scholarly journals Sex‐Dependent Differences in NMDA and GABA Receptor Subunits in the Rat Rostral Ventrolateral Medulla

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Patrick J Mueller ◽  
Toni A Azar ◽  
Bozena E Fyk‐Kolodziej
2015 ◽  
pp. 161-171 ◽  
Author(s):  
Y. LU ◽  
Y. S. WU ◽  
D. S. CHEN ◽  
M. M. WANG ◽  
W. Z. WANG ◽  
...  

Salusin-β is newly identified bioactive peptide of 20 amino acids, which is widely distributed in hematopoietic system, endocrine system, and the central nervous system (CNS). Although salusin-β extensively expressed in the CNS, the central cardiovascular functions of salusin-β are unclear. Our main objective was to determine the cardiovascular effect of microinjection of salusin-β into the nucleus tractus solitarii (NTS) in anesthetized rats. Bilateral or unilateral microinjection of salusin-β (0.94-94 µg/rat) into the NTS dose-dependently decreased blood pressure and heart rate. Bilateral NTS microinjection of salusin-β (9.4 µg/rat) did not alter baroreflex sensitivity. Prior application of the glutamate receptor antagonist kynurenic acid (0.19 µg/rat, n=9) into the NTS did not alter the salusin-β (9.4 µg/rat) induced hypotension and bradycardia. However, pretreatment with the GABA receptor agonist muscimol (0.5 ng/rat) within the rostral ventrolateral medulla (RVLM) completely abolished the hypotension (−14±5 vs. −3±5 mm Hg, P<0.05) and bradycardia (−22±6 vs. −6±5 bpm, P<0.05) evoked by intra-NTS salusin-β (9.4 µg/rat). In addition, we found that vagotomy didn’t influence the actions of salusin-β (9.4 µg/rat) in the NTS. In conclusion, our present study shows that microinjection of salusin-β into the NTS significantly produces hypotension and bradycardia, presumably by suppressing the activities of presympathetic neurons in the RVLM.


Author(s):  
Qi-Jian Sun ◽  
Jane Minson ◽  
Ida J. Llewellyn-Smith ◽  
Leonard Arnolda ◽  
John Chalmers ◽  
...  

Hypertension ◽  
2014 ◽  
Vol 64 (4) ◽  
pp. 815-824 ◽  
Author(s):  
Kay L.H. Wu ◽  
Yung-Mei Chao ◽  
Shiow-Jen Tsay ◽  
Chen Hsiu Chen ◽  
Samuel H.H. Chan ◽  
...  

1990 ◽  
Vol 258 (2) ◽  
pp. R325-R331 ◽  
Author(s):  
D. A. Morilak ◽  
G. Drolet ◽  
J. Chalmers

We have examined the influence of endogenous opioids on the basal and reflex control of arterial blood pressure in the pressor region of the rostral ventrolateral medulla (RVLM) of chloralose-anesthetized rabbits. We tested basal effects both in intact animals and after hypotensive hemorrhage. Bilateral administration of the opiod antagonist naloxone (20 nmol, 100 nl) directly into the RVLM induced a gradual and prolonged increase in mean arterial pressure (MAP) (+17 +/- 2 mmHg). This was preceded by a brief and mild depressor effect (-9 +/- 3 mmHg), which was attributable to a transient reduction in excitability immediately after naloxone injection. When naloxone was administered into the RVLM after hemorrhage (20 ml/kg), it improved recovery of MAP relative to saline controls, again producing a gradual, prolonged pressor response (+29 +/- 5 mmHg). The effect of naloxone on a baroreflex in intact animals was only transient, with a brief, nonsignificant attenuation of the reflex depressor response to aortic nerve stimulation. We conclude that endogenous opioids exert a tonic inhibitory influence on RVLM pressor neurons and that this input remains active after hemorrhage. The RVLM may thus be one site for the beneficial effects of naloxone in preventing circulatory decompensation after hemorrhage. In contrast, opioid neurons are not an essential component of baroreflex-mediated sympathoinhibition in the RVLM.


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