Stereoselective actions of S-nitrosocysteine in central nervous system of conscious rats

1997 ◽  
Vol 272 (5) ◽  
pp. H2361-H2368 ◽  
Author(s):  
R. L. Davisson ◽  
M. D. Travis ◽  
J. N. Bates ◽  
A. K. Johnson ◽  
S. J. Lewis
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Intracerebroventricular Injection ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Recognition Sites ◽  
Pressor Responses ◽  
The Central Nervous System ◽  
Intracerebroventricular Injections

This study examined whether the stereoselective actions of S-nitrosocysteine (SNC) in the central nervous system involves the activation of stereoselective SNC recognition sites. We examined the effects produced by intracerebroventricular injection of the L- and D-isomers of SNC (L- and D-SNC) on mean arterial blood pressure, heart rate, and vascular resistances in conscious rats. We also examined the hemodynamic effects produced by intracerebroventricular injections of 1) L-cystine, the major non-nitric oxide (NO) decomposition product of L-SNC, 2) the parent thiols L- and D-cysteine, and 3) the bulky S-nitrosothiol L-S-nitroso-gamma-glutamylcysteinylglycine [L-S-nitrosoglutathione, (L-SNOG)]. Finally, we examined the decomposition of L- and D-SNC and L-SNOG to NO on their addition to brain homogenates. The intracerebroventricular injection of L-SNC (250-1,000 nmol) produced falls in mean arterial pressure, increases in heart rate, and a dose-dependent pattern of changes in hindquarter, renal, and mesenteric vascular resistances. The intracerebroventricular injections of D-SNC, L-cystine, and L-SNOG produced only minor effects. The intracerebroventricular injection of L-cysteine produced pressor responses and tachycardia, whereas D-cysteine was inactive. L- and D-SNC decomposed equally to NO on addition to brain homogenates. L-SNOG decomposed to similar amounts of NO as L- and D-SNC. These results suggest that SNC may activate stereoselective SNC recognition sites on brain neurons and that S-nitrosothiols of substantially different structure do not stimulate these sites. These recognition sites may be stereoselective membrane-bound receptors for which L-SNC is the unique ligand.

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.

Effect of central administration of motilin on migrating complexes in the dog

1987 ◽  
Vol 252 (2) ◽  
pp. G195-G199 ◽  
Author(s):  
M. Hashmonai ◽  
V. L. Go ◽  
T. Yaksh ◽  
J. H. Szurszewski
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Central Administration ◽  
Intravenous Injections ◽  
Lumbar Level ◽  
The Central Nervous System ◽  
Intracerebroventricular Injections ◽  
Plasma Motilin ◽  
Endogenous Release ◽  
Intrathecal Space

The effects of intravenous, intrathecal, and intracerebroventricular injection of motilin on the interdigestive myoelectric (MMC) activity of the stomach and small intestine were examined in conscious dogs. To monitor electrical activity, electrodes were implanted on the stomach and small bowel. To inject motilin into the central nervous system, catheters were chronically positioned in the intrathecal space at the lumbar level and in one of the lateral cerebral ventricles. In all dogs, intravenous injection of motilin caused a transient increase in the plasma concentration of motilin and initiated gastric MMCs, which propagated aborally to the ileum. Intrathecal and intracerebroventricular injections of motilin did not affect plasma motilin levels and did not induce MMCs. These data suggest that initiation of MMCs after intravenous injections of motilin occurs through receptors for motilin possibly located outside the central nervous system. These data also suggest the hypothesis that initiation of naturally occurring MMCs in the dog may not be dependent on endogenous release of motilin from the central nervous system.

scholarly journals Contribution of Baroreceptor Function to Pain Perception and Perioperative Outcomes

2019 ◽  
Vol 130 (4) ◽  
pp. 634-650 ◽  
Author(s):  
Heberto Suarez-Roca ◽  
Rebecca Y. Klinger ◽  
Mihai V. Podgoreanu ◽  
Ru-Rong Ji ◽  
Martin I. Sigurdsson ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Pain Perception ◽  
Perioperative Outcomes ◽  
Cognitive Responses ◽  
Baroreceptor Function ◽  
Arterial Blood ◽  
Baroreceptor Reflexes ◽  
The Central Nervous System ◽  
Physiologic Responses

Abstract Baroreceptors are mechanosensitive elements of the peripheral nervous system that maintain homeostasis by coordinating physiologic responses to external and internal stimuli. While it is recognized that carotid and cardiopulmonary baroreceptor reflexes modulate autonomic output to mitigate excessive fluctuations in arterial blood pressure and to maintain intravascular volume, increasing evidence suggests that baroreflex pathways also project to key regions of the central nervous system that regulate somatosensory, somatomotor, and central nervous system arousal. In addition to maintaining autonomic homeostasis, baroreceptor activity modulates the perception of pain, as well as neuroimmune, neuroendocrine, and cognitive responses to physical and psychologic stressors. This review summarizes the role that baroreceptor pathways play in modulating acute and chronic pain perception. The contribution of baroreceptor function to postoperative outcomes is also presented. Finally, methods that enhance baroreceptor function, which hold promise in improving postoperative and pain management outcomes, are presented.

