Drugs online research references
Brain Res Mol Brain Res. 1993 Jun;18(4):311-5.
Neuropeptide Y increases the corticotropin-releasing factor messenger ribonucleic acid level in the rat hypothalamus.
Suda T, Tozawa F, Iwai I, Sato Y, Sumitomo T, Nakano Y, Yamada M, Demura H.
Department of Medicine, Tokyo Women's Medical College, Japan.
Neuropeptide Y (NPY) has a stimulatory effect on adrenocorticotropin (ACTH) and corticotropin-releasing factor (CRF) release. In the present study, to investigate the effect of NPY on CRF synthesis, the effect of centrally administered NPY on CRF messenger RNA (mRNA) levels in rat hypothalamus was examined under pentobarbital anesthesia. The administration of 0.01, 0.1 and 1 nmol of NPY into the lateral ventricle dose-dependently Increased the plasma ACTH levels, as well as the levels of proopiomelanocortin mRNA in the anterior pituitary. The CRF mRNA level in the hypothalamus also increased after administration of 0.1 and 1 nmol of NPY in a dose-dependent manner. The administration of 3 nmol of phentolamine or propranolol failed to block 0.1 nmol NPY-induced ACTH release or 1 nmol NPY-stimulated CRF mRNA levels in the hypothalamus. These results Indicate that the central administration of NPY increases the CRF mRNA levels in the hypothalamus and the probable CRF release, which increases the proopiomelanocortin mRNA levels and ACTH secretion in the anterior pituitary. Therefore, NPY seems to play a physiological role in the regulation of the release and synthesis of CRF in the hypothalamus.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8392133&dopt=Abstract
J Appl Physiol. 1993 Jun;74(6):2860-7.
High lactate and NH3 release during arm vs. leg exercise is not due to beta-adrenoceptor stimulation.
Jensen-Urstad M, Ahlborg G, Sahlin K.
Department of Clinical Physiology, Sodersjukhuset, Stockholm, Sweden.
To investigate the differences in metabolic response between arm exercise (AE) and leg exercise (LE) and to elucidate the underlying mechanisms, seven men were studied during 20 min of AE or LE both with (beta) and without (control, C) nonselective beta-blockade (beta B) (propranolol). The work loads corresponded to 59 and 60% of peak pulmonary O2 uptake (VO2) during LE and AE, respectively. Pulmonary VO2 increased more slowly at the onset of exercise during AEC (half time = 61 +/- 9 s) than during LEC (half time = 35 +/- 3 s) and was not affected by beta B. At the onset of exercise the arteriovenous O2 difference across the exercising limb increased above that of steady state during AEC but not during LEC. This demonstrates that the adjustment of O2 delivery is slower than that of arm VO2 during AE. Despite the smaller exercising muscle mass, the release of lactate and NH3 was about twofold higher during AEC than during LEC. The difference in metabolic response between AE and LE was not altered by beta B. Lactate release was not reduced by beta B but, if anything, tended to increase during both AE and LE (beta vs. C). beta B increased NH3 release during LE (beta vs. C) but not during AE (beta vs. C). We conclude that AE compared with LE at the same relative work load is associated with a greater release of lactate and NH3, indicating a more severe metabolic stress during AE. Furthermore, the present data suggest that the increase in blood lactate at these submaximal exercise intensities is caused by factors other than beta-adrenoceptor stimulation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8396108&dopt=Abstract
Acta Physiol Scand. 1998 Nov;164(3):309-15.
Beta-adrenergic stimulation of cellular K+ uptake in rat distal colon.
Aizman R, Aizman O, Celsi G.
Department of Woman and Child Health, Astrid Lindgren Children's Hospital, Karolinska Institutet, Stockholm, Sweden.
We recently demonstrated that the ratio between colonic K+ absorptive and K+ secretive pathways was higher in infant than in adult rats. To test the hypothesis that hormones selectively affect these pathways during ontogeny we examined the effect of adrenergic agonists on cellular K+ uptake in distal colon from infant (10-day-old) and adult (50-day-old) rats. Here we describe that adrenaline (10(-5) M) increased total and ouabain-insensitive 86Rb uptake in both age groups, but it did not affect ouabain-sensitive 86Rb uptake. This stimulation was more pronounced in adult than in infant rats. The effect of adrenaline was mediated via beta-adrenergic receptors. Incubation in vitro with beta-agonist, isoproterenol, stimulated SCH-28080-sensitive, i.e. H+, K(+)-ATPase-dependent, 86Rb uptake in adult but not in infant rats. The threshold dose of beta-agonist was at 10(-7) M, and the maximal activation was observed at 10(-5) M. In vivo inhibition of beta-adrenergic system with propranolol caused a significant decrease in H+, K(+)-ATPase-dependent 86Rb uptake in infant but not in adult colon. In conclusion, this study suggests that the higher colonic K+ absorption in infant rats may be as a result of a selective beta-adrenergic up-regulation leading to stimulation of the apical H+, K(+)-ATPase.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9853019&dopt=Abstract
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