Drugs online research references
Invest Ophthalmol Vis Sci. 1992 Jun;33(7):2340-3.
Nitric oxide and endothelin-1 are important regulators of human ophthalmic artery.
Haefliger IO, Flammer J, Luscher TF.
Department of Ophthalmology, University Hospitals, Basel, Switzerland.
The vascular endothelial cells have the ability to modulate local vascular tone by releasing relaxing factors such as nitric oxide or the vasoconstrictor peptide endothelin-1. Although this regulatory system is found in all vertebrates, there is a great heterogeneity in the release of these endothelium-derived substances, from one organ to an other, between large and small vessels, and between different species. Therefore, observations made in certain vascular beds or animals do not necessarily apply to human ophthalmic circulation. The present study was designed to investigate endothelial mediators in the human ophthalmic artery. The results show that in the human ophthalmic artery, nitric oxide is released under basal conditions and that its production can be markedly stimulated by bradykinin, acetylcholine, and particularly histamine, which cause profound vascular relaxation. In contrast, endothelin-1 evoked potent contractions, which were unaffected by the calcium antagonist nifedipine. However, upon re-exposure of the blood vessels to the peptide, marked tachyphylaxis occurred. These findings demonstrate that in the human ophthalmic artery, endothelium-derived nitric oxide and endothelin are very potent modulators of vascular tone, suggesting that they play an important role in the regulation of local blood flow in the eye. Hence, endothelium dysfunction may represent a new pathogenetic mechanism in disease states associated with altered blood flow to the eye, such as diabetes, hypertension, and some forms of low-tension glaucoma.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1607246&dopt=Abstract
J Cardiovasc Pharmacol. 1997 Jun;29(6):747-54.
Reversal of endothelin-induced vasoconstriction by endothelium-dependent and -independent vasodilators in isolated hearts and vascular rings.
Stowe DF, O'Brien WC, Chang D, Knop CS, Kampine JP.
Department of Anesthesiology, Medical College of Wisconsin, and Veterans Affairs Medical Center, Milwaukee 53226, USA.
Endothelin (ET-1) is a potent endogenous vasoconstrictor. Several factors increase ET-1 release in vitro and ET-1 levels increase in vivo in situations that damage blood vessels. The aim of this study was to test the activity of several differently acting vasodilator drugs on reversing or attenuating the vasoconstrictor effects of exogenously administered ET-1 in isolated guinea-pig hearts, in isolated rings with intact endothelium from canine middle cerebral and basilar arteries, and from guinea-pig aortas. Vasodilator drugs tested up to maximal concentrations were adenosine (ADE), nitroprusside (NP), acetylcholine (ACH), nifedipine (NIF), and butanedione monoxime (BDM), an excitation-uncoupling agent. Variables measured in isolated hearts included coronary flow, percentage oxygen extraction (% O2E), left ventricular pressure (LVP), and myocardial oxygen consumption. It was found that ADE, NP, ACH, and BDM each attenuated the 60% decrease in coronary flow and 20% increase in % O2E elicited by 0.5 nM ET-1 in isolated hearts, but only BDM restored coronary flow, whereas BDM and ADE both restored % O2E. In isolated rings constricted with 20 nM ET-1, BDM restored tone equivalent to that by papaverine, whereas NP and NIF only attenuated the vasoconstriction elicited by ET-1. Ring experiments also demonstrated that the vasodilatory effect of BDM was independent of nitric oxide-dependent pathways and that BDM attenuated vasoconstriction resulting from increased bath KCl. The study suggests that drugs affecting intracellular Ca2+ with a mechanism of action downstream from cell-membrane receptors or intracellular messengers may be more effective for reversing the constrictor effect of ET-1. NP, however, would be a better clinical choice for reversing ET-1-induced vasoconstriction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9234655&dopt=Abstract
Pflugers Arch. 1990 Feb;415(5):526-32.
Mechanisms of endothelin-induced augmentation of the electrical and mechanical activity in rat portal vein.
Nakao K, Inoue Y, Oike M, Kitamura K, Kuriyama H.
Department of Pharmacology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Actions of porcine endothelin (ET) on the electrical and mechanical activity of the rat portal vein were investigated by means of the intracellular microelectrode and isometric tension recording techniques, ET (greater than 0.1 nM) enhanced the amplitude and frequency of the spontaneous contractions which ceased in the presence of 100 nM dihydropyridine derivatives (nifedipine or nicardipine). ET (0.15 nM) increased the frequency of the spontaneous action potentials, with no change in the basal membrane potential. Higher concentrations of ET (greater than or equal to 0.3 nM) further depolarized the membrane potential and increased the spike frequency. After blocking the spontaneous action potentials with nifedipine (100 nM), ET still depolarized the membrane. The depolarization was associated with a reduction in the electrotonic potential and was blocked in a Na-deficient solution (15.5 mM) but not in Ca-free, K-deficient or Cl-deficient solutions. In a Na-deficient solution, ET still evoked action potentials without depolarization. In Ca-free solution, ET depolarized the membrane potential with small oscillations, which were blocked by nifedipine (100 nM). The results indicate that in the rat portal vein, ET enhances electrical and mechanical responses through activation of the dihydropyridine-sensitive and voltage-dependent Ca channels. Acceleration of the Ca entry induced by ET can occur with or without depolarization of the membrane and can enhance the pacemaking mechanism.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2183175&dopt=Abstract
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