Academic literature on the topic 'Clonidine Synthesis'
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Journal articles on the topic "Clonidine Synthesis"
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Ghabbour, Hazem A., Ahmed H. Bakheit, Essam Ezzeldin, and Gamal A. E. Mostafa. "Synthesis Characterization and X-ray Structure of 2-(2,6-Dichlorophenylamino)-2-imidazoline Tetraphenylborate: Computational Study." Applied Sciences 12, no. 7 (March 31, 2022): 3568. http://dx.doi.org/10.3390/app12073568.
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The title compound tetraphenylborate salt of clonidine (Catapres®), 2-(2,6-dichlorophenylamino)-2-imidazoline tetraphenylborate (3), was prepared in 76 % yield by the reaction of 2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride (clonidine hydrochloride) (1) with sodium tetraphenylborate (2) in deionized water through anion exchange reaction at ambient temperature. The structure of the title borate salt was characterized by UV, thermal analysis, mass and NMR analyses. White crystals of (3) suitable for an X-ray structural analysis were obtained by slow growing from acetonitrile. The molecular structure of the titled compound (3) was crystallized in the acetonitrile, P21/c, a = 9.151 (3) Å, b = 12.522 (3) Å, c = 25.493 (6) Å, β = 105.161 (13)° V = 2819.5 (13) Å3, Z = 4. A DFT quantum chemistry calculation method was employed to investigate the interaction mechanism of clonidine with tetraphenylborate. The stable configurations of the complexes of clonidine with tetraphenylborate with electrostatic interactions were obtained. Finally, the interaction strength and type of the complexes were studied through the reduced density gradient (RDG) function. This study provides new theoretical insight into the interaction mechanism and a guide for screening and designing the optimal clonidine and tetraphenylborate reacting to form the complex.
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KALKOTE, U. R., K. C. BRAHME, and N. R. AYYANGAR. "ChemInform Abstract: Synthesis of New Clonidine Analogues." ChemInform 23, no. 21 (August 22, 2010): no. http://dx.doi.org/10.1002/chin.199221182.
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Plato, Craig F., and Jeffrey L. Garvin. "α2-Adrenergic-mediated tubular NO production inhibits thick ascending limb chloride absorption." American Journal of Physiology-Renal Physiology 281, no. 4 (October 1, 2001): F679—F686. http://dx.doi.org/10.1152/ajprenal.2001.281.4.f679.
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Stimulation of α2-adrenergic receptors inhibits transport in various nephron segments, and the thick ascending limb of the loop of Henle (THAL) expresses α2-receptors. We hypothesized that selective α2-receptor activation decreases NaCl absorption by cortical THALs through activation of NOS and increased production of NO. We found that the α2-receptor agonist clonidine (10 nM) decreased chloride flux ( J Cl) from 119.5 ± 15.9 to 67.4 ± 13.8 pmol · mm−1 · min−1 (43% reduction; P < 0.02), whereas removal of clonidine from the bath increased J Cl by 20%. When NOS activity was inhibited by pretreatment with 5 mM N G-nitro-l-arginine methyl ester, the inhibitory effects of clonidine on THAL J Clwere prevented (81.7 ± 10.8 vs. 71.6 ± 6.9 pmol · mm−1 · min−1). Similarly, when the NOS substrate l-arginine was deleted from the bath, addition of clonidine did not decrease THAL J Cl from control (106.9 ± 11.6 vs. 132.2 ± 21.3 pmol · mm−1 · min−1). When we blocked the α2-receptors with rauwolscine (1 μM), we found that the inhibitory effect of 10 nM clonidine on THAL J Cl was abolished, verifying that α2, rather than I1, receptors mediate the effects of clonidine in the THAL. We investigated the mechanism of NOS activation and found that intracellular calcium concentration did not increase in response to clonidine, whereas pretreatment with 150 nM wortmannin abolished the clonidine-mediated inhibition of THAL J Cl, indicating activation of phosphatidylinositol 3-kinase and the Akt pathway. We found that pretreatment of THALs with 10 μM LY-83583, an inhibitor of soluble guanylate cyclase, blocked clonidine-mediated inhibition of THAL J Cl. In conclusion, α2-receptor stimulation decreases THAL J Cl by increasing NO release and stimulating guanylate cyclase. These data suggest that α2-receptors act as physiological regulators of THAL NO synthesis, thus inhibiting chloride transport and participating in the natriuretic and diuretic effects of clonidine in vivo.
