scholarly journals Blockade of Rostral Ventrolateral Medulla Apelin Receptors Does Not Attenuate Arterial Pressure in SHR and L-NAME-Induced Hypertensive Rats

2018 ◽  
Vol 9 ◽  
Author(s):  
Philip R. Griffiths ◽  
Stephen J. Lolait ◽  
Louise E. Pearce ◽  
Fiona D. McBryde ◽  
Julian F. R. Paton ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Hypertensive Rats

Regularly swimming exercise modifies opioidergic neuromodulation in Rostral Ventrolateral Medulla in hypertensive rats

2021 ◽  
pp. 147726
Author(s):  
Roberto L. Almeida ◽  
Cristiana A. Ogihara ◽  
Janaína S. de Souza ◽  
Kelen C. Oliveira ◽  
Eduardo M. Cafarchio ◽  
...  
Keyword(s):  
Rostral Ventrolateral Medulla ◽  
Swimming Exercise ◽  
Ventrolateral Medulla ◽  
Hypertensive Rats

scholarly journals Neurosteroid modulation of arterial baroreflexsensitive neurons in rat rostral ventrolateral medulla

1998 ◽  
Vol 274 (4) ◽  
pp. R903-R911 ◽  
Author(s):  
J. D. Laiprasert ◽  
R. C. Rogers ◽  
C. M. Heesch
Keyword(s):  
Arterial Pressure ◽  
Unit Activity ◽  
Plasma Concentrations ◽  
Saturation Pressure ◽  
Virgin Female ◽  
Rostral Ventrolateral Medulla ◽  
Female Rats ◽  
Ventrolateral Medulla ◽  
Acute Administration ◽  
Positive Modulator

The major metabolite of progesterone, 3α-OH-dihydroprogesterone (3α-OH-DHP), is the most potent endogenous positive modulator of central nervous system GABAA receptors. Acute intravenous administration of 3α-OH-DHP to virgin female rats potentiates arterial baroreflex sympathoinhibitory responses. The current experiments tested the possibility that circulating 3α-OH-DHP potentiates central GABAergic influences in the rostral ventrolateral medulla (RVLM). The unit activity of spontaneously active, spinally projecting, and arterial pressure-sensitive neurons was recorded in the RVLM of urethan-anesthetized rats. Arterial pressure sensitivity of RVLM neurons was tested before (control) and 10 min after bolus injection (44 μl iv) of 3α-OH-DHP (1.12 μg/kg, n = 19) or vehicle (40% β-cyclodextrin, n = 8). Both threshold pressure and saturation pressure for inhibition of RVLM neurons were decreased after acute administration of a physiological dose of 3α-OH-DHP (1.12 μg/kg iv), which produces plasma concentrations similar to those seen during pregnancy (20–30 ng/ml), suggesting potentiated responsiveness to endogenously released GABA. Following suppression by 3α-OH-DHP, high doses of the inactive stereoisomer 3β-OH-DHP (112–224 μg/kg iv; n = 8) restored unit activity, presumably by displacing 3α-OH-DHP from the neurosteroid binding site on GABAA receptors.

scholarly journals Brain Prostaglandin D2 Increases Neurogenic Pressor Activity and Mean Arterial Pressure in Angiotensin II-Salt Hypertensive Rats

Hypertension ◽  
2019 ◽  
Vol 74 (6) ◽  
pp. 1499-1506 ◽  
Author(s):  
Ninitha Asirvatham-Jeyaraj ◽  
A. Daniel Jones ◽  
Robert Burnett ◽  
Gregory D. Fink
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Developmental Stage ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Salt Hypertension ◽  
Pressor Activity

This study tested whether brain L-PGDS (lipocalin-type prostaglandin [PG] D synthase), through prostanoid signaling, might increase neurogenic pressor activity and thereby cause hypertension. Sprague Dawley rats on high-salt diet received either vehicle or Ang II (angiotensin II) infusion. On day 4, the developmental stage of hypertension, brains from different sets of control and Ang II–treated rats were collected for measuring L-PGDS expression, PGD2 levels, and DP1R (type 1 PGD2 receptor) expression. In a different set of 14-day Ang II-salt–treated rats, mini-osmotic pumps were used to infuse either a nonselective COX (cyclooxygenase) inhibitor ketorolac, L-PGDS inhibitor AT56, or DP1R inhibitor BWA868C to test the role of brain COX-PGD2-DP1R signaling in Ang II-salt hypertension. The acute depressor response to ganglion blockade with hexamethonium was used to quantify neurogenic pressor activity. During the developmental stage of Ang II-salt hypertension, L-PGDS expression was higher in cerebrospinal fluid, and PGD2 levels were increased in the choroid plexus, cerebrospinal fluid, and the cardioregulatory brain region rostral ventrolateral medulla. DP1R expression was decreased in rostral ventrolateral medulla. Both brain COX inhibition with ketorolac and L-PGDS inhibition with AT56 lowered mean arterial pressure by altering neurogenic pressor activity compared with vehicle controls. Blockade of DP1R with BWA868C, however, increased the magnitude of Ang II-salt hypertension and significantly increased neurogenic pressor activity. In summary, we establish that the development of Ang II-salt hypertension requires increased COX- and L-PGDS–derived PGD2 production in the brain, making L-PGDS a possible target for treating neurogenic hypertension.

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