Centrally administered naloxone blocks reflex natriuresis after acute unilateral nephrectomy

1985 ◽  
Vol 249 (3) ◽  
pp. F390-F395 ◽  
Author(s):  
S. Y. Lin ◽  
M. H. Humphreys
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Opiate Receptors ◽  
Opiate Receptor ◽  
Unilateral Nephrectomy ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Arterial Blood ◽  
Artificial Cerebrospinal Fluid ◽  
The Central Nervous System

Acute unilateral nephrectomy (AUN) leads to a natriuresis and kaliuresis by the remaining kidney through reflex mechanisms involving opiate receptors. To determine whether the opiate receptors mediating these responses are located in the central nervous system, we carried out AUN in anesthetized rats undergoing continuous ventriculocisternal perfusion (VCP) with artificial cerebrospinal fluid (CSF). AUN caused large increases in both Na (UNaV) and K (UKV) excretion without changes in glomerular filtration rate or arterial blood pressure. When the opiate receptor antagonist naloxone was added to the perfusate to achieve a perfusion rate of 32 micrograms X kg-1 X h-1, AUN failed to increase either UNaV or UKV by the remaining kidney. This dose of naloxone, however, was without effect when infused intravenously. Addition of thyrotropin-releasing hormone (TRH) to the artificial CSF to achieve a VCP rate of 50 micrograms X kg-1 X h-1 also blocked the expected increase in UNaV and UKV by the remaining kidney after AUN. Infusion of TRH intravenously at the same rate did not interfere with the postnephrectomy natriuresis or kaliuresis. Higher intravenous infusion rates of TRH (1 and 2 mg X kg-1h-1) prevented the postnephrectomy natriuresis without affecting the kaliuresis. These results indicate that the effect of naloxone to block the reflex natriuresis and kaliuresis after AUN resides largely in the central nervous system. The blockade by naloxone of the postnephrectomy natriuresis is duplicated by centrally administered TRH, providing another example of the interaction of this hormone with the endogenous opioid system. Large intravenous infusions of TRH also block the postnephrectomy natriuresis but not the kaliuresis.

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.

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.

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.

Interaction of phencyclidines with the muscarinic and opiate receptors in the central nervous system

1978 ◽  
Vol 152 (1) ◽  
pp. 176-182 ◽  
Author(s):  
J.P. Vincent ◽  
D. Cavey ◽  
J.M. Kamenka ◽  
P. Geneste ◽  
M. Lazdunski
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Opiate Receptors ◽  
The Central Nervous System

scholarly journals The influence of occupational environment and professional factors on the risk of cardiovascular disease

Medicina ◽  
2006 ◽  
Vol 43 (2) ◽  
pp. 96 ◽  
Author(s):  
Vytautas Obelenis ◽  
Vilija Malinauskienė
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Circulatory System ◽  
Electrolyte Imbalance ◽  
Vascular Lesions ◽  
Cholesterol Concentration ◽  
Long Term Effects ◽  
Arterial Blood ◽  
The Central Nervous System

The article reviews the recent scientific literature and the authors’ studies on this topic. Occupational conditions and psychological factors have been shown to play an important role in the etiopathogenesis of cardiovascular diseases. Their effect is often indirect, through damage to the central nervous, respiratory, and neuroendocrine systems. Hot climate in the workplace and intense infrared radiation cause the water and electrolyte imbalance and chronic hyperthermia and manifests as neurovegetative dystonia. The long-term effects of low temperatures condition ischemic lesions in circulatory system, trophic organ destruction. The influence of ultrahigh-frequency electromagnetic radiation on the cardiovascular system is directly related to the central nervous system and neurohumoral lesions. “Microwave disease” often manifests as polymorphic dystonia. Exposure to occupational vibration causes “white finger” syndrome or Raynaud’s phenomenon together with cerebral vascular lesions. Recent studies have confirmed that noise as a chronic stressor causes the imbalance in the central and vegetative nervous systems and changes in homeostasis. Noise increases catecholamine and cholesterol concentration in blood, has an effect on plasma lipoprotein levels, increases heart rate, arterial blood pressure, and risk of myocardial infarction. Psychophysiological changes caused by long-term stress influence constant pathological changes in the central nervous system, endocrine and cardiovascular systems. The long-term effect of psychogenic stressors is very important in the etiopathogenesis of psychosomatic diseases.

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