Introduction In a situation of extreme emotional or physical stress, a high plasma concentration of catecholamines, especially epinephrine (Epi), results in cardiac dysfunction. This has been linked to the development of wall motion
Lu Fu, Hongyuan Zhang, Jeremiah Ong’achwa Machuki, Tingting Zhang, Lin Han, Lili Sang, Lijuan Wu, Zhiwei Zhao, Matthew James Turley, Xide Hu, Hongjian Hou, Dongye Li, Sian E Harding, and Hong Sun
Melissa A Davis, Leticia E Camacho, Alexander L Pendleton, Andrew T Antolic, Rosa I Luna-Ramirez, Amy C Kelly, Nathan R Steffens, Miranda J Anderson, and Sean W Limesand
and hypoglycemic conditions, the fetal adrenal chromaffin cells secrete epinephrine and norepinephrine that in combination with the metabolic deficiencies inhibit insulin secretion ( Jackson et al. 2000 , Leos et al. 2010 , Benjamin et al. 2017
P Nguyen, S Khurana, H Peltsch, J Grandbois, J Eibl, J Crispo, D Ansell, and T C Tai
secretion of the catecholamine epinephrine, a neurotransmitter/neurohormone that is physiologically significant in the sympathetic control of blood pressure and cardiovascular activity ( Borkowski & Quinn 1984 , Wong 2006 ). Its synthesis and release is
A L Markel, O E Redina, M A Gilinsky, G M Dymshits, E V Kalashnikova, Yu V Khvorostova, L A Fedoseeva, and G S Jacobson
mechanisms of cardiovascular and kidney functions may contribute largely to the link. When comparisons were based on measurements of plasma corticosterone content, the response of the ISIAH rats to such stressors as restraint, heat stress, epinephrine
R P Rhoads, J W Kim, M E Van Amburgh, R A Ehrhardt, S J Frank, and Y R Boisclair
each injection period. Blood samples were obtained immediately before hormone injection at 0900 h. On day 3, epinephrine challenges were performed twice at 1000 and 1400 h, as described by Baumgard et al. (2002) . At both times, cows were administered
Júlio Cezar de Oliveira, Patrícia Cristina Lisboa, Egberto Gaspar de Moura, Luiz Felipe Barella, Rosiane Aparecida Miranda, Ananda Malta, Claudinéia Conationi da Silva Franco, Tatiane Aparecida da Silva Ribeiro, Rosana Torrezan, Clarice Gravena, and Paulo Cezar de Freitas Mathias
/l), either in the presence of 1 μmol/l epinephrine and an α 2 -adrenoceptor antagonist, yohimbine (10 μmol/l) or in the presence of epinephrine and a β 2 -adrenoceptor antagonist, propranolol (1 μmol/l). Similar to the muscarinic receptor studies, the doses
Sushil K Mahata, Hong Zheng, Sumana Mahata, Xuefei Liu, and Kaushik P Patel
overactivation and progression of HF is less well known. Circulating catecholamines, comprising dopamine (DA), norepinephrine (NE) and epinephrine (EPI), are primarily synthesized and released from the chromaffin cells of the adrenal medulla ( Goldstein et al
MA De Bortoli, MH Garraza, and LI Aguado
The present study investigates the acute consequences of central adrenergic stimulation on the release of steroids from the ovary. The influence of the superior ovarian nerve (SON) and the relationship between the neural effect and peripheral LH levels were also examined. The intracerebroventricular (i.c.v.) injection of 5 microg epinephrine in SON-intact rats on day 1 of dioestrus (D1) increased progesterone levels in ovarian vein blood from 7 to 21 min after injection but the same injection in SON-intact rats on day 2 of dioestrus (D2) decreased progesterone levels in ovarian vein blood from 1 to 25 min. A smaller dose (0.5 microg) of epinephrine injected i.c.v. in SON-intact rats produced a decrease in progesterone levels in ovarian vein blood of shorter duration. In SON-transected (SONt) animals, 0.5 microg epinephrine i.c.v. caused a smaller decrease in progesterone levels compared with SON-intact rats (P<0.05). On the other hand, in SON-intact rats on D2, the i.c. v. injection of 0.5 microg epinephrine did not modify the peripheral LH levels during 25 min, but 5 microg epinephrine injected i.c.v. raised the peripheral LH level from the third minute after injection (P<0.05). Oestradiol levels in the ovarian vein blood did not change after epinephrine i.c.v. injection in rats on D2. To avoid any humoral influence, SONt and SON-intact rats on D2 were injected i.c.v. with 5 microg epinephrine or with vehicle, and 5 min later the ovaries were incubated in vitro with or without LH. Under these conditions, it was demonstrated that the previous injection of epinephrine in SON-intact rats resulted in a diminished release of progesterone from ovaries incubated with or without LH. These results suggest that a central adrenergic stimulus increases progesterone release from the ovary on D1 and decreases it on D2. Also, this neural input would arrive at the ovary through the SON, and would condition the ovarian response to LH on D2. Ovarian progesterone changes could be attributed to signals coming from ganglionar neurons, which are affected by the central adrenergic stimulation.
