Role of ventrolateral medulla in sympatholytic effect of 8-OHDPAT in rats

1991 ◽  
Vol 260 (3) ◽  
pp. R600-R609 ◽  
Author(s):  
A. Nosjean ◽  
P. G. Guyenet

In halothane-anesthetized, paralyzed, and artificially ventilated rats, the putative 5-hydroxytryptamine1A receptor agonist 8-OHDPAT (13.1 micrograms/kg iv) produced hypotension (-14.6 +/- 1.3 mmHg, n = 35), reduced lumbar sympathetic nerve discharge (SND, -17.8%, n = 35), and slowed the discharge rate of sympathoexcitatory neurons recorded in the rostroventrolateral medulla (RVLM, -17.6%, n = 20). The gain of the baroreflex was unaffected by the drug, but SND and RVLM unit discharges were silenced at significantly reduced levels of mean arterial pressure (MAP; 153 vs. 171 mmHg for SND, 155 vs. 172 mmHg for RVLM cells). Subsequent intravenous administration of the alpha 2-adrenergic receptor agonist clonidine (5.3 micrograms/kg) produced an additional decrease in MAP (-21.2 +/- 1.9 mmHg, n = 24) and SND (-24%, n = 24), Bilateral microinjections of 8-OHDPAT into the RVLM (1 nmol/side, n = 9) or into the raphe pallidus-obscurus (2 injections of 1 nmol each, n = 7) also produced hypotension (-22.9 +/- 3.2 and -14.4 +/- 2.8 mmHg, respectively) and sympathoinhibition (-39.1 and -24.6%, respectively). Bilateral microinjection into RVLM of the alpha 2-adrenergic antagonists idazoxan (16 nmol/side, n = 6) or rauwolscine (2 nmol/side, n = 6) attenuated the sympatholytic effect of both 8-OHDPAT (13.1 micrograms/kg, iv) and clonidine (5.3 micrograms/kg iv). These results suggest that 8-OHDPAT may exert a portion of its central sympatholytic effect by activating alpha 2-adrenergic receptors in the rostroventral medulla.

2012 ◽  
Vol 303 (10) ◽  
pp. R1031-R1041 ◽  
Author(s):  
Yusuke Kumai ◽  
Mellissa A. R. Ward ◽  
Steve F. Perry

The potential role of adrenergic systems in regulating Na+ uptake in zebrafish ( Danio rerio) larvae was investigated. Treatment with isoproterenol (a generic β-adrenergic receptor agonist) stimulated Na+ uptake, whereas treatment with phenylephrine (an α1-adrenergic receptor agonist) as well as clonidine (an α2-adrenergic receptor agonist) significantly reduced Na+ uptake, suggesting opposing roles of α- and β-adrenergic receptors in Na+ uptake regulation. The increase in Na+ uptake associated with exposure to acidic water (pH = 4.0) was attenuated in the presence of the nonselective β-receptor antagonist propranolol or the β1-receptor blocker atenolol; the β2-receptor antagonist ICI-118551 was without effect. The stimulation of Na+ uptake associated with ion-poor water (32-fold dilution of Ottawa tapwater) was unaffected by β-receptor blockade. Translational gene knockdown of β-receptors using antisense oligonucleotide morpholinos was used as a second method to assess the role of adrenergic systems in the regulation of Na+ uptake. Whereas β1- or β2B-receptor knockdown led to significant decreases in Na+ uptake during exposure to acidic water, only β2A-receptor morphants failed to increase Na+ uptake in response to ion-poor water. In support of the pharmacology and knockdown experiments that demonstrated an involvement of β-adrenergic systems in the control of Na+ uptake, we showed that the H+-ATPase-rich (HR) cell, a subtype of ionocyte known to be a site of Na+ uptake, is innervated and appears to express β-adrenergic receptors (propranolol binding sites) at 4 days postfertilization. These data indicate an important role of adrenergic systems in regulating Na+ uptake in developing zebrafish.


2009 ◽  
Vol 297 (5) ◽  
pp. R1610-R1614 ◽  
Author(s):  
Ryuhei Inamoto ◽  
Takenori Miyashita ◽  
Kosuke Akiyama ◽  
Terushige Mori ◽  
Nozomu Mori

To clarify the role of the endolymphatic sac (ES) in the regulation of endolymphatic pressure, the effects of isoproterenol, a β-adrenergic receptor agonist, and acetazolamide, a potent carbonic anhydrase inhibitor, both of which decrease ES direct current potential on cochlear hydrostatic pressure, were examined in guinea pigs. When isoproterenol was applied intravenously, hydrostatic pressures of cochlear endolymph and perilymph were significantly increased with no change in endocochlear potential or the hydrostatic pressure of cerebrospinal fluid. Acetazolamide produced no marked change in the hydrostatic pressure of cochlear endolymph. In ears with an obstructed ES, the action of isoproterenol on the hydrostatic pressure of cochlear endolymph and perilymph was suppressed. These results suggest that the ES may regulate the hydrostatic pressure of the endolymphatic system via the action of the agents such as catecholamines on the ES.


2008 ◽  
Vol 294 (5) ◽  
pp. R1435-R1444 ◽  
Author(s):  
Hakan S. Orer ◽  
Gerard L. Gebber ◽  
Susan M. Barman

We studied the changes in inferior cardiac sympathetic nerve discharge (SND) produced by unilateral microinjections of 5-hydroxytryptamine (5-HT) receptor agonists and antagonists into the ventrolateral medulla (VLM) of urethane-anesthetized, baroreceptor-denervated cats. Microinjection of the 5-HT2 receptor antagonist LY-53857 (10 mM) into either the rostral or caudal VLM significantly reduced ( P ≤ 0.05) the 10-Hz rhythmic component of basal SND without affecting its lower-frequency, aperiodic component. The selective depression of 10-Hz power was accompanied by a statistically significant decrease in mean arterial pressure (MAP). Microinjection of LY-53857 into the VLM also attenuated the increase in 10-Hz power that followed tetanic stimulation of depressor sites in the caudal medullary raphé nuclei. Microinjection of the 5-HT2 receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)2-amino-propane (DOI; 10 μM) into the VLM selectively enhanced 10-Hz SND, and intravenous DOI (1 mg/kg) partially reversed the reduction in 10-Hz SND produced by 5-HT2 receptor blockade in the VLM. Microinjection of the 5-HT1A receptor agonist, 8-hydroxy-2-(di- n-propylamino)tetralin (8-OHDPAT; 10 mM), into either the rostral or caudal VLM also selectively attenuated 10-Hz SND and significantly reduced MAP. The reduction in 10-Hz SND produced by 8-OHDPAT was partially reversed by intravenous WAY-100635 (1 mg/kg), which selectively blocks 5-HT1A receptors. These results support the view that serotonergic inputs to the VLM play an important role in expression of the 10-Hz rhythm in SND.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1146-P
Author(s):  
ALANA O'MARA ◽  
AARON CYPESS ◽  
CHERYL CERO ◽  
JAMES W. JOHNSON ◽  
JOYCE D. LINDERMAN ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Barbara Jana ◽  
Jarosław Całka

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.


2004 ◽  
Vol 53 (2) ◽  
pp. 69-75 ◽  
Author(s):  
Shigemi Yoshihara ◽  
Yumi Yamada ◽  
Toshio Abe ◽  
Osamu Arisaka

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