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Alvo, M., A. M. Espinoza, V. Fernandez, and E. T. Marusic. "Alpha 2-agonists block ADH action in toad bladder and this inhibition is not modified by indomethacin." American Journal of Physiology-Renal Physiology 255, no. 1 (July 1, 1988): F74—F77. http://dx.doi.org/10.1152/ajprenal.1988.255.1.f74.
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To identify the type of alpha-adrenoceptors involved in the inhibition of the hydrosmotic effect of antidiuretic hormone (ADH) on the toad bladder, we studied the effect of different alpha-adrenergic agonists and antagonists on ADH-induced water transport. Serosal addition of epinephrine (10(-6) M) and norepinephrine (10(-6) M) in the presence of 10(-4) M propranolol significantly inhibited the hydrosmotic effect of ADH (arginine vasopressin). This inhibitory effect of the catecholamines was completely reversed by 10(-5) M yohimbine but not by prazosin. Clonidine did not block ADH-induced water transport, but guanabenz, another alpha 2-agonist, inhibited water transport in response to ADH. In bladders pretreated with indomethacin to block prostaglandin synthesis, basal water permeability was increased, and even in this condition epinephrine inhibited ADH-induced water transport. These studies indicate that alpha 2-adrenergic receptors are involved in the inhibitory effect of catecholamines on ADH-mediated water permeability in the toad bladder. However, this effect was not mimicked by clonidine, as in the case of rabbit cortical collecting tubule. The inhibitory effect of epinephrine appears to be exerted independently of prostaglandin synthesis.
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Ayyangar, N. R., K. C. Brahme, and K. V. Srinivasan. "A Novel Synthesis of Clonidine, an Anti-Hypertensive Drug fromo-Chloronitrobenzene." Synthesis 1987, no. 01 (1987): 64–65. http://dx.doi.org/10.1055/s-1987-27847.
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Filer, Crist N., and David G. Ahern. "Synthesis and characterization of [phenyl-3H] clonidine hydrochloride at high specific activity." Journal of Labelled Compounds and Radiopharmaceuticals 44, no. 5 (2001): 323–27. http://dx.doi.org/10.1002/jlcr.457.
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Gales, Mark A. "Oral Antihypertensives for Hypertensive Urgencies." Annals of Pharmacotherapy 28, no. 3 (March 1994): 352–58. http://dx.doi.org/10.1177/106002809402800311.
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OBJECTIVE: To review the data describing the use of oral antihypertensive agents in the treatment of hypertensive urgencies (HU). DATA SOURCES: A MEDLINE search of the English-language literature and fan searches of papers evaluating oral antihypertensives in HUs and emergencies were conducted. STUDY SELECTION: Controlled and uncontrolled studies in humans are reviewed. Emphasis was placed on recent trials evaluating individual agents and comparative trials. DATA SYNTHESIS: Comparative trials have demonstrated that four currently available oral agents can lower blood pressure rapidly and predictably. Nifedipine, the most extensively studied, and clonidine have served traditionally as the oral agents of choice for the treatment of HUs. All the agents can lower blood pressure effectively within the first few hours after dosing, but their use also has been associated with adverse effects. Nifedipine and captopril are the two agents with the most rapid onset, within 0.5–1 hour, and may treat hypertensive emergencies as well as urgencies. Clonidine and labetalol have maximal blood pressure lowering effects at 2–4 hours. CONCLUSIONS: Captopril, clonidine, labetalol, and nifedipine are all effective agents for the treatment of HUs. Agent selection should be based on the perceived need for urgent blood pressure control, the cause of HU, and concomitant conditions. A definite benefit from acute blood pressure lowering in HUs has yet to be demonstrated, especially in asymptomatic patients. More controlled trials with less aggressive dosing regimens and placebo controls need to be performed to assess the most appropriate treatments for HUs with the fewest adverse effects.
