scholarly journals Hemodynamic responses to electrical stimulation of carotid sinus in conscious rats (1169.15)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Jaci Castania ◽  
Carlos Alberto Silva ◽  
Gean Souza ◽  
Daniel Dias ◽  
Helio Salgado ◽  
...  
Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Pedro L Katayama ◽  
Jaci A Castania ◽  
Rubens Fazan ◽  
Helio C Salgado

The mechanisms involved in Baroreflex Activation Therapy (BAT) in patients with resistant hypertension require better understanding. It was shown that electrical stimulation of the carotid sinus (ESCS), in conscious carotid body-denervated rats, caused bradycardia and greater hypotensive response when compared with intact control rats. In the current study the activation of the chemoreceptors due to ESCS, in conscious rats, was examined in the absence of the carotid baroreceptors. Wistar rats with unilateral denervation of the right carotid chemoreceptors were divided into three groups: 1) control (CONT, n=7); 2) bilateral carotid chemoreceptor denervation (CD, n=7); 3) unilateral denervation of the left carotid baroreceptors (BD, n=4). Under ketamine/xylazine anesthesia bipolar electrodes were implanted around the left carotid sinus combined with arterial and venous catheters into the femoral vessels. On the next day, after basal hemodynamic recordings, the animals received three ESCS (5V, 1 ms) with 15 Hz, 30 Hz and 60 Hz, applied randomly for 20s. Carotid chemoreceptors denervation was confirmed by the lack of hemodynamic responses after the administration of KCN (40 μg iv). The efficacy of left carotid baroreceptor denervation was confirmed by the absence of hemodynamic responses to changes in the left carotid sinus pressure ranging from 60 mmHg to 180 mmHg. The results showed that ESCS was efficient to cause greater hypotensive responses in the CD as compared with the CONT group at 60 Hz (-37 ± 6 vs -19 ± 3 mmHg) and to cause hypertensive responses in the BD group at 30 Hz and 60 Hz (15 ± 2 and 19 ± 2 mmHg). ESCS caused no alteration of the heart rate in the CONT but caused significant bradycardia in the CD group at 30 Hz and 60 Hz (-31 ± 11 and -35 ± 12 bpm) and in the BD group at 15 Hz, 30 Hz and 60 Hz (-38 ± 6, -37 ± 6 and -34 ± 4 bpm). These data demonstrated that carotid chemoreceptor activation in the absence of the carotid baroreceptors caused hypertension and bradycardia, indicating that when the baroreceptors are intact, the chemoreceptors blunt the hypotensive response caused by ESCS. These findings provide important information for the clinical studies using BAT in patients with resistant hypertension and/or heart failure.


Hypertension ◽  
2015 ◽  
Vol 66 (3) ◽  
pp. 598-603 ◽  
Author(s):  
Pedro L. Katayama ◽  
Jaci A. Castania ◽  
Daniel P.M. Dias ◽  
Kaushik P. Patel ◽  
Rubens Fazan ◽  
...  

2020 ◽  
Vol 43 (10) ◽  
pp. 1057-1067 ◽  
Author(s):  
Gean Domingos-Souza ◽  
Fernanda Machado Santos-Almeida ◽  
César Arruda Meschiari ◽  
Nathanne S. Ferreira ◽  
Camila A. Pereira ◽  
...  

1999 ◽  
Vol 276 (4) ◽  
pp. R1030-R1037 ◽  
Author(s):  
Mohamed K. Mohamed ◽  
Mahmoud M. El-Mas ◽  
Abdel A. Abdel-Rahman

We have recently shown that estrogen enhances baroreceptor control of reflex bradycardia in conscious rats. The present study replicated this finding in pentobarbital sodium-anesthetized rats, and the study was extended to investigate whether this effect of estrogen is centrally or peripherally mediated. Hemodynamic responses to electrical stimulation of the central end of the aortic depressor or the vagal efferent nerve were evaluated in pentobarbital sodium-anesthetized sham-operated (SO), ovariectomized (OVX), and OVX estradiol-treated Sprague-Dawley rats. Phenylephrine (1–16 μg/kg iv) elicited dose-dependent pressor and bradycardic responses. Regression analysis of the baroreflex curves, relating changes in mean arterial pressure and heart rate, revealed a significantly smaller baroreflex sensitivity in OVX compared with SO anesthetized rats (−0.54 ± 0.05 and −0.91 ± 0.12 beats ⋅ min−1 ⋅ mmHg−1, respectively; P < 0.05). Treatment of OVX rats with 17β-estradiol (E2, 50 μg ⋅ kg−1 ⋅ day−1for 2 days subcutaneously) significantly enhanced baroreflex sensitivity to a level similar to that of SO rats ( P < 0.05). The enhancing effect of E2 on the baroreflex-mediated bradycardia, observed in conscious and anesthetized rats, seems to be selective because the baroreflex-mediated tachycardic responses measured in a separate group of conscious rats were not altered by ovariectomy or E2 administration. Electrical stimulation of the aortic nerve elicited frequency-dependent depressor and bradycardic responses that were significantly smaller in OVX compared with SO values ( P < 0.05). Treatment of OVX rats with E2 restored the hemodynamic responses to aortic stimulation to near SO levels. On the other hand, hemodynamic responses to vagal stimulation were not affected by OVX or treatment with E2. These findings suggest that enhancement of reflex bradycardia by estrogen is centrally mediated and involves interaction with central projections of the aortic nerve.


2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Helio Salgado ◽  
Fernanda Brognara ◽  
Daniel Penteado Martins Dias ◽  
Jaci Airton Castania ◽  
Rubens Fazan

1991 ◽  
Vol 70 (6) ◽  
pp. 2539-2550 ◽  
Author(s):  
F. A. Hopp ◽  
J. L. Seagard ◽  
J. Bajic ◽  
E. J. Zuperku

Respiratory responses arising from both chemical stimulation of vascularly isolated aortic body (AB) and carotid body (CB) chemoreceptors and electrical stimulation of aortic nerve (AN) and carotid sinus nerve (CSN) afferents were compared in the anesthetized dog. Respiratory reflexes were measured as changes in inspiratory duration (TI), expiratory duration (TE), and peak averaged phrenic nerve activity (PPNG). Tonic AN and AB stimulations shortened TI and TE with no change in PPNG, while tonic CSN and CB stimulations shortened TE, increased PPNG, and transiently lengthened TI. Phasic AB and AN stimulations throughout inspiration shortened TI with no changes in PPNG or the following TE; however, similar phasic stimulations of the CB and CSN increased both TI and PPNG and decreased the following TE. Phasic AN stimulation during expiration decreased TE and the following TI with no change in PPNG. Similar stimulations of the CB and CSN decreased TE; however, the following TI and PPNG were increased. These findings differ from those found in the cat and suggest that aortic chemoreceptors affect mainly phase timing, while carotid chemoreceptors affect both timing and respiratory drive.


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