Drugs online research references
Comp Biochem Physiol Pharmacol Toxicol Endocrinol. 1994 Feb;107(2):295-304.
Hypoxia inverts the negative chronotropic response to norepinephrine in normoxia in cultured neonatal rat cardiac myocytes: role of the alpha 1 adrenergic signal transduction system.
Kawana S, Kimura H, Miyamoto A, Ohshika H, Namiki A.
Department of Anesthesiology, School of Medicine, Sapporo Medical University, Japan.
In the present study, we investigated the effect of hypoxia on the chronotropic response to norepinephrine (NE) of cultured neonatal rat ventricular myocytes. We measured beating of myocytes with the Fotonic sensor, using a newly developed method for a noncontact displacement measurement. The beating rate counted with the sensor had a high correlation coefficient with that counted visually under a microscope (r = 0.997, P < 0.01). NE concentrations of 10(-8) - 10(-4) M caused negative chronotropy dose dependently in the presence of 5 x 10(-7) M propranolol. NE-induced chronotropy was completely antagonized by 10(-6) M prazosin. Three hours hypoxia decreased the spontaneous beating rate 40% (P < 0.01). Negative chronotropy induced by 10(-4) M NE in normoxia was inverted to positive and was antagonized by prazosin. Hypoxia increased the basal level of inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) to 190% (P < 0.01), while NE-stimulated Ins(1,4,5)P3 production was significantly suppressed. Immunoblotting analysis of G protein subunits demonstrated no quantitative changes in Gi alpha, Gq alpha, Go alpha and G beta common subunits in hypoxia. In a saturation binding assay with [3H]prazosin, Kd values were increased to 152% by hypoxia (P < 0.05) without significant change in Bmax. Basal activity of low Km-GTPase was increased to 122% by hypoxia (P < 0.05). These results suggest that the hypoxia-induced increase in low-Km GTPase activity, which could stimulate phospholipase C by an activated alpha GTP subunit of G protein and consequently induce receptor-independent increase in Ins(1,4,5)P3, may be responsible for the inversion of the NE-induced negative chronotropic response in normoxia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7749596&dopt=Abstract
FEBS Lett. 1995 May 8;364(2):161-4.
ATP opens an electrophoretic potassium transport pathway in respiring yeast mitochondria.
Roucou X, Manon S, Guerin M.
Institut de Biochimie et de Genetique Cellulaires, CNRS, Universite de Bordeaux II, France.
In the presence of KCl and only at low phosphate concentrations, ATP stimulated state 4 of the respiration of isolated yeast mitochondria. This effect could be related to a partial collapse of the transmembrane potential which was created by the respiratory chain or the F0F1-ATPase. Sodium and lithium could not replace potassium ion. Atractyloside prevented the opening of this K+ pathway, suggesting that only matricial ATP operated. All these effects were inhibited by increasing phosphate concentration, or by adding propranolol, quinine, Zn2+ or Mg2+.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7750562&dopt=Abstract
J Appl Physiol. 1995 Feb;78(2):623-8.
Production of PGE2 by bovine cultured airway smooth muscle cells: regulation by cAMP.
Barry T, Delamere F, Holland E, Pavord I, Knox A.
Respiratory Medicine Unit, City Hospital, Nottingham, United Kingdom.
Prostaglandin E2 (PGE2) is thought to be an important inhibitory modulator of inflammatory processes in the airway. Previous studies have shown that it is produced by bovine cultured airway smooth muscle (ASM) cells in large quantities, but its regulation by second messengers has not been studied in this tissue. To determine whether PGE2 production by ASM might be an important action of beta-adrenoceptor agonists in asthma, the regulation of PGE2 production by adenosine 3',5'-cyclic monophosphate (cAMP) was assessed using dibutyryl cAMP (DBcAMP), forskolin, and albuterol. DBcAMP increased PGE2 production over a 24-h time course. Forskolin and albuterol both increased PGE2 production over control cells to similar levels after 24 h. Incubation of albuterol-treated cells with propranolol significantly (70%) reduced the stimulatory effect of albuterol on PGE2 production. Incubation of forskolin-treated cells with Rp-cAMP, a cAMP antagonist, inhibited the PGE2 response evoked by forskolin by 80%. Ro-20-1724, a selective inhibitor of type IV phosphodiesterase, stimulated PGE2 production (P = 0.02). Cycloheximide, a protein-synthesis inhibitor, did not inhibit the response to DBcAMP. The effects of DBcAMP were additive with the effects of bradykinin, a proinflammatory mediator known to increase PGE2 production (P < 0.05). These studies suggest that cAMP may play an important regulatory role in stimulating PGE2 production by ASM. This may be a novel beneficial action of beta-adrenoceptor agonists in asthma.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7759432&dopt=Abstract
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