Hepatic glucose balance in response to direct stimulation of sympathetic nerves in the intact liver of cats

1978 ◽  
Vol 56 (6) ◽  
pp. 1022-1028 ◽  
Author(s):  
W. Wayne Lautt ◽  
Chong Wong
Keyword(s):  
Sympathetic Nerves ◽  
Direct Stimulation ◽  
Blood Flows ◽  
Parasympathetic Nerves ◽  
Hepatic Glucose ◽  
Simultaneous Activation ◽  
Glucose Output ◽  
Hepatic Nerves ◽  
Mixed Nerve ◽  
Stimulation Of

Changes in hepatic glucose balance in response to direct stimulation of the hepatic nerves were measured in cats. Simultaneous measurements were made of glucose concentrations entering and leaving the intact liver; this, combined with measured blood flows, allows calculation of hepatic glucose balance. Stimulation of the hepatic sympathetic nerves (8 Hz, 15 V, 1 ms) produced a rapid increase in hepatic glucose output that was statistically significant after 1 min and reached a peak 3–5 min after onset of stimulation, after which time the output declined somewhat. The half time for deactivation of the response was 1.8–2 min. Variability in the responses was largely accounted for by the variable control base lines measured immediately prior to stimulation. Those animals showing the highest basal output showed the least increase in output in response to the nerves. The response to stimulation of the mixed nerve trunk in the presence and absence of atropine (1 mg/kg, intraportal) was similar. Simultaneous activation of hepatic sympathetic and parasympathetic nerves therefore produces a purely sympathetic type of effect on net glucose balance across the liver. It was also shown that changes in net splanchnic output or simply in arterial – hepatic venous glucose differences are an adequate reflection of liver glucose balance under the currently tested responses.

Hepatic parasympathetic neural effect on glucose balance in the intact liver

1978 ◽  
Vol 56 (4) ◽  
pp. 679-682 ◽  
Author(s):  
W. Wayne Lautt ◽  
Chong Wong
Keyword(s):  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Electromagnetic Flowmeter ◽  
Sympathetic Nerves ◽  
Rapid Reduction ◽  
Parasympathetic Nerves ◽  
Hepatic Glucose ◽  
6 Hydroxydopamine ◽  
Glucose Output ◽  
Neural Effect

Sympathetic nerves to the intact liver of the cat were selectively destroyed by injection of 6-hydroxydopamine into the portal vein 1 week prior to the experiment. Glucose output was calculated from the product of the arterial–venous glucose difference and hepatic blood flow. Hepatic blood flow was monitored by an electromagnetic flowmeter using a hepatic venous long-circuit. Stimulation of the parasympathetic nerves isolated from around the common hepatic artery produced a rapid reduction in hepatic glucose output to one-quarter of control levels by 2 min and to zero by 10 min of nerve stimulation. The data show that hepatic glucose balance is readily influenced by the hepatic parasympathetic nerves.

scholarly journals Lateral Habenula Regulates Cardiovascular Autonomic Responses via the Serotonergic System in Rats

2021 ◽  
Vol 15 ◽  
Author(s):  
Tri Huu Doan ◽  
Yuma Sato ◽  
Masayuki Matsumoto ◽  
Tadachika Koganezawa
Keyword(s):  
Receptor Antagonist ◽  
Cardiovascular Responses ◽  
Sympathetic Nerves ◽  
Stressful Events ◽  
Serotonergic System ◽  
High Dose ◽  
Lateral Habenula ◽  
Autonomic Responses ◽  
Parasympathetic Nerves ◽  
Stimulation Of

The lateral habenula (LHb) plays essential roles in behavioral responses to stressful events. Stress is tightly linked to autonomic responses such as cardiovascular responses, yet how the LHb regulates these responses is not well understood. To address this issue, we electrically stimulated the LHb in rats, measured its effects on heart rate (HR) and mean arterial pressure (MAP), and investigated the neural circuits that mediate these LHb-induced cardiovascular responses via the autonomic nervous system. We observed that stimulation of the LHb induced bradycardia and pressor responses, whereas stimulation of the adjacent areas changed neither the HR nor the MAP. Bilateral vagotomy and administration of a muscarinic receptor antagonist suppressed the LHb stimulation effect on the HR but not on the MAP, whereas administration of a β-adrenoceptor antagonist partly attenuated the effect on the MAP but not on the HR. Thus, the LHb-induced cardiovascular responses of the HR and the MAP were likely caused by activations of the cardiac parasympathetic nerves and the cardiovascular sympathetic nerves, respectively. Furthermore, administration of a non-selective 5-HT receptor antagonist significantly attenuated the LHb stimulation effects on both the MAP and the HR. A 5-HT2 receptor antagonist also attenuated the LHb stimulation effects. A low dose of a 5-HT1A receptor antagonist enhanced the LHb stimulation effects, but a high dose of the drug attenuated them. 5-HT1B and 5-HT1D receptor antagonists as well as a 5-HT7 receptor antagonist did not affect the LHb stimulation effects. Taken together, our findings suggest that the LHb regulates autonomic cardiovascular responses at least partly through the serotonergic system, particularly via the 5-HT1A and 5-HT2 receptors.

