Corticotropin-releasing factor: Central nervous system effects on baroreflex control of heart rate

Life Sciences ◽  
1988 ◽  
Vol 42 (25) ◽  
pp. 2645-2649 ◽  
Author(s):  
Laurel A. Fisher
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Corticotropin Releasing Factor ◽  
Baroreflex Control

Isoflurane Depresses Baroreflex Control of Heart Rate in Decerebrate Rats

2002 ◽  
Vol 96 (5) ◽  
pp. 1214-1222 ◽  
Author(s):  
Jong S. Lee ◽  
Don Morrow ◽  
Michael C. Andresen ◽  
Kyoung S. K. Chang
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Baroreflex Sensitivity ◽  
Baroreflex Control ◽  
Beta Adrenoceptor ◽  
Reflex Bradycardia ◽  
Reflex Tachycardia ◽  
Map Data ◽  
Regulatory Sites

Background Isoflurane inhibits baroreflex control of heart rate (HR) by poorly understood mechanisms. The authors examined whether suprapontine central nervous system cardiovascular regulatory sites are required for anesthetic depression. Methods The effects of isoflurane (1 and 2 rat minimum alveolar concentration [MAC]) on the baroreflex control of HR were determined in sham intact and midcollicular-transected decerebrate rats. Intravenous phenylephrine (0.2-12 microg/kg) and nitroprusside (1-60 microg/kg) were used to measure HR responses to peak changes in mean arterial pressure (MAP). Sigmoidal logistic curve fits to HR-MAP data assessed baroreflex sensitivity (HR/MAP), HR range, lower and upper HR plateau, and MAP at half the HR range (BP50). Four groups (two brain intact and two decerebrate) were studied before, during, and after isoflurane. To assess sympathetic and vagal contributions to HR baroreflex, beta-adrenoceptor (1 mg/kg atenolol) or muscarinic (0.5 mg/kg methyl atropine) antagonists were administered systemically. Results Decerebration did not alter resting MAP and HR or baroreflex parameters. Isoflurane depressed baroreflex slope and HR range in brain-intact and decerebrate rats. In both groups, 1 MAC reduced HR range by depressing peak reflex tachycardia. Maximal reflex bradycardia during increases in blood pressure was relatively preserved. Atenolol during 1 MAC did not alter maximum reflex tachycardia. In contrast, atropine during 1 MAC fully blocked reflex bradycardia. Therefore, 1 MAC predominantly depresses sympathetic components of HR baroreflex. Isoflurane at 2 MAC depressed both HR plateaus and decreased BP50 in both groups. Conclusions Isoflurane depresses HR baroreflex control by actions that do not require suprapontine central nervous system sites. Isoflurane actions seem to inhibit HR baroreflex primarily by the sympathetic nervous system.

Effect of a central CRF antagonist on cardiovascular and thermoregulatory responses induced by stress or IL-1 beta

1993 ◽  
Vol 265 (4) ◽  
pp. R834-R839 ◽  
Author(s):  
T. Nakamori ◽  
A. Morimoto ◽  
N. Murakami
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1 ◽  
Corticotropin Releasing Factor ◽  
Mild Stress ◽  
Induced Responses ◽  
Interleukin 1 Beta ◽  
The Central Nervous System ◽  
Beta 2

We investigated the role of central corticotropin-releasing factor (CRF) in the development of cardiovascular and thermal responses induced by stress or by interleukin-1 beta (IL-1 beta) in free-moving rats. Intracerebroventricular (icv) injection of alpha-helical CRF9-41 (10 micrograms), a CRF receptor antagonist, significantly attenuated hypertension, tachycardia, and a rise in body temperature induced by cage-switch stress, a mild stress. However, icv injection of alpha-helical CRF9-41 (10 micrograms) had no effect on hypertension, tachycardia, or fever induced by intraperitoneal (ip) injection of IL-1 beta (2 micrograms/kg) or icv prostaglandin E2 (PGE2, 100 ng). In contrast, icv injection of alpha-helical CRF9-41 (10 micrograms) significantly attenuated hypertension, tachycardia, or fever induced by icv injection of IL-1 beta (20 ng). The present results suggest that central CRF has an important role in the development of the cage-switch stress-induced responses, but it does not seem to contribute to the hypertension, tachycardia, and fever induced by ip IL-1 beta or by central PGE2. However, it is possible that when IL-1 beta directly acts on the central nervous system, some of its actions are mediated by central CRF.

scholarly journals Fractal fluctuations in the cardiovascular dynamical system : from the autonomic control to the central nervous system influence

