Catecholamine stimulation

Lovstad, R.A. (1984). Catecholamine stimulation of copper-dependent haemolysis protective action of superoxide dismutase, catalase, hydroxyl radical scavengers and scrum proteins (ceruloplasmin, albumin and apotransferrin). Acta Pharmacol. Toxicol. 54, 340-345. 

Kessar, P. and Sa erson, E.D. (1980). Evidence that catecholamines stimulate renal gluconeogenesis through a-type of adrenoceptor. Biochem. J. 190, 119-123. 

Singh AP, Shanker K, Parvez SH. 1984. Effect of Kepone on catecholamine-stimulated sodium, potassium-ATPase of rat brain. Biogenic Amines 1 (4) 313-318. 

Kaye and Fainstat 1987 Wooten et al. 1983). The risk of cerebral hemorrhage is even greater when combining ephedrine with other catecholamine stimulants such as the over-the-counter stimulant phenyl-propanolamine (StoessI et al. 1985). Pseudoephedrine may be safer than ephedrine in some respects (Porta et al. 1986). In a large sample (n > 100,000) of pseudoephedrine users, there were no reports of cerebrovascular disorders within 15 days after administration. The incidence of myocardial infarction, seizures, and neuropsychiatric disorders were no greater than base rates in the general population. 

Hajo-Tello N, Dupont C, Wepierre J, Cohen Y, Miller R, Godfraind T. (1985). Effects of tabernanthine on calcium and catecholamine stimulated contractions of isolated vascular and cardiac muscle. Arch Int Pharmacodyn Then 276(1) 35-43. 

Propranolol decreases Purkinje fiber membrane responsiveness and reduces action potential amplitude. His-Purkinje tissue excitability also is reduced. These changes result in a decrease in His-Purkinje conduction velocity. However, these electrophysiological alterations are observed at propranolol concentrations in excess of those normally used in therapy. The most striking electrophysiological property of propranolol at usual therapeutic concentrations is a depression of catecholamine-stimulated automaticity. 

Many of the manifestations of thyroid hyperactivity resemble sympathetic nervous system overactivity (especially in the cardiovascular system), although catecholamine levels are not increased. Changes in catecholamine-stimulated adenylyl cyclase activity as measured by cAMP are found with changes in thyroid activity. Possible explanations include increased numbers of 13 receptors or enhanced amplification of the 13 receptor signal. Other clinical symptoms reminiscent of excessive epinephrine activity (and partially alleviated by adrenoceptor antagonists) include lid lag and retraction, tremor, excessive sweating, anxiety, and nervousness. The opposite constellation of effects is seen in hypothyroidism (Table 38-4). 

LaMonica DA, Frohloff N, Dobson JG (1985) Adenosine inhibition of catecholamine-stimulated cardiac membrane adenylate cyclase. Am J Physiol 248(5 Pt 2) H737-H744 Lasley RD, Narayan P, Jahania MS, Partin EL, Kraft KR, Mentzer RM Jr (1999) Species-dependent hemodynamic effects of adenosine A,-receptor agonists IB-MECA and Cl-IB-MECA. Am J Physiol 276 6 Pt 2 H2076-H2084... 

Kranias, E.G., and Solaro, R.J., 1982, Phosphorylation of troponin I and phospholamban during catecholamine stimulation of rabbit heart. Nature, 298(5870), pp 182-4. 

Metabolic effects Prostaglandin Ej inhibits basal and catecholamine-stimulated lipo-lysis. 

The authors speculated that cocaine and amfeta-mine-induced catecholamine stimulation of a-adrenocep-tors may cause intense vasoconstriction and thus a reduced blood supply to an ulcer, resulting in a giant ulcer. 

All three subtypes of P-ARs are expressed in the heart (73). Despite the existence of species-related differences (reviewed in ref. 74), prARs are the predominant form of ARs. The positive chronotropic and inotropic response of the heart to catecholamine stimulation is mediated almost exclusively by prARs (75-77). Coupling of (32-ARs to cardiac contractility is less defined and species related, showing a positive effect in human hearts (77) but not affecting contractility in the mouse (75). Better defined is the role of P2-ARs in the regulation of vascular tone and blood pressure (78). P3-ARs, atypical P-ARs, are expressed in the adipose tissue, where they mediate lipolysis and thermogenesis (79,80), and in smooth muscle cells, where they mediate vasorelaxation (81). 

Gao MH, Lai NC, Roth DM, et al. Adenylyl cyclase increases responsiveness to catecholamine stimulation in transgenic mice. Circulation 1999 99 1618-1622. 

The previous review mentioned CN-induced changes in myocardial, calcium, and as factors in myocardial depression caused by this agent. Marked CN-induced increases in circulating catecholamine stimulate the heart,but, at the same time, energy metabolism is impaired and heart failure results. ... 

An anti-lipolytic signal is transduced by the otj-adrenergics, and the a,-adrenergics are involved in a separate pathway. In short, although lipolysis is the observed outcome of catecholamine stimulation, it is the steady-state result of competition between two opposing pathways triggered by the same signal. 

Asano,T., Pedersen, S. E., Scott, C. W and Ross, E. M. (1984) Reconstitution of catecholamine-stimulated binding of guanosine 5 -0-(3-thiotriphosphate) to the stimulatory GTP-binding protein of adenylate cyclase. Biochemistry 23,5460-5467... 

Carlson, L. A., Studies on the effect of nicotinic acid on catecholamine stimulated lipolysis in adipose tissue, Acta med. scand. 173, 719 (1963). 

Since endothelial and vascular smooth muscle cells can rapidly synthesize and metabolize histamine, a possible homeostatic role for histamine in cardiovascular physiology has been suggested (Gross et al., 1984). Catecholamine-stimulated histamine release from vascular tissue (Schayer, 1960 Rand et al., 1982) may function to attenuate the effect of catecholamines on heart rate, contractility, and coronary resistance (Gross et ai, 1984 Giacomini and Reis, 1986). Histamine may exert its effects on catecholamine activity by forcing an uncoupling of the P-receptor from the transductional protein, Gs (Levi et ai, 1991). 

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