scholarly journals Role of beta-adrenergic receptor subtypes in pig uterus contractility with inflammation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Barbara Jana ◽  
Jarosław Całka
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Domestic Animals ◽  
Inhibitory Effect ◽  
Receptor Subtypes ◽  
Beta Adrenergic Receptor ◽  
Pharmacological Modulation ◽  
Uterine Inflammation ◽  
Myometrial Contractility

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.

scholarly journals Regulatory Influence of Galanin and GALR1/GALR2 Receptors on Inflamed Uterus Contractility in Pigs

2021 ◽  
Vol 22 (12) ◽  
pp. 6415
Author(s):  
Barbara Jana ◽  
Jarosław Całka ◽  
Bartosz Miciński
Keyword(s):  
Protein Expression ◽  
Domestic Animals ◽  
Receptor Subtypes ◽  
E Coli ◽  
Regulatory Influence ◽  
Pretreatment Period ◽  
Uterine Inflammation ◽  
Myometrial Contractility

Uterine inflammation is a very common and serious pathology in domestic animals, the development and progression of which often result from disturbed myometrial contractility. We investigated the effect of inflammation on the protein expression of galanin (GAL) receptor subtypes (GALR)1 and GALR2 in myometrium and their role in the contractile amplitude and frequency of an inflamed gilt uterus. The gilts of the E. coli and SAL groups received E. coli suspension or saline in their uteri, respectively, and only laparotomy was performed (CON group). Eight days later, the E. coli group developed severe acute endometritis and lowered GALR1 protein expression in the myometrium. Compared to the pretreatment period, GAL (10−7 M) reduced the amplitude and frequency in myometrium and endometrium/myometrium of the CON and SAL groups, the amplitude in both stripes and frequency in endometrium/myometrium of the E. coli group. In this group, myometrial frequency after using GAL increased, and it was higher than in other groups. GALR2 antagonist diminished the decrease in amplitude in myometrium and the frequency in endometrium/myometrium (SAL, E. coli groups) induced by GAL (10−7 M). GALR1/GALR2 antagonist and GAL (10−7 M) reversed the decrease in amplitude and diminished the decrease in frequency in both examined stripes (CON, SAL groups), and diminished the drop in amplitude and abolished the rise in the frequency in the myometrium (E. coli group). In summary, the inflammation reduced GALR1 protein expression in pig myometrium, and GALR1 and GALR2 participated in the contractile regulation of an inflamed uterus.

Role of supraspinal and spinal α1-adrenergic receptor subtypes in micturition reflex in conscious rats

2010 ◽  
Vol 299 (4) ◽  
pp. F785-F791 ◽  
Author(s):  
Masaru Yoshizumi ◽  
Kazumasa Matsumoto-Miyai ◽  
Akihiko Yonezawa ◽  
Masahito Kawatani
Keyword(s):  
Spinal Cord ◽  
Receptor Antagonist ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Intrathecal Injection ◽  
Receptor Subtypes ◽  
Lumbosacral Spinal Cord ◽  
Micturition Reflex ◽  
Conscious Rats

α1-Adrenergic receptor subtypes are widely distributed in the central nervous system and are involved in autonomic functions such as micturition. We investigated the presence and the role of supraspinal and/or spinal α1-adrenergic receptors in modulating the micturition reflex in conscious female Wistar rats. The expression of α1-adrenergic receptor subtypes in rat brain and lumbosacral spinal cord was studied using RT-PCR. Continuous-infusion cystometrograms were obtained in conscious rats, and α1-adrenergic receptor antagonists were administered via intracerebroventricular or intrathecal routes. The mRNA expression of α1A-, α1B-, and α1D-adrenergic receptors was detected in rat brain (midbrain and pons) and lumbosacral spinal cord (dorsal and ventral parts of spinal cord). In addition, intracerebroventricular injection of the α1-adrenergic receptor antagonist tamsulosin (1–10 μg), the selective α1A-adrenergic receptor antagonist silodosin (1–10 μg), and the selective α1D-adrenergic receptor antagonist BMY 7378 (1–10 μg) significantly prolonged the intercontraction interval (ICI) but did not alter maximum voiding pressure (MVP). Although intrathecal injection of BMY 7378 (0.0001–10 μg) did not affect ICI, tamsulosin and silodosin prolonged ICI in a dose-dependent manner. MVP was significantly reduced by intrathecal injection of tamsulosin (10 μg) but not by silodosin or BMY 7378 (0.0001–10 μg). Supraspinal α1A- and α1D-adrenergic receptors are apparently important for the regulation of reflex-bladder activity in conscious rats. Noradrenergic projection from the brain stem to the lumbosacral spinal cord may promote the afferent limb rather than the efferent limb of the micturition reflex pathway via α1A-adrenergic receptors.

