Correlation between endogenous noradrenaline and glucose released from the liver upon hepatic sympathetic nerve stimulation in anesthetized dogs

1984 ◽  
Vol 62 (9) ◽  
pp. 1086-1091 ◽  
Author(s):  
Denis Garceau ◽  
Nobuharu Yamaguchi ◽  
Robert Goyer ◽  
Francine Guitard
Keyword(s):  
Nerve Stimulation ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Metabolic Role ◽  
Hepatic Venous Blood ◽  
Anesthetized Dogs ◽  
Na Release ◽  
Induced Changes ◽  
Hepatic Nerves

The metabolic role of neurally released noradrenaline (NA) was studied in the liver of anesthetized dogs. Sustained stimulation with various frequencies was directly applied on the anterior plexus of hepatic nerves. Stimulation-induced changes in plasma concentrations of endogenous catecholamines in hepatic venous blood were determined in correlation with concomitant changes in those of glucose (GL). Mean basal values for hepatic venous NA, adrenaline, dopamine, and GL were 0.062, 0.022, 0.032 ng/mL, and 97.9 mg%, respectively. Among these catecholamines, NA was the only one being released significantly during stimulation. While hepatic venous NA increased rapidly during stimulation, being maximum within 3 min, hepatic venous GL increased gradually, reaching a maximum value 5 min after the onset of stimulation. A highly significant correlation (r = 0.90, P < 0.001) was found between changes in hepatic venous NA and GL concentrations observed during stimulation at various frequencies (2–16 Hz). However, hepatic vasoconstricting responses to stimulation were not correlated with increased hepatic venous GL. An α-blockade with phentolamine (2 mg/kg, iv) resulted in diminished release of GL by approximately 50% (P < 0.05) and reduced hepatic arterial vasoconstriction by approximately 47% (P < 0.01) upon stimulation (8 Hz, 5 min), even though NA release was markedly enhanced. We conclude that in the dog, NA is the sole catecholamine released within the liver in response to direct hepatic nerve stimulation, and NA thus released mediates the hepatic glycogenolysis via α-adrenoceptors.

Evidence for increased hepatic sympathetic nerve activity resulting in hyperglycemia in response to hemorrhage-induced reflex stimulation in anesthetized dogs

1985 ◽  
Vol 63 (9) ◽  
pp. 1209-1213 ◽  
Author(s):  
Nobuharu Yamaguchi
Keyword(s):  
Adrenal Glands ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Correlation Coefficients ◽  
Sympathetic Nerves ◽  
Maximum Output ◽  
Venous Blood Flow ◽  
Large Measure ◽  
Hepatic Venous Blood ◽  
Anesthetized Dogs

To investigate the role of the sympathoadrenal system in glucose mobilization by the liver during hemorrhage, catecholamine (CA) output from both adrenal glands was determined in anesthetized dogs. Venous blood draining from both adrenal glands was combined in a Y-tube that was connected to an electromagnetic flow probe to measure total adrenal venous blood flow. Plasma concentrations of norepinephrine (NE), epinephrine (E), dopamine (DA), and glucose (GL) were determined in various vascular regions. Adrenal CA output (nanograms per minute) under basal conditions was 50.2 ± 13.6, 181.4 ± 41.9, and 13.7 ± 4.8 for NE, E, and DA, respectively. These values were found to increase significantly (P < 0.05) in response to 5 min of hemorrhage, reaching a maximum output (nanograms per minute) of 663.6 ± 160.6 (NE), 2503.4 ± 607.8 (E), and 141.7 ± 43.7 (DA). Aortic CAs (nanograms per millilitre) increased significantly with a predominant increase in E (0.33 ± 0.08 to 3.75 ± 1.03, P < 0.05). In contrast, increases in portal and hepatic venous CAs (nanograms per millilitre) were characterized by a predominant increase in NE (0.30 ± 0.06 to 0.64 ± 0.11 and 0.17 ± 0.02 to 0.31 ± 0.07, respectively, P < 0.05). Hepatic venous and aortic GL concentrations also increased significantly during hemorrhage. Among the various correlations between plasma CA and GL concentrations, the strongest correlation was found between hepatic venous NE and hepatic venous GL (r = 0.804, P < 0.001). Correlation coefficients obtained with aortic NE and E were weaker but significant (r = 0.603 and r = 0.608, respectively, P < 0.01). Both the predominant increase in NE observed in hepatic-venous blood and the marked correlation of hepatic venous NE with hepatic venous GL suggest that, in dogs with normal sympathoadrenal systems, hemorrhage-induced hyperglycemia results from increased hepatic glycogenosis, due in large measure to increased activation of hepatic sympathetic nerves.