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Wang, Xinyan, Mable M. S. Chu, and Anderson O. L. Wong. "Signaling mechanisms for α2-adrenergic inhibition of PACAP-induced growth hormone secretion and gene expression grass carp pituitary cells." American Journal of Physiology-Endocrinology and Metabolism 292, no. 6 (June 2007): E1750—E1762. http://dx.doi.org/10.1152/ajpendo.00001.2007.
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Pituitary adenylate cyclase-activating polypeptide (PACAP) is a potent growth hormone (GH)-releasing factor in lower vertebrates. However, its functional interactions with other GH regulators have not been fully characterized. In fish models, norepinephrine (NE) inhibits GH release at the pituitary cell level, but its effects on GH synthesis have yet to be determined. We examined adrenergic inhibition of PACAP-induced GH secretion and GH gene expression using grass carp pituitary cells as a cell model. Through activation of pituitary α2-adrenoreceptors, NE or the α2-agonist clonidine reduced both basal and PACAP-induced GH release and GH mRNA expression. In carp pituitary cells, clonidine also suppressed cAMP production and intracellular Ca2+ levels and blocked PACAP induction of these two second messenger signals. In GH3 cells transfected with a reporter carrying the grass carp GH promoter, PACAP stimulation increased GH promoter activity, and this stimulatory effect could be abolished by NE treatment. In parallel experiments, clonidine reduced GH primary transcript and GH promoter activity without affecting GH mRNA stability, and these inhibitory actions were mimicked by inhibiting adenylate cyclase (AC), blocking protein kinase A (PKA), removing extracellular Ca2+ in the culture medium, or inactivating L-type voltage-sensitive Ca2+ channels (VSCC). Since our recent studies have shown that PACAP can induce GH secretion in carp pituitary cells through cAMP/PKA- and Ca2+/calmodulin-dependent mechanisms, these results, taken together, suggest that α2-adrenergic stimulation in the carp pituitary may inhibit PACAP-induced GH release and GH gene transcription by blocking the AC/cAMP/PKA pathway and Ca2+ entry through L-type VSCC.
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Seuwen, K., I. Magnaldo, B. K. Kobilka, M. G. Caron, J. W. Regan, R. J. Lefkowitz, and J. Pouysségur. "Alpha 2-adrenergic agonists stimulate DNA synthesis in Chinese hamster lung fibroblasts transfected with a human alpha 2-adrenergic receptor gene." Cell Regulation 1, no. 6 (May 1990): 445–51. http://dx.doi.org/10.1091/mbc.1.6.445.
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To test the hypothesis that agents activating receptors negatively coupled to adenylyl cyclase (AC) can stimulate cell proliferation, we have expressed a human alpha 2-adrenergic receptor (alpha 2-C10) in CCL39 cells and studied the effects of alpha 2-agonists on reinitiation of DNA synthesis in quiescent cells. We report that the alpha 2-agonists epinephrine and clonidine stimulate [3H]-thymidine incorporation in synergy with fibroblast growth factor and that the alpha 2-antagonist yohimbine efficiently inhibits this response. Epinephrine- and clonidine-stimulated DNA synthesis is completely blocked by pertussis toxin and correlates well with the inhibition of prostaglandin E1-stimulated AC. Thus, their action closely resembles the action of serotonin in the same cell system, which is mediated through 5-HT1b receptors. In fact, serotonin- and epinephrine-stimulated DNA synthesis reinitiation is not additive, suggesting that both agents act through a common pathway. Interestingly, alpha 2-agonists also induced a moderate release of inositol phosphates, indicating that alpha 2-adrenergic receptors can interact both with the AC and phospholipase C messenger system. Activation of phosphoinositide (PI) turnover by epinephrine leads to a significant stimulation of Na+/H+ exchange but is insufficient to trigger a mitogenic response in CCL39 cells, as will be discussed. We found no evidence for epinephrine-induced activation of Na+/H+ exchange by a mechanism independent of PI breakdown.Our data show that alpha 2-adrenergic receptors can play a role in the regulation of cell proliferation in an appropriate context; also, the data support the hypothesis that receptors negatively coupled to AC must be taken into account as mediators of growth factor action in fibroblasts, in particular when activated in parallel with receptor tyrosine kinases.