scholarly journals Genetic regulation of β2-adrenergic receptors in 3T3-L1 fibroblasts

1989 ◽  
Vol 260 (1) ◽  
pp. 53-59 ◽  
Author(s):  
M T Nakada ◽  
K M Haskell ◽  
D J Ecker ◽  
J M Stadel ◽  
S T Crooke
Keyword(s):  
Phorbol Ester ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Genetic Regulation ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Regulatory Sequences ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Beta 2

The beta 2-adrenergic receptor from mouse 3T3-L1 cells is up-regulated through genetic mechanisms by glucocorticoids and butyrate. To study the genetic regulation of these receptors, we sequenced a 5 kb region of genomic DNA from 3T3-L1 cells, containing the beta-adrenergic receptor gene and approx. 1.5 kb of both 5′ and 3′ flanking sequences. The sequence contained one copy of an 8 bp consensus sequence which can confer phorbol ester-responsiveness to genes. Phorbol esters attenuated the up-regulation of beta 2-adrenergic receptors by glucocorticoids but not by butyrate. This effect was probably due to a phorbol ester-induced decrease in glucocorticoid receptor number. Using methylation-sensitive restriction enzymes, we examined the methylation of a CG-rich region occurring 5′ to the gene and did not detect any changes in methylation of this region upon dexamethasone or butyrate treatment. A total of 16 putative glucocorticoid response elements were found which may mediate the glucocorticoid-induced increase in beta 2-adrenergic receptors. A comparison of the regulatory sequences of the two beta-adrenergic receptor subtypes from human and mouse confirms the observed physiological controls of receptor subtype expression and offers an explanation as to why the subtypes differ in genetic regulation.

The role of the hypothalamic β-adrenergic system in controlling the LH rise in short-term castrated rats

1987 ◽  
Vol 114 (2) ◽  
pp. 167-172 ◽  
Author(s):  
M. H. Al-Hamood ◽  
D. P. Gilmore ◽  
C. A. Wilson ◽  
P. Tuohy-Jones ◽  
S. Drummond ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Concomitant Administration ◽  
Inhibitory Effect ◽  
Adrenergic System ◽  
Receptor Subtypes ◽  
Short Term ◽  
Pharmacological Agents ◽  
Inhibitory Component ◽  
Lh Release

ABSTRACT Intraventricular infusions of adrenaline and various pharmacological agents acting on β-adrenergic receptor subtypes were carried out in rats orchidectomized 16 h previously. Infusions (10 μl) of solutions containing the drugs were administered under anaesthesia induced with alphaxalone and alphadolone. Levels of LH were measured in plasma collected immediately before and at predetermined intervals after the infusion. The acute rise in LH levels after castration was increased still further by isoprenaline (a mixed β1- and β2-agonist), fenoterol (a β2-agonist) and atenolol (a β1-antagonist). In contrast, prenalterol (a β1-agonist) and (2RS,3RS)-3-isopropylamino-1-(7-methylindan-4-yloxy)butan-2-ol (ICI 118 551) (a selective β2-antagonist) were inhibitory to LH release. Adrenaline itself, salbutamol (another selective β2-agonist), propranolol (a mixed β-antagonist) and metoprolol (a β1-antagonist) did not significantly alter plasma LH concentrations at the doses administered. The stimulatory effect of isoprenaline on LH release was partially reduced when given together with ICI 118 551, but was not affected when administered simultaneously with atenolol. The inhibitory effect of ICI 118 551 was, however, prevented by concomitant administration with fenoterol, as was that of prenalterol when infused with atenolol. The results suggest that the hypothalamic mediation of the short-term changes in LH release in response to castration is exerted, at least in part, through the activation of a β2-stimulatory component and the suppression of a β1-inhibitory component. J. Endocr. (1987) 114, 167–172

scholarly journals Overexpression of beta-arrestin and beta-adrenergic receptor kinase augment desensitization of beta 2-adrenergic receptors.

1993 ◽  
Vol 268 (5) ◽  
pp. 3201-3208
Author(s):  
S. Pippig ◽  
S. Andexinger ◽  
K. Daniel ◽  
M. Puzicha ◽  
M.G. Caron ◽  
...  
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Kinase ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Beta 2
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