Drugs online research references
Biol Psychiatry. 1991 Jan 15;29(2):127-38.
The cholinergic-adrenergic hypothesis of depression reexamined using clonidine, metoprolol, and physostigmine in an animal model.
Hasey G, Hanin I.
Department of Psychiatry, Faculty of Medicine, University of Toronto, Ontario, Canada.
The role of central nervous system (CNS) cholinergic and noradrenergic mechanisms in the pathogenesis of depression and hypothalamic-pituitary-adrenal (HPA) axis hyperactivity is examined using the Behavioral Despair rat model of depression. Immobility (IM), the analog of depression in this model, and plasma corticosterone (C) were increased by physostigmine (PHYSO). Neostigmine (NEO), which does not cross the blood-brain barrier, produced the same peripheral cholinomimetic effects and motor inhibition as PHYSO, but did not change IM. PHYSO's effects on C and IM were blocked by metoprolol pretreatment and partially blocked by clonidine pretreatment. PHYSO increased acetylcholine in the striatum. In this animal model of depression, cholinergic and noradrenergic mechanisms are interactively involved in the regulation of behavioral depression and the HPA axis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1847308&dopt=Abstract
Basic Res Cardiol. 1985 Nov-Dec;80(6):642-52.
Prevention of hypertensive hypertrophy by medical therapy: effects on systolic wall stress and systolic function.
Motz W, Strauer BE.
Left ventricular (LV) hypertrophy and LV systolic pumping function of spontaneously hypertensive rats (SHR) treated for 40 weeks with hydralazine (n = 8), metoprolol (n = 8) and both metoprolol and hydralazine (n = 9) were compared with those of 25 age-matched untreated SHR. LV pressure (PLV), peak systolic wall stress (SWS), cardiac index (CI), LV ejection fraction (EF), LV muscle mass to body weight ratio (LV/BW) and the mass volume ratio (M/V) were determined. In the rats treated with hydralazine and metoprolol and hydralazine combined PLV was 28.7% (129 +/- 19 mm Hg) and 31.5% (124 +/- 17 mm Hg) lower compared to the untreated control group (181 +/- 18 mm Hg). In spite of the same amount of blood pressure reduction, LV hypertrophy was less expressed after treatment with metoprolol and hydralazine than after hydralazine only (LV/BW: 2.48 +/- 0.17 versus 2.67 +/- 0.24 mg/g, p less than 0.01; M/V: 2.43 +/- 0.59 versus 3.09 +/- 0.47 mg/microliter, p less than 0.05 respectively). In the group treated with metoprolol and hydralazine LV systolic ejection function parameters (CI, EF) did not differ from those untreated due to an unchanged LV afterload as demonstrated by identical systolic wall stress values (169 +/- 43.4 X 10(3) versus 171 +/- 26.0 X 10(3) dyn/cm2, ns). The identical systolic wall stress values indicate that cardiac hypertrophy had regressed in proportion to the reduced LV peak systolic pressure. Following hydralazine therapy systolic wall stress was even lower (140 +/- 26.5 X 10(3) dyn/cm2) in comparison to the untreated group (171 +/- 26.0 X 10(3) dyn/cm3, p less than 0.05). This reflects an inappropriate low muscle mass reduction in relation to blood pressure reduction. In conclusion (I) antihypertensive therapy with an arteriolar vasodilator in combination with a beta-receptor blocker is more effective in preventing cardiac hypertrophy than therapy with a vasodilator only. (II) Myocardial working capacity remained unaltered after prevention of cardiac hypertrophy as well as LV pumping function.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2936329&dopt=Abstract
J Clin Endocrinol Metab. 1982 Aug;55(2):341-6.
Trophoblastic cells of the hydatidiform mole contain a beta 1-subtype adrenergic receptor.
Moore JJ Jr, Workman L, Whitsett JA.
Both beta 1- and beta 2-adrenergic receptors have been previously described in normal human placental homogenates; the cells upon whose surface membranes these receptors reside have not been identified. In order to show that a beta 1-adrenergic receptor is present on trophoblastic cells, the cells which mediate maternal-fetal transport and produce placental hormones, beta-adrenergic receptors were demonstrated in membrane fractions of human hydatidiform mole. Microscopic sections of the mole samples used demonstrated edematous villi lined by trophoblastic cells with minimal nontrophoblastic (stromal or vascular) contamination compared with placenta. (--)-[3H]Dihydroalprenolol [(--)-[3H]DHA] binding to molar membranes was reversible and saturable to a single class of sites (Kd = 0.97 +/- 0.12 nM; n = 7; maximum binding capacity, 72.9 +/- 6.4 fmol/mg protein). (--)-[3H]DHA binding was associated with catecholamine-stimulated adenylate cyclase activity. Agonist competition for the molar beta-adrenergic receptor showed the order of potency to be (--)isoproterenol much greater than norepinephrine = epinephrine, characteristic of a beta 1-adrenergic receptor subtype. Competition for (--)-[3H]DHA binding to trophoblastic membranes by the beta-adrenergic receptor subtype-specific agents metoprolol (beta 1 selective) and zinterol (beta 2 selective) was also characteristic of a homogeneous subtype of beta 1-adrenergic receptors. Because beta 1-adrenergic receptors alone were seen on trophoblast cells, the beta 2-adrenergic receptor in placenta must reside on nontrophoblastic elements (stromal or vascular endothelium). No differences in beta-adrenergic receptor binding were seen related with ploidy (2 or 3 N), the presence or absence of a fetus, or the progression of the mole to choriocarcinoma. Two choriocarcinoma cell lines, BeWo and JEG-3, however, showed no specific (--)-[3H]DHA binding. Human trophoblast contains beta 1-adrenergic receptors coupled to catecholamine-sensitive adenylate cyclase, supporting a role for catecholamines in the regulation of placental metabolism.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6282922&dopt=Abstract
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