Visceral nociception: peripheral and central aspects of visceral nociceptive systems

1985 ◽  
Vol 308 (1136) ◽  
pp. 325-337 ◽  
Keyword(s):  
Central Nervous System ◽  
Intestinal Tract ◽  
Sympathetic Nerves ◽  
Noxious Stimulation ◽  
Visceral Sensation ◽  
Parasympathetic Nerves ◽  
The Central Nervous System ◽  
Specific Receptors ◽  
Gastro Intestinal Tract ◽  
Stimulation Of

Discomfort and pain are the sensations most commonly evoked from viscera. Most nociceptive signals that originate from visceral organs reach the central nervous system (c.n.s.) via afferent fibres in sympathetic nerves, whereas parasympathetic nerves contain mainly those visceral afferent fibres concerned with the non-sensory aspects of visceral afferent function. Noxious stimulation of viscera activates a variety of specific and non-specific receptors, the vast majority of which are connected to unmyelinated afferent fibres. Studies on the mechanisms of visceral sensation can thus provide information on the more general functions of unmyelinated afferent fibres. Specific visceral nociceptors have been found in the heart, lungs, testes and biliary system, whereas noxious stimulation of the gastro-intestinal tract appears to be detected mainly by non-specific visceral receptors that use an intensity-encoding mechanism.

Responses of hepatic glucose output to electro-acupuncture stimulation of the hindlimb in anaesthetized rats

2004 ◽  
Vol 115 (1-2) ◽  
pp. 7-14 ◽  
Author(s):  
Rie Shimoju-Kobayashi ◽  
Hitoshi Maruyama ◽  
Masashi Yoneda ◽  
Mieko Kurosawa
Keyword(s):  
Hepatic Glucose Output ◽  
Acupuncture Stimulation ◽  
Hepatic Glucose ◽  
Anaesthetized Rats ◽  
Glucose Output ◽  
Stimulation Of

scholarly journals Stimulation by vasopressin of glycogen breakdown and gluconeogenesis in the perfused rat liver

1973 ◽  
Vol 136 (3) ◽  
pp. 705-709 ◽  
Author(s):  
Douglas A. Hems ◽  
Patricia D. Whitton
Keyword(s):  
Liver Glycogen ◽  
Haemorrhagic Shock ◽  
Perfused Rat Liver ◽  
Hepatic Glucose Output ◽  
Diuretic Hormone ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Glycogen Breakdown ◽  
Stimulation Of ◽  
Intact Rats

1. Vasopressin (anti-diuretic hormone, [8-arginine]vasopressin) stimulated the breakdown of glycogen in perfused livers of fed rats, at concentrations (50–600μunits/ml) that have been reported in the blood of intact rats, especially during acute haemorrhagic shock. 2. In perfused livers from starved rats, vasopressin (30–150μunits/ml) stimulated gluconeogenesis from a mixture of lactate, pyruvate and glycerol. 3. Vasopressin prevented accumulation of liver glycogen in the perfused liver of starved rats, or in starved intact rats. 4. The action of vasopressin on hepatic carbohydrate metabolism thus resembles that of glucagon; the minimum effective circulating concentrations of these hormones are of the same order (100pg/ml). 5. The stimulation of hepatic glucose output by vasopressin is discussed in connexion with the release of glucose and water from the liver.

scholarly journals Direct Stimulation of Ghrelin Secretion by Sympathetic Nerves

Endocrinology ◽  
2006 ◽  
Vol 147 (6) ◽  
pp. 2893-2901 ◽  
Author(s):  
Thomas O. Mundinger ◽  
David E. Cummings ◽  
Gerald J. Taborsky
Keyword(s):  
Sympathetic Nerves ◽  
Direct Stimulation ◽  
Ghrelin Secretion ◽  
Stimulation Of

Effect of phlorizin on hepatic glucose output

1962 ◽  
Vol 202 (1) ◽  
pp. 149-154 ◽  
Author(s):  
Edwin H. Kolodny ◽  
Robert Kline ◽  
Norman Altszuler
Keyword(s):  
Plasma Glucose ◽  
Vena Cava ◽  
The Body ◽  
Hepatic Veins ◽  
Hepatic Glucose Output ◽  
Direct Stimulation ◽  
Indwelling Catheters ◽  
Glucose Levels ◽  
Hepatic Glucose ◽  
Glucose Output

Using phlorizin as an experimental tool, an investigation of the mechanisms responsible for the maintenance of plasma glucose levels was undertaken. Infusion of phlorizin has been shown to produce a prompt glucosuria and increase in hepatic glucose output (HGO), but without discernable hypoglycemia. This raises the question as to the nature of the stimulus for the increased HGO. The effect of phlorizin on net HGO was studied in anesthetized dogs with indwelling catheters in the portal and hepatic veins. Infusion of phlorizin into normal dogs produced a prompt glucosuria and a concomitant increase in HGO, without significant changes in the plasma glucose concentration in the portal vein. In functionally nephrectomized dogs, phlorizin did not change HGO nor circulating glucose levels. In dogs with intact kidneys, when glucosuria was prevented by urine recirculation into the inferior vena cava, the infusion of phlorizin again failed to alter HGO or circulating glucose levels. The data indicate that the phlorizin-induced increase in HGO is dependent on loss of glucose from the body. The enhancement of HGO could not be ascribed to a direct stimulation of the liver, kidney, or endocrine glands, or to an impairment of glucose utilization. Possible mechanisms to explain this effect of phlorizin are discussed.

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