J Claustre, S Brechet, P Plaisancie, JA Chayvialle, and JC Cuber
Postprandial release of peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) from L cells results from both nutrient transit in the ileal lumen and neural drive of endocrine cells. The adrenosympathetic system and its effectors have been shown to induce secretion of L cells in vivo or in vitro. Because these transmitters act through three receptors, beta, alpha1, alpha2, coupled to different intracellular pathways, we evaluated the responses of L cells to specific agonists, using the model of isolated vascularly perfused rat ileum. General stimulation of adrenergic receptors with epinephrine (10(-7) M) induced significant GLP-1 and PYY secretions (94+/-38 and 257+/-59 fmol/8 min respectively) which were abolished upon propranolol (10(-7) M) pretreatment and strongly decreased upon infusion with 10(-8) M prazosin. Blockade of alpha2-receptors with idazoxan (10(-8) M) did not alter epinephrine-induced peptide secretion. The beta-adrenergic agonist isoproterenol (10(-6) M) infused for 30 min induced a transient release of GLP-1 and PYY (integrated release over the 8 min of the peak secretion: 38+/-16 and 214+/-69 fmol for GLP-1 and PYY respectively, P<0.05). Because terbutaline but not dobutamine or BRL 37,344 (10(-5) M) induced significant GLP-1 and PYY secretions (135+/-30 and 305+/-39 fmol/8 min respectively), isoproterenol-induced secretions are suggested to result mainly from stimulation of the beta2-isoreceptor type. In contrast, the alpha1-agonist phenylephrine (10(-7) M) did not stimulate peptide release. When co-infused with 10(-6) M or 10(-7) M isoproterenol, 10(-7) M phenylephrine raised GLP-1 release to 174+/-53 and 108+/-28 fmol/8 min respectively (vs 38+/-16 and 35+/-10 fmol/8 min for isoproterenol alone, P<0.05) whereas PYY secretion was not significantly increased. Clonidine (10(-7) M), an alpha2-agonist, induced a moderate and delayed increase of GLP-1 and PYY but abolished the isoproterenol-induced peptide secretion. Our results showed that general stimulation of adrenergic receptors stimulates the secretory activity of ileal endocrine L cells. The net peptide secretion results from the activation of the beta2-isoreceptor type. Additionally, GLP-1 and PYY secretions are positively modulated by alpha1-receptor stimulation and inhibited by alpha2-receptor activation upon beta-receptor occupation.
TH Kruger, P Haake, D Chereath, W Knapp, OE Janssen, MS Exton, M Schedlowski, and U Hartmann
We have demonstrated that sexual activity produces transient sympathoadrenal activation and a pronounced, long-lasting increase in prolactin in men and women. However, by analyzing endocrine alterations at 10-min intervals, a precise assignment of these changes to the pre-, peri- and postorgasmic periods was not possible. Thus, the current study aimed to accurately differentiate the endocrine response to sexual arousal and orgasm in men using an automatic blood collection technique with 2-min sampling intervals. Blood was drawn continuously before, during and after orgasm over a total period of 40 min in 10 healthy subjects and were compared with samples obtained under a control condition. Sexual activity induced transient increases of plasma epinephrine and norepinephrine levels during orgasm with a rapid decline thereafter. In contrast, prolactin levels increased immediately after orgasm and remained elevated throughout the experiment. Although oxytocin was acutely increased after orgasm, these changes were not consistent and did not reach statistical significance. Vasopressin, LH, FSH and testosterone plasma concentrations remained unaltered during sexual arousal and orgasm. These data confirm that prolactin is secreted after orgasm and, compared with oxytocin, seems to represent a more reliable and sustained marker for orgasm in man. The results further reinforce a role for prolactin either as a neuroendocrine reproductive reflex or as a feedback mechanism modulating dopaminergic systems in the central nervous system that are responsible for appetitive behavior.