Drugs online research references
Neuroscience. 1993 Apr;53(3):855-64.
Histamine enhances the depolarizing afterpotential of immunohistochemically identified vasopressin neurons in the rat supraoptic nucleus via H1-receptor activation.
Smith BN, Armstrong WE.
Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee, Memphis 38163.
Previous studies have demonstrated that histamine primarily excites unidentified neurons in the rat supraoptic nucleus. We investigated the neuromodulatory effects of histamine on immunohistochemically identified vasopressin neurons in the rat supraoptic nucleus using intracellular recording techniques from the hypothalamo-neurohypophysial explant. Exogenous application of histamine (0.1-100 microM) to vasopressinergic neurons produced a small membrane depolarization accompanied by an increase of up to 100% in the amplitude of the depolarizing afterpotential that follows current-evoked trains of action potentials. The enhancement of the depolarizing afterpotential by histamine did not depend upon the depolarization. Further, histamine enhanced the amplitude of the depolarizing afterpotential when blocking the afterhyperpolarizing potential with d-tubocurarine or apamin, and in the presence of tetrodotoxin and d-tubocurarine or apamin, indicating a postsynaptic action of histamine on the depolarizing afterpotential that is not simply a reflection of a decrease in the afterhyperpolarizing potential. These toxins also had no effect on the histamine-induced depolarization. The enhancement of the depolarizing afterpotential by histamine was mimicked by the histamine H1-receptor agonist 2-thiazolylethylamine and was reduced or blocked by the H1-receptor antagonist promethazine, but was not blocked or reduced in the presence of the histamine H2-receptor antagonist, cimetidine. In summary, these results show that the excitatory effect of histamine on immunohistochemically identified vasopressin neurons in the supraoptic nucleus is due in part to the H1-receptor-mediated enhancement of the depolarizing afterpotential independent of any change in the afterhyperpolarizing potential or membrane potential.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8098142&dopt=Abstract
J Pharm Sci. 1988 Jul;77(7):586-90.
Effects of phenothiazine derivatives on the microclimate-pH in the rat jejunum.
Iwatsubo T, Sugiyama Y, Miyamoto Y, Leibach FH, Suzuki H, Iga T, Hanano M.
Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
The effects of several phenothiazine derivatives (PTDs) and quinidine (QD) on the jejunal microclimate-pH in rats were studied using a microelectrode. Chlorpromazine, thioridazine, chlorpromazine sulfoxide (CPZSO), trifluoperazine, prochlorperazine, and QD at concentrations of 1 mM increased this microclimate-pH by 0.15-0.3 pH units, while 1 mM diethazine and 1 mM promethazine had little effect on it. The increases in the microclimate-pH caused by PTDs and QD were concentration dependent and reversible. We studied the effects of PTDs on the fluidity of intestinal brush border membranes and on the release of proteins from the intestinal tissue to the lumen. The PTD-induced changes in microclimate-pH could not be explained by either of these nonspecific effects on the membranes. Then, the effects of PTDs on Na+,K+-ATPase activity and Mg2+-ATPase activity were studied using the jejunal homogenate. Each PTD inhibited Na+,K+-ATPase and Mg2+-ATPase activity to some extent. The inhibitory effects on Na+,K+-ATPase and Mg2+-ATPase activity were compared with the PTD-induced increases in the microclimate-pH. No good correlation was obtained between the IC50 values of PTDs for Na+,K+-ATPase activity and the concentrations required to increase the microclimate-pH by 0.1 pH unit, while IC50 values of PTDs for Mg2+-ATPase activity showed a relatively good correlation, except for that of CPZSO. These findings suggest that the effects of PTDs on the microclimate-pH were not nonspecific, although the increases in the microclimate-pH caused by PTDs cannot be fully explained by the inhibitory effects of these compounds on either Na+,K+-ATPase activity or Mg2+-ATPase activity alone.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2845051&dopt=Abstract
Br J Pharmacol. 1981 Sep;74(1):143-8.
Effects of mianserin, desipramine and maprotiline on blood pressure responses evoked by acetylcholine, histamine and 5-hydroxytryptamine in rats.
Cavero I, Lefevre-Borg F, Roach AG.
1 In rats anaesthetized with pentobarbitone, intravenous administration of desipramine (0.1 mg/kg), maprotiline (0.5 mg/kg) or mianserin (0.3-3.0 mg/kg) did not modify the blood pressure lowering effects of acetylcholine (0.25-1.0 micrograms/kg, i.v.) which were significantly reduced by atropine (3.0 micrograms/kg, i.v.). 2 Maprotiline and mianserin, like promethazine (0.1 mg/kg, i.v.), inhibited the vasodepressor responses evoked by histamine (2.5-10.0 micrograms/kg,i.v.). however, desipramine was inactive against histamine. 3 In pithed rats, the pressor effects of intravenous 5-hydroxytryptamine (5-HT: 5.0-20.0 micrograms/kg) were antagonized by mianserin (0.01-0.3 mg/kg, i.v.) and cyproheptadine (0.01 mg/kg) but were unaffected by maprotiline and desipramine. 4 In syrosingopine pretreated rats given mianserin 0.1 mg/kg, intravenously, 5-HT (20.0 micrograms/kg, i.v.) produced a significant fall in blood pressure which could be reduced by a large dose of mianserin (10.0 mg/kg, i.v.). 5 In conclusion, desipramine, maptrotiline and mianserin, in doses previously found to inhibit noradrenaline neuronal reuptake in the rat cardiovascular system, lack muscarinic receptor antagonist properties. Whilst maprotiline and mianserin blocked vascular histamine receptors, only mianserin (10.0 mg/kg, i.v.). 5 In conclusion, desipramine, maptrotiline and mianserin, in doses previously found to inhibit noradrenaline neuronal reuptake in the rat cardiovascular system, lack muscarinic receptor antagonist properties. Whilst maprotiline and mianserin blocked vascular histamine receptors, only mianserin, like cyproheptadine, was a potent antagonist of the 5-HT receptors that mediate increases in blood pressure in rats. Finally, the vasodepressor effects of 5-HT in syrosingopine pretreated rats given a small dose of mianserin were antagonized by a large dose of mianserin, suggesting that 5-HT may activate two distinct types of receptors in the rat.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6115693&dopt=Abstract
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