Carotid chemoreceptors influence arterial pressure in intact and aortic-denervated rats

1992 ◽  
Vol 262 (4) ◽  
pp. R677-R683 ◽  
Author(s):  
K. G. Franchini ◽  
E. M. Krieger

The objective of the present study was to analyze the role of the arterial chemoreceptors in arterial pressure alterations produced by sinoaortic denervation (SAD) in rats. The mean arterial pressure during 2 h of continuous computerized beat-to-beat recordings was higher after aortic denervation (AD; 130 +/- 2 and 124 +/- 3 mmHg, respectively), lower after sinus denervation (SD; 101 +/- 1 and 101 +/- 3 mmHg), and remained unaltered after SAD (121 +/- 3 and 108 +/- 2 mmHg) 1 and 20 days after denervation compared with control rats (114 +/- 1 mmHg). Hypotensive effect of SD was confirmed when arterial pressure was recorded in the same animal before and after SD (from 112 +/- 2 to 103 +/- 2 mmHg). A similar effect was observed after isolated carotid body artery (CBA) ligation (from 114 +/- 3 to 104 +/- 3 mmHg). Furthermore, CBA ligation attenuated by 13% the hypertension after AD (from 136 +/- 2 to 118 +/- 3 mmHg). Bradycardic response to phenylephrine and arterial pressure variability were markedly altered by SAD and AD but remained normal after SD. In contrast, the chemoreflex (intravenous KCN) was abolished after SAD, SD, and CBA ligation but was preserved after AD. These data suggest that the arterial pressure alteration produced by SAD in rats represents the net effect of the abolition of inhibitory (baroreceptor deafferentation) and excitatory (chemoreceptor deafferentation) influences on the arterial pressure.

2013 ◽  
Vol 305 (9) ◽  
pp. H1382-H1386 ◽  
Author(s):  
Matthew D. Muller ◽  
Charity L. Sauder ◽  
Chester A. Ray

Melatonin attenuates muscle sympathetic nerve responses to sympathoexcitatory stimuli, but it is unknown whether melatonin similarly attenuates reflex changes in skin sympathetic nerve activity (SSNA). In this double-blind, placebo-controlled, crossover study, we tested the hypothesis that melatonin (3 mg) would attenuate the SSNA response to mental stress (mental arithmetic). Twelve healthy subjects underwent experimental testing on two separate days. Three minutes of mental stress occurred before and 45 min after ingestion of melatonin (3 mg) or placebo. Skin temperature was maintained at 34°C. Reflex increases in SSNA (peroneal nerve), mean arterial pressure, and heart rate (HR) to mental stress before and after melatonin were determined. Melatonin lowered HR (pre, 66 ± 3 beats/min; and post, 62 ± 3 beats/min, P = 0.046) and SSNA (pre, 14,282 ± 3,706 arbitrary units; and post, 9,571 ± 2,609 arbitrary units, P = 0.034) at rest. In response to mental stress, SSNA increases were significantly attenuated following melatonin ingestion (second minute, 114 ± 30 vs. 74 ± 14%; and third minute, 111 ± 29 vs. 54 ± 12%, both P < 0.05). The mean arterial pressure increase to mental stress was blunted in the third minute (20 ± 2 vs. 17 ± 2 mmHg, P = 0.032), and the HR increase was blunted in the first minute (33 ± 3 vs. 29 ± 3 beats/min, P = 0.034) after melatonin. In summary, exogenous melatonin attenuates the SSNA response to mental stress.


2006 ◽  
Vol 291 (3) ◽  
pp. R736-R741 ◽  
Author(s):  
Léa Emonnot ◽  
Charles Bakhos ◽  
Bruno Chapuis ◽  
Valérie Oréa ◽  
Christian Barrès ◽  
...  

Previous studies have shown that the sympathetically mediated oscillations of arterial pressure (AP), the so-called Mayer waves, are shifted from 0.4 to 0.6 Hz after acute α-adrenoceptor blockade in conscious rats. This raises the possibility that, under physiological conditions, Mayer waves are mediated by the conjoint action of norepinephrine and other sympathetic cotransmitters. To evaluate the possible role of the cotransmitter ATP in determining the frequency of Mayer waves, AP and renal sympathetic nerve activity (RSNA) were simultaneously recorded in 10 conscious rats with cardiac autonomic blockade before and after acute blockade of P2 receptors with pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid. P2 receptor blockade did not alter the mean level and overall variability of AP and RSNA but shifted peak coherence between AP and RSNA from 0.43 ± 0.02 to 0.22 ± 0.01 Hz. A model of the sympathetic limb of the arterial baroreceptor reflex was designed to simulate Mayer waves at 0.2 and 0.6 Hz, with norepinephrine and ATP, respectively, acting as the sole sympathetic cotransmitter. When both cotransmitters acted in concert, a single oscillation was observed at 0.4 Hz when the gain ratio of the adrenergic to the purinergic components was set at 15. The model thus accounted for an important role for ATP in determining Mayer wave frequency, but not in sustaining the mean level of AP or controlling its overall variability.


