β-Adrenergic receptors and stimulatory effects of (−) isoproterenol on testosterone production in fetal mouse Leydig cells

1988 ◽  
Vol 151 (3) ◽  
pp. 1454-1460 ◽  
Author(s):  
M. Breuiller ◽  
A. Tahri-Joutei ◽  
F. Ferré ◽  
G. Pointis
Keyword(s):  
Adrenergic Receptors ◽  
Leydig Cells ◽  
Fetal Mouse ◽  
Testosterone Production ◽  
Β Adrenergic Receptors

Sustained in vivo blockade of α1-adrenergic receptors prevented some of stress-triggered effects on steroidogenic machinery in Leydig cells

2013 ◽  
Vol 305 (2) ◽  
pp. E194-E204 ◽  
Author(s):  
Natasa J. Stojkov ◽  
Marija M. Janjic ◽  
Aleksandar Z. Baburski ◽  
Aleksandar I. Mihajlovic ◽  
Dragana M. Drljaca ◽  
...  
Keyword(s):  
Adrenergic Receptors ◽  
Leydig Cells ◽  
High Affinity ◽  
Testosterone Production ◽  
Transcription Profiles ◽  
Steroidogenic Cells ◽  
Main Regulator ◽  
Stimulatory Factor

This study was designed to systematically analyze and evaluate the effects of in vivo blockade of α1-adrenergic receptors (α1-ADRs) on the stress-induced disturbance of steroidogenic machinery in Leydig cells. Parameters followed 1) steroidogenic enzymes/proteins, transcription factors, and cAMP/testosterone production; 2) the main hallmarks of stress (epinephrine, glucocorticoids); and 3) transcription profiles of ADRs and oxidases with high affinity to inactivate glucocorticoids. Results showed that sustained blockade of α1-ADRs prevented stress-induced 1) decrease of the transcripts/proteins for main steroidogenic CYPs (CYP11A1, CYP17A1); 2) decrease of Scarb1 and Hsd3b1 transcripts; 3) decrease of transcript for Nur77, one of the main activator of the steroidogenic expression; and 4) increase of Dax1 and Arr19, the main steroidogenic repressors in Leydig cells. In the same cells, the expression of steroidogenic stimulatory factor Creb1, StAR, and androgen receptor increased. In this signaling scenario, stress-induced stimulation of Adra1a/Adra1b/Adrbk1 and Hsd11b2 (the unidirectional oxidase with high affinity to inactivate glucocorticoids) was not changed. Blockade additionally stimulated stress-increased transcription of the most abundantly expressed ADRs Adra1d/Adrb1/Adrb2 in Leydig cells. In the same cells, stress-decreased testosterone production, the main marker of Leydig cells functionality, was completely prevented, while reduction of cAMP, the main regulator of androgenesis, was partially prevented. Accordingly, the presented data provide a new molecular/transcriptional base for “fight/adaptation” of steroidogenic cells and new molecular insights into the role of α1-ADRs in stress-impaired Leydig cell steroidogenesis. The results are important in term of wide use of α1-ADR selective antagonists, alone/in combination, to treat high blood pressure, nightmares associated with posttraumatic stress disorder, and disrupted sexual health.

Repeated immobilization stress disturbed steroidogenic machinery and stimulated the expression of cAMP signaling elements and adrenergic receptors in Leydig cells

2012 ◽  
Vol 302 (10) ◽  
pp. E1239-E1251 ◽  
Author(s):  
Natasa J. Stojkov ◽  
Marija M. Janjic ◽  
Maja M. Bjelic ◽  
Aleksandar I. Mihajlovic ◽  
Tatjana S. Kostic ◽  
...  
Keyword(s):  
Adrenergic Receptors ◽  
Leydig Cells ◽  
Immobilization Stress ◽  
Regulatory Protein ◽  
Camp Signaling ◽  
Partial Recovery ◽  
Transcription Analysis ◽  
Releasing Hormone ◽  
Testosterone Production ◽  
Glucocorticoid Signaling