An intracaval cannulation for obtaining pure, mixed hepatic venous blood samples

1978 ◽  
Vol 235 (2) ◽  
pp. H262-H265
Author(s):  
W. W. Lautt ◽  
C. Wong ◽  
J. S. Durham ◽  
P. Taillon
Keyword(s):  
Blood Pressure ◽  
Venous Blood ◽  
Vena Cava ◽  
Direct Stimulation ◽  
Blood Samples ◽  
Arterial Blood ◽  
Vascular Congestion ◽  
Hepatic Venous Blood ◽  
Surgical Preparation ◽  
Hepatic Nerves

A method for obtaining pure, mixed hepatic venous blood is described and evaluated in anesthetized cats. Hepatic vascular congestion does not occur with this “intracaval cannulation”, however small elevations in central venous blood pressure were noted. Although these changes persisted they did not result in systemic vascular congestion, judging from the normal arterial and portal pressures and from the lack of progressive decrease in arterial blood pressure. Blood samples obtained using the intracaval cannulation were shown to contain identical levels of oxygen as those obtained using a more complex surgical preparation. Reflux of blood from the vena cava does not occur during sampling. The responsiveness of this sampling method to rapid changes in venous content was evaluated by following the changes in glucose balance caused by direct stimulation of the hepatic nerves. The responses measured were similar to those measured in a separate set of experiments obtained using blood samples from a surgically isolated hepatic venous supply.

Activation of histamine H3 receptors inhibits renal noradrenergic neurotransmission in anesthetized dogs

2001 ◽  
Vol 280 (5) ◽  
pp. R1450-R1456 ◽  
Author(s):  
Tomoyuki Yamasaki ◽  
Isao Tamai ◽  
Yasuo Matsumura
Keyword(s):  
Receptor Antagonist ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urinary Sodium ◽  
Renal Nerve ◽  
Anesthetized Dogs ◽  
Induced Changes ◽  
Antidiuretic Action

To investigate the possible involvement of histamine H3 receptors in renal noradrenergic neurotransmission, effects of (R)alpha-methylhistamine (R-HA), a selective H3-receptor agonist, and thioperamide (Thiop), a selective H3-receptor antagonist, on renal nerve stimulation (RNS)-induced changes in renal function and norepinephrine (NE) overflow in anesthetized dogs were examined. RNS (0.5–2.0 Hz) produced significant decreases in urine flow and urinary sodium excretion and increases in NE overflow rate (NEOR), without affecting renal hemodynamics. When R-HA (1 μg · kg−1 · min−1) was infused intravenously, mean arterial pressure and heart rate were significantly decreased, and there was a tendency to reduce basal values of urine flow and urinary sodium excretion. During R-HA infusion, RNS-induced antidiuretic action and increases in NEOR were markedly attenuated. Thiop infusion (5 μg · kg−1 · min−1) did not affect basal hemodynamic and excretory parameters. Thiop infusion caused RNS-induced antidiuretic action and increases in NEOR similar to the basal condition. When R-HA was administered concomitantly with Thiop infusion, R-HA failed to attenuate the RNS-induced antidiuretic action and increases in NEOR. However, in the presence of pyrilamine (a selective H1-receptor antagonist) or cimetidine (a selective H2-receptor antagonist) infusion, R-HA attenuated the RNS-induced actions, similarly to the case without these antagonists. Thus functional histamine H3 receptors, possibly located on renal noradrenergic nerve endings, may play the role of inhibitory modulators of renal noradrenergic neurotransmission.

