Dynamics of acute retention in prostatic patient and role of adrenergic receptors

AbstractUterine inflammation is a very common and serious condition in domestic animals. To development and progression of this pathology often lead disturbances in myometrial contractility. Participation of β1-, β2- and β3-adrenergic receptors (ARs) in noradrenaline (NA)-influenced contractility of the pig inflamed uterus was studied. The gilts of SAL- and E.coli-treated groups were administered saline or E.coli suspension into the uterine horns, respectively. Laparotomy was only done in the CON group. Compared to the period before NA administration, this neurotransmitter reduced the tension, amplitude and frequency in uterine strips of the CON and SAL groups. In the E.coli group, NA decreased the amplitude and frequency, and these parameters were lower than in other groups. In the CON, SAL and E.coli groups, β1- and β3-ARs antagonists in more cases did not significantly change and partly eliminated NA inhibitory effect on amplitude and frequency, as compared to NA action alone. In turn, β2-ARs antagonist completely abolished NA relaxatory effect on these parameters in three groups. Summarizing, NA decreases the contractile amplitude and frequency of pig inflamed uterus via all β-ARs subtypes, however, β2-ARs have the greatest importance. Given this, pharmacological modulation of particular β-ARs subtypes can be used to increase inflamed uterus contractility.

Download Full-text

Recovery of beta-adrenergic receptors following long term exposure of astrocytoma cells to catecholamine. Role of protein synthesis.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(18)43267-x ◽

1981 ◽

Vol 256 (23) ◽

pp. 12281-12286 ◽

Cited By ~ 4

Author(s):

R.C. Doss ◽

J.P. Perkins ◽

T.K. Harden

Keyword(s):

Protein Synthesis ◽

Adrenergic Receptors ◽

Beta Adrenergic Receptors ◽

Beta Adrenergic ◽

Astrocytoma Cells

Download Full-text

Contraction of dog trachealis muscle in vivo: role of alpha-adrenergic receptors

Journal of Applied Physiology ◽

10.1152/jappl.1980.48.2.329 ◽

1980 ◽

Vol 48 (2) ◽

pp. 329-336 ◽

Cited By ~ 3

Author(s):

W. H. Beinfield ◽

J. Seifter

Keyword(s):

Adrenergic Receptors ◽

Beta Blockers ◽

Systemic Arterial Pressure ◽

Alpha Adrenergic Receptors ◽

Bilateral Vagotomy ◽

Cervical Trachea ◽

Spontaneously Breathing ◽

Trachealis Muscle

Contraction, relaxation, and longitudinal tension were recorded by isometric strain gauge arches attached to cervical tracheal muscle (CTM) in 60 spontaneously breathing dogs anesthetized with pentobarbital. Intravenous norepinephrine (NE) (3 X 10(-9), 6 X 10(-9), 1.2 X 10(-8), and 2.4 x 10(-8) mol/kg) increased spontaneous mechanical activities (SMA) and caused dose related contraction of CTM in all dogs even though there was no pretreatment with beta-blockers. These activities were first potentiated by propranolol and then prevented by phentolamine. NE briefly decreased SMA and induced CTM relaxation prior to the onset of contraction in one-third of dogs. Propranolol prevented this initial relaxation. CTM responses induced by NE were 1) not significantly altered by atropine, tripelennamine, bilateral vagotomy, curarization, and complete tracheal transection below transducer sites; 2) unrelated to passive constriction of cervical trachea associated with airway elongation; and 3) independent of reflexes initiated by elevations of systemic arterial pressure. The moles per kilogram doses of acetylcholine were found to exceed those of NE when their intravenous administration caused equal CTM contractions in the same dog. These findings are consistent with the existence of alpha-adrenergic receptors in CTM.

Download Full-text

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

Physiology ◽

10.1152/physiol.00011.2013 ◽

2013 ◽

Vol 28 (4) ◽

pp. 216-224 ◽

Cited By ~ 21

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.

Download Full-text

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

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00100.2013 ◽

2013 ◽

Vol 305 (2) ◽

pp. E194-E204 ◽

Cited By ~ 12

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.

Download Full-text