Drugs online research references
J Appl Physiol. 1993 Mar;74(3):1195-9.
Beta 2-adrenoceptor agonists inhibit NANC neural bronchoconstrictor responses in vitro.
Verleden GM, Belvisi MG, Rabe KF, Miura M, Barnes PJ.
Department of Thoracic Medicine, National Heart and Lung Institute, London, United Kingdom.
Nonadrenergic noncholinergic (NANC) contractile responses in guinea pig bronchi are due to the release of tachykinins from airway sensory nerves. The purpose of this study was to determine whether beta 2-receptor agonists modulate NANC contractions in guinea pig bronchi in vitro. Bronchial rings were suspended in organ baths for isometric measurement of tension, and comparable contractions were induced by electrical field stimulation (EFS; 40 V, 0.5 ms, 8 Hz for 20 s) or by exogenous substance P (3 microM). Aformoterol and salbutamol produced concentration-dependent inhibition of the NANC contraction, with aformoterol being ninefold more potent than salbutamol; approximate 50% inhibitory concentrations for aformoterol and salbutamol were 1.03 nM (n = 6) and 9.3 nM (n = 6), respectively. Aformoterol also inhibited the contraction induced by exogenous substance P but to a far lesser extent than its inhibition of EFS-induced responses. The inhibitory effects of formoterol (10 nM) on responses to EFS at 8 Hz were significantly prevented by propranolol (1 microM) and ICI 118551 (a beta 2-antagonist, 0.1 microM) but not by atenolol (a beta 1-antagonist, 1 microM) or phentolamine (10 microM). These experiments demonstrate that beta 2-agonists may modulate the release of tachykinins from airway sensory nerves by prejunctional receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7683310&dopt=Abstract
Clin Exp Pharmacol Physiol. 1993 May;20(5):355-8.
Neurogenic vasodilatation in isolated perfused segments of rabbit jejunal artery.
La M, Rand MJ.
Department of Pharmacology, University of Melbourne, Parkville, Victoria, Australia.
1. Vasodilator responses were elicited by field stimulation in isolated perfused segments of rabbit jejunal arteries when noradrenergic and purinergic vasoconstrictor responses had been abolished and the smooth muscle partly contracted by endothelin. 2. The stimulation-induced vasodilator responses were abolished by tetrodotoxin, but were not affected by atropine, propranolol or a nitric oxide synthase inhibitor. 3. After recovery from the vasodilator action of capsaicin, the stimulation-induced vasodilator responses were greatly reduced or abolished. 4. A competitive antagonist of calcitonin gene-related peptide (CGRP) blocked vasodilator responses elicited by field stimulation and exogenously administered CGRP. 5. The findings indicated that the mediator of the stimulation-induced vasodilator responses is neurogenic in origin, and it is not acetylcholine, noradrenaline acting on beta-adrenoceptors, nitric oxide or an endothelium-dependent vasodilator. It appears to be CGRP, presumably released from sensory nerves in the periarterial plexus.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7686829&dopt=Abstract
Gastroenterology. 1993 Aug;105(2):449-61.
Histamine secretion from rat enterochromaffinlike cells.
Prinz C, Kajimura M, Scott DR, Mercier F, Helander HF, Sachs G.
Department of Physiology and Medicine, University of California, Los Angeles.
BACKGROUND: In vivo studies have suggested an important role for gastric enterochromaffinlike (ECL) cells in mediating acid secretion. Direct evidence for this function is lacking and requires a preparation of highly purified ECL cells. This work investigates the possible role and mechanism of histamine release from the ECL cell in the peripheral regulation of acid secretion, using purified ECL cells from rat fundic mucosa. METHODS: A combination of elutriation and density-gradient centrifugation was used to purify rat fundic ECL cells. Enrichment was determined by the presence of acidic vacuoles containing a V type adenosine triphosphatase, electron microscopy, immunostaining, and histamine content and release. RESULTS: ECL cells were enriched at least 65-fold with respect to the fundic epithelium. Gastrin (EC50 0.2 nmol/L) and cholecystokinin octapeptide (nonsulfated, EC50 0.04 nmol/L) stimulated histamine release in a time- and dose-dependent manner, suggesting a CCK-B receptor subtype, confirmed by the inhibition of gastrin/CCK stimulation with the CCK-B antagonist L365,260. Somatostatin also inhibited gastrin-mediated histamine release. Single cell imaging showed that gastrin elevated intracellular cytosolic calcium concentration biphasically. Carbachol and the C kinase activator 120-tetradecanoylphorbol-13-acetate also stimulated histamine release. Epinephrine (blocked by propranolol), forskolin, and dibutyryl-5'-cyclic adenosine monophosphate were also effective, implicating a beta-adrenergic pathway. The H3 agonist R-alpha-methyl-histamine inhibited, whereas the H3-antagonist thioperamide potentiated gastrin/CCK stimulated histamine release. CONCLUSIONS: These in vitro results support a central role for the ECL cell in the peripheral regulation of gastric acid secretion.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7687574&dopt=Abstract
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