Presynaptic inhibitory effects of sotalol, propranolol, and acebutolol on noradrenaline release upon cardiac sympathetic nerve stimulation in anesthetized dogs

1986 ◽  
Vol 64 (8) ◽  
pp. 1076-1084 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Michel Naud ◽  
Daniel Lamontagne ◽  
Reginald Nadeau ◽  
Jacques de Champlain
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Inhibitory Effect ◽  
Cardiac Sympathetic Nerve ◽  
Sympathetic Nerve Stimulation ◽  
Flow Response ◽  
Anesthetized Dogs ◽  
Na Release

Effect of sotalol (STL) was compared with that of (±)-propranolol, (+)-propranolol (PPL), and acebutolol (ABL) on noradrenaline (NA) release as measured in coronary sinus (CS) blood during postganglionic stimulation (2 Hz, 30 s) of the left cardiac sympathetic nerves in anesthetized dogs. In control dogs receiving saline, increasing responses of CS-NA concentration, mean CS blood flow, and CS-NA output to repetitive stimulation were relatively stable throughout a given experimental period. Both STL (1, 2.5, and 5 mg/kg, i.v.) and (±)-PPL (0.5 and 2.5 mg/kg, i.v.) diminished the increased CS-NA concentration by approximately 35 (P < 0.05) to 60% (P < 0.01) in a dose-dependent fashion. However, (+)-PPL (0.02–2.5 mg/kg, i.v.) and ABL (0.5–5 mg/kg, i.v.) did not significantly alter the increasing response of CS-NA concentration upon stimulation. STL, (±)-PPL, and ABL markedly inhibited the CS blood flow response to stimulation at all doses tested, while (+)-PPL did not significantly diminish the flow response even at the highest dose tested. Consequently, CS-NA output decreased significantly (p < 0.01) in the presence of STL, (±)-PPL, and ABL at all doses tested but not with (+)-PPL at any dose tested. The inhibitory effect of STL and (±)-PPL on the increasing response of CS-NA concentration upon stimulation could be related to their beta-blocking effect, which exerts presumably on postulated presynaptic β-adrenoceptors, as (+)-PPL did not at all diminish the response. On the other hand, ABL does not seem to exert a similar presynaptic inhibitory effect, owing presumably either to its β-1 selectivity or to its intrinsic sympathetic activity. The results support the existence of facilitatory presynaptic β-adrenoceptors in the normal dog heart under in vivo conditions. The findings also suggest that NA release upon cardiac sympathetic nerve stimulation may be reflected more precisely by CS-NA concentration than by NA output.

Effects of nifedipine and Bay K 8644 on stimulation-induced adrenal catecholamine secretion in the dog

1993 ◽  
Vol 265 (1) ◽  
pp. R28-R34 ◽  
Author(s):  
R. Gaspo ◽  
N. Yamaguchi ◽  
J. De Champlain
Keyword(s):  
Pulse Duration ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Splanchnic Nerve ◽  
Bay K 8644 ◽  
Control Group ◽  
Total Period ◽  
Aortic Blood ◽  
Anesthetized Dogs

The effects of nifedipine and BAY K 8644 on the adrenal medullary secretion in response to direct splanchnic nerve stimulation were studied in anesthetized dogs. Supramaximal stimulation (12 V) was given on the left splanchnic nerve at a frequency of 2 Hz with three different pulse durations (0.2, 2, and 20 ms) for a total period of 1.5 min. Each stimulation was given for 30 s without interruption between each stimulation. Plasma concentrations of epinephrine and norepinephrine were measured in adrenal venous and aortic blood. In the vehicle control group, epinephrine and norepinephrine concentrations in adrenal venous blood proportionally increased with the lengthening of the pulse duration without significant changes in catecholamine concentrations in aortic blood. In dogs receiving nifedipine (100 micrograms/kg iv), the net increase in adrenal venous epinephrine concentration during stimulation with 20-ms pulse duration was attenuated by approximately 50% (P < 0.05). In dogs treated with BAY K 8644 (30 micrograms.kg-1.min-1 iv), both adrenal venous epinephrine and norepinephrine secretions evoked by stimulation with 20-ms pulse duration were significantly enhanced by approximately 50%. The present results suggest that the secretion of adrenal catecholamines under in vivo conditions is controlled through mechanism(s) involving dihydropyridine sensitive L-type Ca2+ channels presumably localized on the surface of adrenal medullary chromaffin cells.

