Catecholamine activation of pyruvate dehydrogenase in white adipose tissue of the rat in vivo. Regulation of mitochondrial pyruvate carboxylation and gluconeogenesis in rat hepatocytes via an alpha-adrenergic, adenosine 3':5'-monophosphate-independent mechanism. Right ventricular diastolic pressure-volume relations and regional dimensions during acute alterations in loading conditions. Rx drugs

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Biochem J. 1987 Jan 15;241(2):415-9.
Catecholamine activation of pyruvate dehydrogenase in white adipose tissue of the rat in vivo.

Kilgour E, Vernon RG.

Intraperitoneal injections of noradrenaline or adrenaline into rats increased the proportion of pyruvate dehydrogenase in the active state in white adipose tissue; this effect of catecholamines was also apparent in streptozotocin-diabetic rats, showing that it was not due to an increase in serum insulin concentration. The catecholamine-induced increase in pyruvate dehydrogenase of white adipose tissue in vivo was completely blocked by prior injection of either the beta-antagonist propranolol or the alpha 1-antagonist prazosin. Cervical dislocation of conscious rats increased pyruvate dehydrogenase activity of white adipose tissue, which was prevented by prior injection of propranolol. Adrenaline (30 nM) activated pyruvate dehydrogenase in white adipocytes in vitro; the maximum effect of adrenaline required activation of both alpha 1- and beta-receptors. The results show that catecholamines activate pyruvate dehydrogenase of white adipose tissue both in vivo and in vitro and that this effect is mediated by a combination of alpha 1- and beta-adrenergic receptors.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3297031&dopt=Abstract

J Biol Chem. 1979 Feb 25;254(4):1129-33.
Regulation of mitochondrial pyruvate carboxylation and gluconeogenesis in rat hepatocytes via an alpha-adrenergic, adenosine 3':5'-monophosphate-independent mechanism.

Garrison JC, Borland MK.

Experiments were performed to determine if catecholamines can regulate control points in the gluconeogenic pathway, such as mitochondrial pyruvate carboxylation and pyruvate kinase activity, via an alpha-adrenergic, adenosine 3':5'-monophosphate-independent mechanism. Of a number of alpha agonists tested, only norepinephrine, epinephrine, and phenylephrine caused an increase in mitochondrial pyruvate metabolism. The effects of catecholamines on pyruvate carboxylation were not attenuated by 1-propranolol which abolishes changes in cyclic nucleotide levels but were blocked by alpha antagonists such as ergotamine, phenoxybenzamine, and phentolamine. Time course experiments demonstrated that the effects of catecholamines on the mitochondria and on carbohydrate metabolism correlated temporally with the concentration of epinephrine in the medium but not with the small changes in adenosine 3':5'-monophosphate. The effects of catecholamines appeared to require extracellular Ca2+ ion. The observation that catecholamines do not increase gluconeogenesis to the same extent as glucagon was not due to a differential effect on mitochondrial CO2 fixation. Rather, catecholamines caused a smaller inhibition of pyruvate kinase activity than did glucagon. The effects of catecholamines on pyruvate kinase also appeared to be mediated by an alpha-adrenergic, adenosine 3':5'-monophosphate-independent mechanism.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=33183&dopt=Abstract

Circulation. 1988 Jun;77(6):1276-82.
Right ventricular diastolic pressure-volume relations and regional dimensions during acute alterations in loading conditions.

Dell'Italia LJ, Walsh RA.

Department of Medicine, University of Texas Health Science Center, San Antonio 78284.

Acute pharmacologically mediated parallel shifts in the left ventricular diastolic pressure-volume relation may be due to the restraining effect of the pericardium and/or leftward displacement of the interventricular septum. The existence and cause of this phenomenon in the right ventricle has not been studied in animals or in man. Accordingly, we altered right ventricular pressure with intravenous phenylephrine (0.2 to 0.3 mg) and nitroprusside (0.5 to 1.5 micrograms/kg/min) to achieve three disparate peak right ventricular pressures in nine normal subjects after partial autonomic blockade with atropine (1 mg) and propranolol (0.15 mg/kg). Simultaneous high-fidelity right ventricular pressures and biplane cineventriculographic volumes were acquired during the three resultant loading conditions. Right atrial pacing maintained heart rate constant at each pressure level. Peak right ventricular systolic pressure (23 +/- 3 vs 31 +/- 9 vs 45 +/- 6 mm Hg, all p less than .01) and right ventricular end-diastolic pressure (4 +/- 2 vs 8 +/- 4 vs 11 +/- 3 mm Hg, all p less than .01) were significantly different at low, medium, and high loading conditions, respectively. Right ventricular diastolic pressure-volume relations were, in parallel, shifted upward with altered loading in each patient. This was manifest by an unchanged dynamic chamber stiffness constant and a significant increase in the diastolic pressure volume y intercept at each load (1.98 +/- 2.21 vs 5.33 +/- 5.39 vs 8.51 +/- 3.99 mm Hg, p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3370767&dopt=Abstract

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