A comparison of some pharmacological effects of naloxone and N-methylnaloxone in mice

1982 ◽  
Vol 60 (5) ◽  
pp. 715-719 ◽  
Author(s):  
K. Ramabadran ◽  
C. Suaudeau ◽  
J. J. C. Jacob
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Subcutaneous Administration ◽  
Intracerebroventricular Injection ◽  
Pharmacological Effects ◽  
Opioid Antagonists ◽  
Hot Plate ◽  
Two Factors ◽  
The Central Nervous System ◽  
Derivatives Of

The effects of N-methylnaloxone following subcutaneous and intracerebroventricular administrations on nociception were investigated using the hot plate technique. Unlike naloxone, subcutaneous administration of N-methylnaloxone did not enhance the nociceptive reactions. In contrast, intracerebroventricular injection of N-methylnaloxone produced antinociception and tremor. Compared with naloxone, N-methylnaloxone was very weak in precipitating the signs of abstinence in mice rendered acutely dependent on morphine. Two factors, poor penetration into the central nervous system and steric hindrance, might render N-methylnaloxone very weak and hence both these factors must be taken into consideration while analyzing the effects following quaternary derivatives of opioid antagonists.

Central Nervous System Pressor Responses in Rats Susceptible and Resistant to Sodium Chloride Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 225s-227s ◽  
Author(s):  
T. Ikeda ◽  
L. Tobian ◽  
J. Iwai ◽  
Patricia Goossens
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Sodium Chloride ◽  
Angiotensin Ii ◽  
Hypertonic Saline ◽  
Pressor Effect ◽  
Left Lateral Ventricle ◽  
Pressor Responses ◽  
The Central Nervous System

1. The pressor responses to hypertonic saline and angiotensin II introduced into the left lateral ventricle were both significantly greater in salt-sensitive (S) rats compared with salt-resistant (R) rats, with all rats on a low Na diet. 2. When S rats were given thiazide to nullify the pressor effect of dietary NaCl, their blood pressure averaged only 5 mmHg higher than that of the R rats; nevertheless, these S rats had significantly higher central nervous system pressor responses to angiotensin II and hypertonic saline. 3. Thus, if excessive dietary Na increases blood pressure by way of action on the central nervous system, these heightened pressor responses could partially account for the NaCl hypertension in S rats. Alternatively, depressed central nervous system pressor responses in R rats could partially explain the resistance of R rats to NaCl hypertension.

scholarly journals Role of Catecholamine in Pressor Responses to Stimulation of the Central Nervous System

1963 ◽  
Vol 4 (2) ◽  
pp. 118-130 ◽  
Author(s):  
Hideo UEDA ◽  
Akiyuki YAMADA ◽  
Hitoshi GOTO ◽  
Iwao ITO ◽  
Yutaka TAKABATAKE ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Pressor Responses ◽  
The Central Nervous System ◽  
Stimulation Of

Suppressed basal antidiuretic hormone release during cyclooxygenase inhibition in conscious dogs

1983 ◽  
Vol 244 (4) ◽  
pp. R487-R491
Author(s):  
B. R. Walker
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Antidiuretic Hormone ◽  
Plasma Osmolality ◽  
Blood Gases ◽  
Conscious Dogs ◽  
Arterial Blood ◽  
The Central Nervous System

Both in vitro and in vivo experiments suggest that prostaglandins may affect antidiuretic hormone (ADH) release centrally. In addition, other studies show that prostaglandins administered peripherally may cause ADH release. However, these latter studies have been flawed by hemodynamic alterations and the use of anesthetics, which make interpretation difficult. The present study was designed to test for involvement of prostaglandins produced outside the central nervous system in ADH release in conscious dogs. Administration of meclofenamate (2 mg/kg and 2 mg X kg-1 X h 1, iv) resulted in a consistent fall in plasma ADH levels in five dogs. This diminution of ADH release occurred with no change in systemic hemodynamics, arterial blood gases, or plasma osmolality, suggesting that prostaglandins are important mediators of basal ADH release in the conscious dog. Because meclofenamate does not cross the blood-brain barrier, prostaglandins produced outside the central nervous system appear to be involved in this process. The specific prostaglandin involved or the site of action of prostaglandins on ADH release is not clear at this time.

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