Effects of yohimbine and desipramine on cardiac noradrenaline release and ventricular arrhythmias during acute coronary artery occlusion and reperfusion in anesthetized dogs

1987 ◽  
Vol 65 (11) ◽  
pp. 2244-2253 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Daniel Lamontagne ◽  
Ghislain Boudreau ◽  
Reginald Nadeau ◽  
Jacques de Champlain
Keyword(s):  
Coronary Artery ◽  
Nerve Stimulation ◽  
Left Ventricular Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Neuronal Uptake ◽  
Ischemic Region ◽  
Anesthetized Dogs ◽  
Na Release

Effects of yohimbine (YHMB, an α2-antagonist) and desipramine (DMI, a neuronal uptake inhibitor) were compared on cardiac noradrenaline (NA) release either upon left ansa subclavia nerve stimulation during acute occlusion of the left anterior descending coronary artery (LAD) or upon subsequent LAD reperfusion without stimulation in anesthetized dogs. In control dogs, before LAD occlusion, coronary sinus (CS) NA output increased from 5.4 ± 1.0 to 26.8 ± 4.0 ng/min (p < 0.05) upon stimulation (2 Hz, 30 s). The response to stimulation remained unchanged 25 min after LAD occlusion. During reperfusion 60 min after occlusion, the output of CS-NA and lactate increased from 6.1 ± 0.8 to 51.3 ± 19.4 ng/min (p < 0.05) and from 2.7 ± 0.5 to 6.7 ± 1.3 mg/min (p < 0.05), respectively. In dogs treated with YHMB, the stimulation-induced increase in NA output was potentiated at least fourfold (p < 0.05) either before or during LAD occlusion, but not during reperfusion. In dogs receiving DMI, stimulation-induced CS-NA output was enhanced to a similar extent (approximately twofold, p < 0.05) either before or during occlusion, while reperfusion-induced NA output was markedly potentiated by approximately ninefold (p < 0.05). Maximum dP/dt of left ventricular pressure remained unchanged upon reperfusion in all groups. The total arrhythmic ratio in the drug-treated groups did not significantly differ from the ratio in control dogs upon either stimulation or reperfusion. The data suggest that an abrupt increase in NA output upon reperfusion may result from a washout of NA locally accumulated in the ischemic and (or) peri-ischemic region during the preceding occlusion period, and that N A thus released does not have substantial hemodynamic effects. The results indicate that in the presence of YHMB or DMI, the potentiated increase in NA release in response to either nerve stimulation during LAD occlusion or to reperfusion without stimulation did not aggravate ventricular arrhythmia, most probably owing to the antiarrhythmic properties of these substances.

Plasma 4-pregnene-17α,20α-diol-3-one (17α,20α-dihydroxyprogesterone) and 17α-hydroxyprogesterone in man

1983 ◽  
Vol 102 (2) ◽  
pp. 271-276 ◽  
Author(s):  
Judith A. Whitworth ◽  
Aldona Butkus ◽  
J. P. Coghlan ◽  
D. A. Denton ◽  
Dianne Saines ◽  
...  
Keyword(s):  
Venous Blood ◽  
Plasma Concentrations ◽  
Normal Subjects ◽  
Dietary Sodium ◽  
Lower Amplitude ◽  
Induced Hypertension ◽  
Male Subjects ◽  
Mineralocorticoid Activity

Abstract. Investigation of the mechanisms involved in ACTH induced hypertension in sheep led to delineation of the major role of 4-pregnene-17α,20α-diol-3-one (17α,20α-OHP) in ovine adrenal venous blood. It has been shown in this model of steroid induced hypertension that 17α,20α-OHP is 'hypertensinogenic' i.e. capable of raising blood pressue when infused concurrently with the major mineralocorticoid and glucocorticoid steroid hormones, but in itself it has no significant blood pressure elevating effect and no significant glucocorticoid or mineralocorticoid activity. The present study examines the regulation of 17α,20α-OHP and 17α-hydroxyprogesterone (17-OHP) in man. The plasma concentration of 17α,20α-OHP in normal ambulant subjects (n = 29) bled at 08.00 to 10.00 h was 14.5 ± 0.8 nmol/l compared with 17-OHP 7.8 ± 0.6 nmol/l. Administration of ACTH (20 μg/kg/day) to normotensive male subjects (n = 6) produced after 5 days of rise in 17α,20α-OHP from 16.6 ± 2.2 to 48.9 ± 7.9 nmol/l and in 17-OHP from 10.9 ± 1.12 to 29.3 ± 4.2 nmol/l. In normal subjects, 17α,20α-OHP had a diurnal rhythm similar to that of cortisol but of lower amplitude. Plasma concentrations of both steroids rose with stepped 30 min ACTH infusions and were suppressed by dexamethasone administration. Angiotensin II infusion, dietary sodium restriction and 9α-fluorocortisol administration had no effect on plasma 17α,20α-OHP. There was no change in 17α,20α-OHP throughout the menstrual cycle but 17-OHP increased during the luteal phase of the cycle. 17-OHP was lower in women on oral contraceptives than in control women, but values for 17α,20α-OHP were unchanged. The mean plasma clearance rate for 17α,20α-OHP in 3 normal subjects was 30.2 l/day/kg, similar to that for aldosterone (31.2 l/day/kg). Unlike the sheep there was no in vitro conversion of 17-OHP to 17α,20α-OHP in human blood. These studies show that 17α,20α-OHP is present in human plasma in higher concentration than 17-OHP. The secretion of 17α,20α-OHP appears to be primarily under the control of ACTH.