2021 ◽  
Author(s):  
Asif Hasan Sharif
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Dynamic Feature ◽  
Scale Free ◽  
Autonomic Nervous ◽  
Factorization Technique ◽  
The Central Nervous System

The fractal component in the complex fluctuations of the human heart rate represents a dynamic feature that is widely observed in diverse fields of natural and artificial systems. It is also of clinical significance as the diminishing of the fractal dynamics appears to correlate with heart disease processes and adverse cardiac events in old age. While the autonomic nervous system directly controls the pacemaker cells of the heart, it does not provide an immediate characterization of the complex heart rate variability (HRV). The central nervous system (CNS) is known to be an important modulator for various cardiac functions. However, its role in the fractal HRV is largely unclear. In this research, human experiments were conducted to study the influence of the central nervous system on fractal dynamics of healthy human HRV. The head up tilt (HUT) maneuver is used to provide a perturbation to the autonomic nervous system. The subsequent fractal effect in the simultaneously recorded electroencephalography and beat-to-beat heart rate data was examined. Using the recently developed multifractal factorization technique, the common multifractality in the data fluctuation was analyzed. An empirical relationship was uncovered which shows the increase (decrease) in HRV multifractality is associated with the increase (decrease) in multifractal correlation between scale-free HRV and the cortical expression of the brain dynamics in 8 out of 11 healthy subjects. This observation is further supported using surrogate analysis. The present findings imply that there is an integrated central-autonomic component underlying the cortical expression of the HRV fractal dynamics. It is proposed that the central element should be incorporated in the fractal HRV analysis to gain a more comprehensive and better characterization of the scale-free HRV dynamics. This study provides the first contribution to the HRV multifractal dynamics analysis in HUT. The multivariate fractal analysis using factorization technique is also new and can be applied in the more general context in complex dynamics research.

Cardioregulatory properties of the abdominal ganglia in Limulus

1970 ◽  
Vol 48 (6) ◽  
pp. 333-341 ◽  
Author(s):  
R. Von Burg ◽  
W. C. Corning
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Heart Function ◽  
Inhibitory Effect ◽  
Bioelectrical Activity ◽  
Inhibitory Influence ◽  
Dorsal Nerves

The abdominal ganglia of the Limulus central nervous system exert a net inhibitory effect on heart rate. This influence is mediated mainly by the dorsal nerves in the first three ganglia. When the dorsal nerves are sectioned, cardioacceleration results; when these nerves are stimulated, a reduction in rate is obtained. However, cardioaccelerators can be unmasked by splitting a ganglion. This selectively removes the inhibitory output, leaving only a cardioaccelerator influence. Inhibition of bioelectrical activity in the intact abdominal ganglia with GABA also resulted in an increased heart rate, confirming their net inhibitory influence on heart function. Possible models of abdominal ganglia organization are discussed.

Hypophysectomy alters cardiorespiratory variables: central effects of pituitary endorphins in shock

1981 ◽  
Vol 241 (4) ◽  
pp. H479-H485 ◽  
Author(s):  
J. W. Holaday ◽  
M. O'Hara ◽  
A. I. Faden
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Mean Arterial Pressure ◽  
Hypovolemic Shock ◽  
Cardiovascular Effects ◽  
Central Effects ◽  
Hypophysectomized Rats ◽  
The Central Nervous System

The possible involvement of pituitary endorphins in the pathophysiology of shock was evaluated by measuring cardiorespiratory variables after naloxone injection in conscious hypophysectomized and sham-hypophysectomized rats subjected to controlled hemorrhage. Additionally, the role of the central nervous system (CNS) in mediating the cardiodepressant effects of endorphins in shock was studied. After the induction of hypovolemic shock (20 min at below 40 mmHg), hypophysectomized and sham-hypophysectomized rats received intraventricular (ivt) injections of naloxone HCl (10 micrograms) or an equivalent volume of saline (20 microliters over 20 s). In sham-hypophysectomized rats, both injections significantly elevated mean arterial pressure and pulse pressure; however, the increase produced by naloxone was significantly greater than that produced by saline. By contrast, hypophysectomized rats showed no response to naloxone or saline. Intravenous (iv) administration of naloxone HCl (3 mg/kg) or saline to these same hypophysectomized rats 15 min after ivt administration had no additional cardiovascular effects; as before, only animals with intact pituitaries responded to naloxone. Heart rate and respiration rate were unaffected by ivt or iv naloxone. From these data we suggest that pituitary endorphins contribute to the pathophysiology of hypovolemic shock, at least in part through actions within the CNS.

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