2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Ida Royani ◽  
Suryani As’ad ◽  
Nasrudin A Mappaware ◽  
Mochammad Hatta ◽  
Rabia

Background. Preeclampsia is the major problem and the main leading cause of fetal and maternal mortality worldwide. The early prediction of preeclampsia in pregnant women is required to prevent the occurrence of preeclampsia. The mean arterial pressure (MAP) and roll-over test (ROT) are the combination of measurement which can be used to predict preeclampsia. On the contrary, Ajwa dates were reported to have an enormous activity which contributes to its role in improving health conditions. In this study, we aimed to evaluate the effect of daily consumption of seven Ajwa dates on prevention of preeclampsia, through MAP and ROT changes. Methods. Forty pregnant women (n = 40) were randomly assigned into the control group (n = 10) and the intervention group which received a daily intake of Ajwa dates (n = 30). The MAP and ROT were assessed before and after the 8-week intervention period. Results. The intervention group showed the significant reduction in MAP and ROT following the 8-week intervention period (p<0.05). Conclusion. Daily consumption of seven Ajwa dates has a remarkable potential to decrease the MAP and ROT in pregnant women at risk of developing preeclampsia, and thus, it can contribute to prevent the development of preeclampsia.


2003 ◽  
Vol 112 (4) ◽  
pp. 373-378 ◽  
Author(s):  
Ageliki K. Pandazi ◽  
Antonios A. Louizos ◽  
John M. Stivaktakis ◽  
Dimitrios J. Davilis ◽  
Loucas G. Georgiou

We studied the effects of sevoflurane, remifentanil hydrochloride, and alfentanil anesthesia in terms of the hemodynamic responses and emergence characteristics of patients scheduled for elective microlaryngeal surgery. Sixty patients (ASA I to III) were randomly allocated into 2 groups: group S-R (sevoflurane-remifentanil) and group S-A (sevoflurane-alfentanil; 1:20 and 1:4 ratios of remifentanil to alfentanil for induction and maintenance of anesthesia, respectively; doses not strictly equipotent). The mean arterial pressure and heart rate were measured before and after induction of anesthesia, 1 and 3 minutes after endotracheal intubation, at the insertion of the operating laryngoscope, and every 3 minutes during surgery. The emergence times and side effects during the first 30 minutes after surgery were also recorded. The mean arterial pressure values at the insertion of the operating laryngoscope and throughout the procedure were significantly greater (p < .05) in group S-A than in group S-R. The emergence times and postoperative side effects did not differ, except for the greater pain score (p < .05) in group S-R. In conclusion, sevoflurane with remifentanil seems to maintain cardiovascular stability during microlaryngeal surgery more effectively than sevoflurane with alfentanil. Both anesthetic regimens seem to provide rapid and uneventful emergence.


2007 ◽  
Vol 103 (6) ◽  
pp. 1958-1963 ◽  
Author(s):  
Ivan Palada ◽  
Davor Eterović ◽  
Ante Obad ◽  
Darija Bakovic ◽  
Zoran Valic ◽  
...  

We investigated the spleen volume changes as related to the cardiovascular responses during short-duration apneas at rest. We used dynamic ultrasound splenic imaging and noninvasive photoplethysmographic cardiovascular measurements before, during, and after 15–20 s apneas in seven trained divers. The role of baroreflex was studied by intravenous bolus of vasodilating drug trinitrosan during tidal breathing. The role of lung volume was studied by comparing the apneas at near-maximal lung volume with apneas after inhaling tidal volume, with and without cold forehead stimulation. In apneas at near maximal lung volume, a 20% reduction in splenic volume ( P = 0.03) was observed as early as 3 s after the onset of breath holding. Around that time the heart rate increased, the mean arterial pressure abruptly decreased from 89.6 to 66.7 mmHg ( P = 0.02), and cardiac output decreased, on account of reduction in stroke volume. Intravenous application of trinitrosan resulted in ∼6-mmHg decrement in mean arterial pressure, while the splenic volume decreased for ∼13%. In apneas at low lung volume, the early splenic contraction was also observed, 10% without and 12% with cold forehead stimulation, although the mean arterial pressure did not change or even increased, respectively. In conclusion, the spleen contraction is present at the beginning of apnea, accentuated by cold forehead stimulation. At large, but not small, lung volume, this initial contraction is probably facilitated by downloaded baroreflex in conditions of decreased blood pressure and cardiac output.


