Drugs online research references
Neuroscience. 1999;94(4):1245-52.
Brain alpha 1-adrenergic neurotransmission is necessary for behavioral activation to environmental change in mice.
Stone EA, Zhang Y, Rosengarten H, Yeretsian J, Quartermain D.
Department of Psychiatry, New York University School of Medicine, NY 10016, USA.
Terazosin, a water-soluble alpha 1 antagonist that can be administered in high doses intraventricularly was used to study the relationship between brain alpha 1 adrenoceptor neurotransmission and behavioral activation in the mouse. The antagonist was found to produce a dose-dependent, complete inhibition of motor activity and catalepsy which were reversed preferentially by coinfusion of an alpha 1 agonist (phenylephrine) compared to a D1 (SKF38393) or a D2 agonist, (quinpirole). Blockade of central beta-1 (betaxolol), alpha-2 (RX821002) or beta-2 (ICI 118551) adrenoceptors had smaller or non-significant effects. Terazosin's selectivity for alpha 1 receptors versus dopaminergic receptors was verified under the present conditions by showing that the intraventricularly administered antagonist protected striatal and cerebral cortical alpha 1 receptors but not striatal or cortical D1 receptors from in vivo alkylation by N-ethoxycarbonyl-2-ethoxy-1, 2-dihydroxyquinoline. That its effect was due to blockade of brain rather than peripheral receptors was shown by the finding that intraperitoneal doses of terazosin three to 66 times greater than the maximal intraventricular dose produced less behavioral inhibition. Intraventricular terazosin also produced hypothermia and a reduced respiratory rate suggestive of a reduced sympathetic outflow. However, external heat did not affect the inactivity, and captopril, a hypotensive agent, did not mimic it. Terazosin did not impair performance on a horizontal wire test or the ability to make co-ordinated movements in a swim test suggesting that its activity-reducing effect was not due to sedation and may have a motivational or sensory gating component. It is concluded that central alpha 1-noradrenergic neurotransmission is required for behavioral activation to environmental change in the mouse and may operate on sensorimotor and motivational processes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10625064&dopt=Abstract
J Cardiovasc Pharmacol. 1993 May;21(5):786-90.
Influence of alpha 1- and alpha 2-adrenoceptor antagonist therapy on the development of hypertension in spontaneously hypertensive rats.
Young RL, Jonsson JR, Mano MT, Frewin DB, Head RJ.
Department of Clinical and Experimental Pharmacology, University of Adelaide, Australia.
There is general agreement that the sympathetic nervous system is involved in the development of hypertension in spontaneously hypertensive rats (SHR). However, in a previous study we established that chronic administration of the selective alpha 1-adrenoceptor antagonist terazosin to SHR failed to prevent this phenomenon. In the present study, we extended that investigation further by examining the effects of another selective alpha 1-antagonist (doxazosin), an alpha 2-adrenoceptor antagonist (yohimbine), and a combination of these agents. Chronic administration of doxazosin and yohimbine produced receptor blockade, as determined by their effect on blood pressure (BP) responses to norepinephrine (NE) and phenylephrine. Chronic administration of either antagonist alone or the two in combination failed to prevent the development of hypertension in SHR, however. These findings suggest that although there may be a need for involvement of the sympathetic nervous system in the development of hypertension in SHR, its influence on this process is not mediated through activation of alpha-adrenoceptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7685450&dopt=Abstract
Naunyn Schmiedebergs Arch Pharmacol. 1993 Apr;347(4):384-93.
Alpha 1-adrenoceptor-mediated inhibition of cellular cAMP accumulation in neonatal rat ventricular myocytes.
Barrett S, Honbo N, Karliner JS.
Cardiology Section, Veterans Affairs Medical Center, San Francisco, CA 94121.
We studied adrenergic regulation of cellular cAMP in neonatal rat ventricular myocytes. Since cAMP content depends on synthesis, breakdown and egress, the contribution of each of these mechanisms was assessed. In the presence of the phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine, cAMP accumulation stimulated by the beta-adrenoceptor agonist (-)-isoprenaline was diminished when the mixed alpha + beta adrenoceptor agonist (-)-noradrenaline was coincubated with (-)-isoprenaline. Moreover, adenylyl cyclase activation stimulated by (-)-isoprenaline was decreased by (-)-noradrenaline and by the selective alpha 1-adrenoceptor agonists (-)-phenylephrine and methoxamine, suggesting that alpha-adrenoceptor agonism regulates cAMP metabolism through its effect on the synthetic pathway. Evidence for alpha 1-adrenoceptor mediation of this response was enhancement of (-)-noradrenaline-induced cAMP generation by the selective alpha 1-adrenoceptor antagonist terazosin (10 nmol/l). The selective alpha 2-adrenoceptor antagonist yohimbine (10 nmol/l) had no effect. The alpha 1-adrenoceptor mediated depression of (-)-isoprenaline-stimulated cAMP generation and adenylyl cyclase activation was prevented by terazosin and in separate experiments markedly enhanced by pertussis toxin pretreatment, suggesting involvement of a guanine-nucleotide regulatory protein in this process. Occupation of the alpha 1-adrenoceptor by (-)-noradrenaline did not accelerate the rate of cAMP breakdown in the absence of phosphodiesterase inhibition. Furthermore, there was no enhancement of total phosphodiesterase activity by (-)-noradrenaline in the presence of (-)-propranolol. By contrast, pertussis toxin pretreatment augmented phosphodiesterase activity. Neither pertussis toxin nor (-)-noradrenaline increased cAMP egress. We conclude that in rat neonatal cardiac myocytes agonist occupation of the alpha 1-adrenoceptor inhibits beta-adrenoceptor stimulated cAMP accumulation most likely by coupling to a guanine nucleotide inhibitory protein.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7685501&dopt=Abstract
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