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Gaida, W., R. E. Lang, K. Kraft, Th Unger, and D. Ganten. "Altered Neuropeptide Concentrations in Spontaneously Hypertensive Rats: Cause or Consequence?" Clinical Science 68, no. 1 (January 1, 1985): 35–43. http://dx.doi.org/10.1042/cs0680035.
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1. Changes in brain neuropeptide content in spontaneously hypertensive rats may be primarily related to the development of hypertension or may be secondary consequences of it. 2. We have measured brain concentrations of β-endorphin, Leu-enkephalin, arginine vasopressin (AVP) and oxytocin (OXT) in stroke-prone spontaneously hypertensive rats (SHRSP) and in age-matched normotensive Wistar Kyoto (WKY) controls, as well as in SHRSP with normalized blood pressure by chronic treatment with clonidine. Opioid peptide contents were measured in 12-, 18- and 24-week-old rats. β-Endorphin was measured in the neuro-intermediate and anterior lobes of the pituitary, the hypothalamus, midbrain and brain stem; Leu-enkephalin in the neuro-intermediate lobe of the pituitary, hypothalamus, mid-brain, brain stem, as well as in the spinal cord and adrenal glands. AVP and OXT were measured in the neuro-intermediate lobe of the pituitary, hypothalamus, brain stem and spinal cord. 3. β-Endorphin in the neuro-intermediate lobe of the pituitary was significantly higher in 12- and 18-week-old SHRSP. Adrenal gland Leu-enkephalin was lower in SHRSP as compared with the WKY. 4. OXT and AVP contents were markedly reduced in all brain regions of SHRSP except the neuro-intermediate lobe of the pituitary, where no significant changes were found. 5. In no case did long-term antihypertensive treatment with clonidine reverse the altered peptide content in the SHRSP. 6. We conclude that alterations in brain neuropeptide content in SHRSP are not secondary to hypertension. The blood pressure lowering activity of clonidine appears not to depend on major alterations of peptide concentrations. A genetic defect in the synthesis of adrenal enkephalins and hypothalamic OXT and AVP seems likely from these studies.
Dissertations / Theses on the topic "Clonidine Synthesis"
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Schann, Stephan. "Synthese d'isosteres pyrroliniques de la rilmenidine et de la clonidine." Université Louis Pasteur (Strasbourg) (1971-2008), 2001. http://www.theses.fr/2001STR13053.
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Au cours de ce travail, nous nous sommes attaches a obtenir des nouveaux ligands selectifs des recepteurs des imidazolines par rapport aux sites de liaison des imidazolines de sous-type 2 et aux recepteurs 2-adrenergiques. De tels ligands sont en effet d'une grande utilite d'une part pour la caracterisation des recepteurs des imidazolines et l'etude de l'effet hypotenseur provoque par les drogues imidazoliniques, mais aussi pour obtenir de nouveaux prototypes d'agents antihypertenseurs centraux. Pour obtenir ces ligands selectifs, nous avons synthetise des isosteres pyrroliniques des deux drogues de reference que sont la rilmenidine et la clonidine. Ces syntheses ont notamment conduit a : - une serie d'analogues pyrroliniques de la rilmenidine, selectifs des recepteurs des imidazolines et capables de faire baisser la pression arterielle apres administration centrale. Un de ces analogues, le lnp 509, s'est d'ores et deja avere tres utile pour l'etude de l'effet hypotenseur des imidazolines. - deux analogues pyrroliniques de la clonidine, originaux et hypotenseurs apres administration systemique (les lnp 541 et lnp 560) qui constituent deux nouveaux prototypes d'agents antihypertenseurs centraux. - l'obtention d'un ligand radiomarque (lnp 911) et d'un ligand de photoaffinite (lnp 906) tous deux tres selectifs et possedant une affinite subnanomolaire pour les recepteurs d'interet. Ces deux molecules constituent deux nouveaux outils pour l'etude des recepteurs des imidazolines.