Drugs online research references
Neuroendocrinology. 1993 Apr;57(4):670-7.
Activation of the adrenergic beta-receptor stimulates prolactin release from primary cultured pituitary cells.
Shin SH, Barton RE.
Department of Physiology, Queen's University, Kingston, Canada.
Prolactin release from primary cultured pituitary cells was investigated using a dynamic perifusion system. Although epinephrine (1 mumol/l) produced an elevation in the mean value of the prolactin concentration at the onset of the perifusion, the elevation was not statistically significant, and the overall effect of the epinephrine was to produce an inhibition of prolactin release. The alpha- and D2-receptors of the primary cultured cells were functionally removed by a pretreatment with phenoxybenzamine (0.1 or 1 mumol/l). Since phenoxybenzamine irreversibly inactivates both the adrenergic alpha- and the D2-receptors but does not block the beta-receptors, the enhanced stimulatory action of the epinephrine (1 mumol/l) on the phenoxybenzamine pretreated cells suggests the involvement of adrenergic beta-receptors in prolactin release. Perifusion of isoproterenol (1 mumol/l), a beta-receptor agonist, stimulated prolactin release. This stimulation was blocked by beta-receptor antagonism with propranolol (1 mumol/l) supporting the implication of the beta-receptor in prolactin release. In order to differentiate between beta 1- and beta 2-receptor involvement, we investigated the effects of ICI 118,551 (1 mumol/l) on isoproterenol-induced prolactin release. ICI 118,551, a selective beta 2-receptor antagonist, blocked the stimulatory action of isoproterenol on prolactin release indicating that the beta-receptor responsible for the stimulation of prolactin release belongs to the beta 2-receptor family. Moreover, the demonstration that salbutamol, a selective beta 2-receptor agonist, stimulated prolactin secretion offers further evidence in support of the role of the beta 2-receptor in the stimulation of prolactin release.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8396220&dopt=Abstract
J Electrocardiol. 1993 Jul;26(3):219-23.
Effect of autonomic blockade on digoxin-induced ECG changes at rest and during exercise in healthy subjects.
Sundqvist K, Jogestrand T.
Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden.
The effect of pharmacological autonomic blockade on digoxin-induced electrocardiographic changes at rest and during exercise was studied in nine healthy men. The subjects performed bicycle exercise tests on four occasions after: (1) intravenous injection of sodium chloride, (2) intravenous injection of propranolol and atropine, (3) oral ingestion of digoxin 0.5 mg daily for 2 weeks and intravenous injection of sodium chloride, and (4) oral ingestion of digoxin 0.5 mg daily for 2 weeks and intravenous injection of propranolol and atropine. The ST-T segment was significantly depressed after digoxin plus sodium chloride and digoxin plus propranolol and atropine in comparison with sodium chloride only and propranolol and atropine only. The digoxin-induced ST-T changes after sodium chloride and propranolol-atropine injections were not significantly different. Thus, judging from the results of this study, an effect mediated via the autonomic nervous system is an unlikely explanation of digitalis-induced ST-T changes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8409815&dopt=Abstract
Am J Obstet Gynecol. 1993 Feb;168(2):605-11.
Possible physiologic role of calcitonin gene-related peptide in the human uterine artery.
Nelson SH, Steinsland OS, Suresh MS.
Department of Anesthesiology, University of Texas Medical Branch, Galveston 77555-0749.
OBJECTIVE: The purpose of our study was to determine the potential physiologic role of calcitonin gene-related peptide as an endogenous vasodilator of human uterine arteries during pregnancy. STUDY DESIGN: Isolated, suffused uterine arteries from pregnant patients (n = 9) and nonpregnant patients (n = 19) were used in the study. RESULTS: Calcitonin gene-related peptide (1 nmol/L to 0.1 mumol/L) produced a concentration-dependent relaxation of norepinephrine (1 mumol/L)-induced contractions. The values of calcitonin gene-related peptide that inhibited norepinephrine-induced contractions by 50% were 0.9 +/- 0.7 nmol/L (n = 8) and 6.5 +/- 1.5 nmol/L (n = 12) in pregnant and nonpregnant arteries, respectively. The calcitonin gene-related peptide-induced relaxation was not affected by propranolol (1 mumol/L), indomethacin (5 mumol/L), methylene blue (10 mumol/L), or by the removal of the endothelium. The relaxant effect of calcitonin gene-related peptide was inhibited by human calcitonin gene-related peptide(8-37). The endogenous levels of calcitonin gene-related peptide were 110.2 +/- 13.5 pmol/L/gm wet weight in pregnant arteries and 14.8 +/- 3.2 pmol/L/gm wet weight in nonpregnant arteries. CONCLUSIONS: These results demonstrate that the vasodilatory effect of calcitonin gene-related peptide is mediated by calcitonin gene-related peptide1 receptors and does not involve beta-adrenoceptors, vasodilator prostanoids, increased levels of guanosine 3',5'-cyclic monophosphate, or endothelium-derived relaxing factor. The findings that calcitonin gene-related peptide acts as a potent dilator and that pregnancy increases both the sensitivity to calcitonin gene-related peptide and the endogenous levels of calcitonin gene-related peptide support the view that calcitonin gene-related peptide has a physiologic role in dilating the uterine vasculature, especially during pregnancy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8438937&dopt=Abstract
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