dependent on the presence of extracellular calcium and are blocked by nitrendipine, nifedipine, or nickel. Endothelin-evoked uptake of 45Ca into aortic tissue is also independent of extracellular sodium or potassium and is blocked by nifedipine. These data strongly suggest that endothelin acts at a site closely coupled to the calcium channel and that depolarization by sodium influx through voltage-dependent channels is not involved in endothelin-induced vasoconstriction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2546692&dopt=Abstract
Am Heart J. 1989 Oct;118(4):674-8.
Vasoconstrictor effect of endothelin on the canine coronary artery: is a novel endogenous peptide involved in regulating myocardial blood flow and coronary spasm?
Igarashi Y, Aizawa Y, Tamura M, Ebe K, Yamaguchi T, Shibata A.
First Department of Internal Medicine, Niigata University School of Medicine, Japan.
We examined the effect of endothelin on the canine coronary artery (N = 20). The left circumflex coronary artery was cannulated and perfused with arterial blood at constant pressure. Coronary blood flow was monitored by an electromagnetic flowmeter. Intracoronary endothelin provoked a vasoconstriction that was dose-dependent. At a dose of 500 pmol, coronary blood flow was reduced remarkably (91.0 +/- 5.4%, n = 4), and endothelin subsequently produced a fall in systemic blood pressure and ST elevation in the electrocardiogram. At a dose of 100 pmol (n = 9), coronary flow decreased from 16.4 +/- 1.5 ml/min to 12.5 +/- 1.5 ml/min (p less than 0.001) and coronary vascular resistance increased from 6.3 +/- 0.8 mm Hg/ml/min to 9.9 +/- 1.9 mm Hg/ml/min (p less than 0.005). A cumulative dose-response curve to endothelin was obtained and the curves were shifted to the right after both verapamil and nifedipine administration. Therefore endothelin has a potent vasoconstrictor action that is attenuated by the calcium-channel blocker.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2679015&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 ||