Drugs online research references
Circ Res. 1985 Jun;56(6):884-94.
Stimulation of hypertrophy of cultured neonatal rat heart cells through an alpha 1-adrenergic receptor and induction of beating through an alpha 1- and beta 1-adrenergic receptor interaction. Evidence for independent regulation of growth and beating.
Simpson P.
Catecholamines may be one of the molecular signals linking increased circulatory demand to myocardial hypertrophy, and I have found previously that norepinephrine stimulates hypertrophy of cultured neonatal rat heart muscle cells through an alpha 1-adrenergic receptor. Since catecholamine stimulation of contractility is believed to be under beta-adrenergic control, I asked whether these cultured heart cells had dual pathways regulating growth and contractility through alpha- and beta-adrenergic receptors, respectively. I examined the effect of adrenergic agents on hypertrophy and beating of myocytes in serum-free cultures. Hypertrophy was defined as an increase in myocyte surface area and in cell protein content, measured by a radioisotopic method, and chronotropic activity was examined visually. Norepinephrine and epinephrine were equipotent stimulants of hypertrophy and beating, increasing cell protein and area 1.5- to 2-fold, and the proportion of beating cells from 5% or less to 95%. Response maxima occurred 24-48 hours after exposure, and EC50 were 20-200 nM. Studies with other agonists (phenylephrine, methoxamine, clonidine, isoproterenol, dopamine) and antagonists (prazosin, terazosin, yohimbine, propranolol, betaxolol, ICI 118,551) indicated that hypertrophy was mediated through an alpha 1-adrenergic receptor, whereas the induction of beating required both alpha 1- and beta 1-receptor activation. Hypertrophied cells with minimal beating were produced by alpha-stimulation, alone. In contrast, alpha-plus beta-stimulation in the presence of cycloheximide to inhibit protein synthesis resulted in maximum beating but no hypertrophy. These findings imply that growth and beating can be regulated independently through separate cellular pathways.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2988814&dopt=Abstract
Proc Natl Acad Sci U S A. 1986 Nov;83(21):8348-50.
Cardiac myocyte hypertrophy is associated with c-myc protooncogene expression.
Starksen NF, Simpson PC, Bishopric N, Coughlin SR, Lee WM, Escobedo JA, Williams LT.
The mechanism of hormonally induced cell hypertrophy is unknown. Stimulation of cardiac myocytes by alpha 1-adrenergic agents, phorbol esters, and serum induces an increase in the cell size of nondividing cardiac myocytes in primary culture. Expression of the c-myc gene, known to be increased in growth factor-induced cell division, was studied in this model of cell hypertrophy. The alpha-adrenergic agonist norepinephrine (0.002-20 microM) increased levels of c-myc-encoded mRNA to 10-fold over control levels. This increase was detectable at 30 min, peaked at 2 hr, and returned to baseline by 6 hr after stimulation. The norepinephrine response was abolished by the alpha 1-antagonist terazosin (2 microM) but was not affected by the beta-adrenergic antagonist propranolol (2 microM) and was only slightly (25%) attenuated by the alpha 2-adrenergic antagonist yohimbine (2 microM). Serum and the phorbol ester tumor promoter phorbol 12-myristate 13-acetate also enhanced c-myc expression in cardiac myocyte cultures. These findings show that the induction of cardiac myocyte hypertrophy is associated with enhanced expression of the c-myc gene and suggest that hormonally induced cell hypertrophy and cell division share common mechanistic pathways.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3022291&dopt=Abstract
Circ Res. 1988 Jul;63(1):126-34.
Role of adrenoceptors and dopamine receptors in modulating left ventricular diastolic function.
Lang RM, Carroll JD, Nakamura S, Itoh H, Rajfer SI.
Section of Cardiology, University of Chicago, IL 60637.
Although both dopamine and dobutamine are potent positive inotropic agents, multiple studies indicate that dopamine may produce a rise in left ventricular (LV) filling pressure, while dobutamine often has the opposite effect. To ascertain the pharmacological and hemodynamic mechanisms responsible for the elevation in LV filling pressure observed with dopamine, we administered incremental infusions (2, 4, and 6 micrograms/kg/min) of dopamine to 18 open-chest, anesthetized dogs in the presence and absence of rauwolscine (selective alpha 2-adrenoceptor antagonist) (n = 7), terazosin (selective alpha 1-antagonist) (n = 6), and domperidone (selective dopamine2 antagonist) (n = 5), while measuring pressures in the LV and left atrium and changes in dimension in the LV short-axis (with ultrasonic piezo crystals). Dobutamine (2, 4, and 6 micrograms/kg/min) was infused in five additional dogs before and after administration of rauwolscine. The time constant of isovolumic pressure decay, peak lengthening rate (mm/sec), LV end-diastolic pressure, and diastolic pressure-dimension relation were computed. A significant elevation in LV end-diastolic pressure and a parallel increase in LV end-diastolic chamber size was observed with dopamine, while a decline in LV end-diastolic pressure occurred with dobutamine. Yet both dopamine and dobutamine caused a dose-related acceleration of pressure decay and augmentation of peak lengthening rate. Furthermore, heart rate declined during the administration of dopamine but rose with dobutamine. In the presence of either rauwolscine or terazosin, dopamine infusion resulted in a positive chronotropic effect and dose-dependent reductions in LV end-diastolic pressure and end-diastolic chamber dimension; arterial pressure fell only after terazosin administration.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3383371&dopt=Abstract
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