Metabolic role of the exercise-induced increment in epinephrine in the dog

1988 ◽  
Vol 255 (4) ◽  
pp. E428-E436 ◽  
Author(s):  
J. M. Moates ◽  
D. B. Lacy ◽  
R. E. Goldstein ◽  
A. D. Cherrington ◽  
D. H. Wasserman
Keyword(s):  
Glucose Production ◽  
Plasma Glucagon ◽  
Metabolic Role ◽  
Exercise Period ◽  
Exercise Induced ◽  
Glucagon And Insulin ◽  
Induced Changes ◽  
Response To Exercise ◽  
Rest And Exercise

The role of the exercise-induced increment in epinephrine was studied in five adrenalectomized (ADX) and in six normal dogs (C). Experiments consisted of an 80-min equilibration period, a 40-min basal period, and a 150-min exercise period. ADX were studied with epinephrine replaced to basal levels during rest and to increased levels during exercise to simulate its normal rise (HE) and on a separate day with epinephrine maintained at basal levels throughout the study (BE). Cortisol was replaced during rest and exercise in ADX so as to simulate the levels seen in C. Glucose was infused as needed in ADX to maintain the glycemia evident during exercise in C. Glucose production (Ra) and utilization (Rd) were assessed isotopically. In C, epinephrine had risen by 95 +/- 25 pg/ml by the end of exercise. In HE, the increment in epinephrine (117 +/- 29 pg/ml) was similar to that seen in C, whereas in BE epinephrine fell by 18 +/- 9 pg/ml. Basal norepinephrine levels were 139 +/- 9, 260 +/- 25, and 313 +/- 33 pg/ml in C, HE, and BE, respectively. In response to exercise, norepinephrine increased by nearly twofold in all protocols. Basal and exercise-induced changes in plasma glucagon and insulin were similar in C and ADX. Ra increased similarly in C (5.3 +/- 0.6 mg.kg-1.min-1) and HE (4.9 +/- 0.6 mg.kg-1.min-1). In BE, Ra rose normally for the initial 90 min but then declined resulting in a rise of only 2.9 +/- 0.5 mg.kg-1.min-1 after 150 min of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Neural activation of α-adrenoreceptors in glucose mobilization from liver

1979 ◽  
Vol 57 (9) ◽  
pp. 1037-1039 ◽  
Author(s):  
W. Wayne Lautt
Keyword(s):  
Nerve Stimulation ◽  
Adrenergic Receptors ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Venous Blood ◽  
Pressure Change ◽  
Neural Activation ◽  
Parasympathetic Nerve ◽  
Hepatic Venous Blood ◽  
Glucose Output

Using a newly described method for obtaining pure, mixed hepatic venous blood samples, it was demonstrated that glucose mobilization from the liver of the anesthetized cat in response to hepatic nerve stimulation is via α-adrenergic receptors. Neither the elevation of portal pressure nor the amount of glucose generated by the liver was affected by intraportal administration of 1 mg propranolol/kg (β blockade). In the presence of α-receptor blockade (3 mg phentolamine/kg) the portal venous pressure change was minor and the glucose output actually decreased slightly upon nerve stimulation, a response consistent with our previously demonstrated reduction of glucose output by parasympathetic nerve stimulation. The present responses to nerve stimulation were not due to activation of pancreatic nerves since these nerves were routinely ligated.

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