1990 ◽  
Vol 259 (6) ◽  
pp. R1172-R1180 ◽  
Author(s):  
J. W. Osborn ◽  
S. K. England

Studies in several species have demonstrated that mean arterial pressure (MAP) is normal or only slightly elevated after chronic arterial baroreceptor denervation. We hypothesized that the absence of sustained hypertension after barodenervation was the result of a pressure natriuresis response, secondary to sympathetic vasoconstriction of nonrenal vasculature. To test this hypothesis, MAP, sodium balance (NaBal), and water balance were measured before and after aortic baroreceptor denervation (ABD), sinoaortic denervation (SAD), or sham surgery in conscious rats. MAP was increased 20.0 +/- 3.7 mmHg 1 day after ABD but returned to control by day 3. ABD had no significant effect on daily NaBal or water balance. The responses to SAD were similar to those after ABD, with the exception that a significant natriuresis was observed the first day after SAD. However, this was followed by a significant antinatriuresis on day 2, when MAP was still elevated. By day 3 after SAD, MAP, NaBal, and water balance were not significantly different from control. These results suggest that the normalization of MAP after ABD or SAD is not the result of pressure natriuresis but rather failure to maintain a chronic elevation of sympathetic activity after barodenervation.


1990 ◽  
Vol 69 (3) ◽  
pp. 880-884 ◽  
Author(s):  
G. L. Jones ◽  
C. G. Lane ◽  
P. M. O'Byrne

Airway hyperresponsiveness after inhaled ozone in dogs may occur as a result of thromboxane release in the airway. In this study, two thromboxane receptor antagonists, L-655,240 and L-670,596, were used in doses that inhibit the response to an inhaled thromboxane mimetic, U-46619, to determine further the role of thromboxane in ozone-induced airway hyperresponsiveness. Dogs were studied on 2 days separated by 1 wk. On each day, the dogs inhaled ozone (3 ppm) for 30 min. On one randomly assigned day, 10 dogs received an infusion of L-655,240 (5 mg.kg-1.h-1) and 5 dogs received an infusion of L-670,596 (1 mg.kg-1.h-1); on the other day dogs received a control infusion. Airway responses to doubling doses of acetylcholine were measured before and after inhalation of ozone and were expressed as the concentration of acetylcholine giving a rise in resistance of 5 cmH2O.l-1.s from baseline (acetylcholine provocation concentration). The development of airway hyperresponsiveness after ozone was not inhibited by the thromboxane antagonists. The mean log difference in the acetylcholine provocative concentration before and after ozone on the L-655,240 treatment day was 0.62 +/- 0.12 (SE) and on the control day was 0.71 +/- 0.12 (P = 0.48); on the L-670,596 treatment day the mean log difference was 0.68 +/- 0.15 (SE) and on the control day it was 0.75 +/- 0.19 (P = 0.45). These results do not support an important role for thromboxane in causing ozone-induced airway hyperresponsiveness.


2018 ◽  
Vol 315 (2) ◽  
pp. R336-R343 ◽  
Author(s):  
Corbin A. Shields ◽  
Maggie McCalmon ◽  
Tarek Ibrahim ◽  
Dakota L. White ◽  
Jan M. Williams ◽  
...  

Previous studies have demonstrated that T-helper 17 (TH17) cells and cytolytic natural killer (cNK) cells are increased in women with preeclampsia. In this study we investigated the role of placental ischemia-stimulated TH17 cells in induction of cNK cells in pregnancy. We further assessed the role of TH17 cell-mediated oxidative stress in facilitation of cNK cell activation in pregnancy by treating rats with the SOD mimetic tempol. CD4+/CD25− cells were isolated from reduced uterine perfusion pressure (RUPP) rats and differentiated into TH17 cells in vitro. On day 12 of gestation ( GD12), 1 × 106 placental ischemia-stimulated TH17 cells were injected into normal pregnant (NP) rats (NP + RUPP TH17 rats), and a subset of rats were treated with tempol (30 mg·kg−1·day−1) from GD12 to GD19 (NP + RUPP TH17 + tempol rats). On GD19, cNK cells, mean arterial pressure, fetal weight, and cNK cell-associated cytokines and proteins were measured. Placental cNK cells were 2.9 ± 1, 14.9 ± 4, and 2.8 ± 1.0% gated in NP, NP + RUPP TH17, and NP + RUPP TH17 + tempol rats, respectively. Mean arterial pressure increased from 96 ± 5 mmHg in NP rats to 118 ± 2 mmHg in NP + RUPP TH17 rats and was 102 ± 3 mmHg in NP + RUPP TH17 + tempol rats. Fetal weight was 2.37 ± 0.04, 1.95 ± 0.14, and 2.3 ± 0.05 g in NP, NP + RUPP TH17, and NP + RUPP TH17 + tempol rats, respectively. Placental IFNγ increased from 1.1 ± 0.6 pg/mg in NP rats to 3.9 ± 0.6 pg/mg in NP + RUPP TH17 rats. Placental perforin increased from 0.18 ± 0.18 pg/mg in NP rats to 2.4 ± 0.6 pg/mg in NP + RUPP TH17 rats. Placental levels of granzymes A and B followed a similar pattern. Treatment with tempol did not lower placental cNK cytokines or proteins. The results of the present study identify TH17 cells as a mediator of aberrant NK cell activation that is associated with preeclampsia.


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