Drugs online research references
J Appl Physiol. 1990 Mar;68(3):973-8.
Influence of thyroid hormones and catecholamines on myosin of swim-exercised rats.
Rupp H, Wahl R.
Institute of Physiology II, University of Tubingen, Federal Republic of Germany.
To define the physiological signals involved in the redirection of myosin expression in the swim-exercised rat, the relative influence of thyroid hormones and beta-adrenergic blockade was determined. Swimming exercise resulted in an increased proportion of myosin V1 (60.9 +/- 9.7 vs. 38.0 +/- 4.1% of sedentary rats fed ad libitum) but did not increase serum concentrations of total and free thyroxine or triiodothyronine determined either 17-21 h or immediately after swimming. The proportion of V1 increased, although intermittently food-deprived rats with the body weight of swimming rats exhibited a reduced proportion of V1 (23.5 +/- 2.7). When swimming rats had only intermittent access to food, they had reduced concentrations of all thyroid hormones, but the proportion of V1 (51.5 +/- 7.6) was nonetheless increased. Thus the redirection of myosin expression cannot be attributed to an increased secretion of thyroid hormones. The influence of the adrenergic system was assessed by treating swimming rats with the beta-blocking drug atenolol. Because the proportion of V1 was reduced, but thyroid hormones were not affected, beta-adrenergic blockade seems to influence myosin expression independently of thyroid hormones.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2140349&dopt=Abstract
Pediatr Res. 1988 Apr;23(4):393-7.
Atenolol enhances growth hormone release to exogenous growth hormone-releasing hormone but fails to alter spontaneous nocturnal growth hormone secretion in boys with constitutional delay of growth.
Martha PM Jr, Blizzard RM, Rogol AD.
Department of Pediatrics, University of Virginia, School of Medicine, Charlottesville 22908.
We tested the hypothesis that selective beta 1-adrenergic blockade will enhance growth hormone (GH) secretion in boys with constitutional delay of growth in response to both exogenously administered growth hormone-releasing hormone as well as to endogenous GH-releasing hormone pulsations. The study group comprised eight healthy, short, prepubertal boys ranging from 7 2/12 to 15 0/12 yr old with bone ages delayed 15 to 42 months. All had demonstrated GH levels of greater than 10 ng/ml following a pharmacologic or physiologic stimulus. During two consecutive nights, blood samples were withdrawn every 20 min for GH determination between 2000 and 0800 h. Immediately after each 0800 h blood withdrawal, 1 microgram/kg of GH-releasing hormone (1-40)-OH was administered intravenously to each subject and blood was withdrawn every 15 min for an additional 2 h. During the day before the second overnight sampling period each subject received atenolol, 25 mg orally, at 1030 and 1600 h to induce beta-adrenergic blockage. The six subjects in whom beta-adrenergic blockade could be documented had enhanced GH release after GH-releasing hormone administration on the atenolol treatment day both in terms of higher peak GH levels achieved (p less than 0.05) as well as greater total GH secretion (3916 +/- 701 versus 5624 +/- 986 ng/ml.min, p less than 0.01). In contrast, there were no differences in endogenous, unstimulated nocturnal GH pulse characteristics between study and control days.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3131726&dopt=Abstract
Life Sci. 1989;44(23):1767-75.
Beta 1-adrenoceptors in rat hepatoma. Desensitization by isoproterenol and phorbol-myristate-acetate.
Garcia-Sainz JA, Alcantara R, Hernandez-Sotomayor SM, Mas-Oliva J.
Instituto de Fisiologia Celular, Universidad Nacional Autonoma de Mexico, D.F., Mexico.
The beta-adrenergic responsiveness of hepatocytes obtained from hypothyroid rats and of a transplantable hepatoma cell line (AS-30D) were studied by measuring the accumulation of cyclic AMP. The potency order for agonists in hepatocytes was: isoproterenol greater than epinephrine much greater than norepinephrine whereas in the hepatoma cells the potency order was: isoproterenol greater than norepinephrine greater than or equal to epinephrine. The effect of isoproterenol was antagonized in hepatocytes by low concentrations of ICI 118551 and only partially by concentrations of atenolol as high as 100 microM. In hepatoma cells the effect of isoproterenol was inhibited by both antagonists with the potency order atenolol greater than ICI 118551. These data indicate that in hepatocytes the effect is mediated by beta 2-adrenoceptors whereas in hepatoma cells it is through beta 1-adrenoceptors. Preincubation of hepatoma cells with isoproterenol or phorbol-myristate-acetate diminished the subsequent beta-adrenergic responsiveness of the cells. Interestingly, when both isoproterenol and phorbol-myristate-acetate were present during the preincubation the beta-adrenergic desensitization observed was bigger than that induced by any of these agents alone.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2543879&dopt=Abstract
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