This study was designed to evaluate the effect of acute (2 h daily) and repeated (2 h daily for 2 or 10 consecutive days) immobilization stress (IMO) on: 1) the steroidogenic machinery homeostasis; 2) cAMP signaling; and the expression of receptors for main markers of 3) adrenergic and 4) glucocorticoid signaling in Leydig cells of adult rats. The results showed that acute IMO inhibited steroidogenic machinery in Leydig cells by downregulation of Scarb1 (scavenger receptor class B), Cyp11a1 (cholesterol side-chain cleavage enzyme), Cyp17a1 (17α-hydroxylase/17,20 lyase), and Hsd17b3 (17β-hydroxysteroid dehydrogenase) expression. In addition to acute IMO effects, repeated IMO increased transcription of Star (steroidogenic acute regulatory protein) and Arr19 (androgen receptor corepressor 19 kDa) in Leydig cells. In the same cells, the transcription of adenylyl cyclases (Adcy7, Adcy9, Adcy10) and cAMP-specific phosphodiesterases ( Pde4a, Pde4b, Pde4d, Pde7a, Pde8a) was stimulated, whereas the expression of the genes encoding protein kinase A subunits were unaffected. Ten times repeated IMO increased the levels of all adrenergic receptors and β-adrenergic receptor kinase ( Adrbk1) in Leydig cells. The transcription analysis was supported by cAMP/testosterone production. In this signaling scenario, partial recovery of testosterone production in medium/content was detected. The physiological significance of the present results was proven by ex vivo application of epinephrine, which increased cAMP/testosterone production by Leydig cells from control rats in greater fashion than from stressed. IMO did not affect the expression of transcripts for Crhr1/Crhr2 (corticotropin releasing hormone receptors), Acthr (adrenocorticotropin releasing hormone receptor), Gr (glucocorticoid receptor), and Hsd11b1 [hydroxysteroid (11-β) dehydrogenase 1], while all types of IMO stimulated the expression of Hsd11b2, the unidirectional oxidase with high affinity to inactivate glucocorticoids. Thus, presented data provide new molecular/transcriptional base for “fight/adaptation” of Leydig cells and new insights into the role of cAMP, epinephrine, and glucocorticoid signaling in recovery of stress-impaired Leydig cell steroidogenesis.

Molecular Docking and Drug Discovery in β-Adrenergic Receptors

2017 ◽  
Vol 24 (39) ◽  
Author(s):  
Santiago Vilar ◽  
Eduardo Sobarzo-Sanchez ◽  
Lourdes Santana ◽  
Eugenio Uriarte
Keyword(s):  
Molecular Docking ◽  
Drug Discovery ◽  
Adrenergic Receptors ◽  
Β Adrenergic Receptors

scholarly journals Role of β-Adrenergic Receptors and Nitric Oxide Signaling in Exercise-Mediated Cardioprotection

Physiology ◽  
2013 ◽  
Vol 28 (4) ◽  
pp. 216-224 ◽  
Author(s):  
John W. Calvert ◽  
David J. Lefer
Keyword(s):  
Nitric Oxide ◽  
Risk Factors ◽  
Adrenergic Receptors ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Signaling ◽  
Factors Associated ◽  
Cardioprotective Effects ◽  
Β Adrenergic Receptors

Exercise promotes cardioprotection in both humans and animals not only by reducing risk factors associated with cardiovascular disease but by reducing myocardial infarction and improving survival following ischemia. This article will define the role that nitric oxide and β-adrenergic receptors play in mediating the cardioprotective effects of exercise in the setting of ischemia-reperfusion injury.

Chronic Effects of Metoprolol on Myocardial β-Adrenergic Receptors in Doxorubicin-Induced Cardiac Damage in Rats

1991 ◽  
Vol 17 (4) ◽  
pp. 656-661 ◽  
Author(s):  
Naoya Fujita ◽  
Michiaki Hiroe ◽  
Yotihiko Ohta ◽  
Toshinobu Horie ◽  
Saichi Hosoda
Keyword(s):  
Adrenergic Receptors ◽  
Cardiac Damage ◽  
Chronic Effects ◽  
Β Adrenergic Receptors
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