PACAP enhances stimulation-induced norepinephrine release in canine pancreas in vivo

1998 ◽  
Vol 76 (7-8) ◽  
pp. 788-797 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Yuka Fukushima
Keyword(s):  
Nerve Stimulation ◽  
Venous Blood ◽  
Facilitatory Effect ◽  
Local Administration ◽  
Plasma Catecholamine ◽  
Venous Blood Flow ◽  
Dependent Manner ◽  
Uptake Mechanism ◽  
Amine Uptake ◽  
Plasma Catecholamine Concentrations

The present study was to investigate whether pituitary adenylate cyclase activating polypeptide (PACAP) can modify norepinephrine (NE) release in response to pancreatic nerve stimulation in anesthetized dogs. Plasma catecholamine concentrations in aortic and superior pancreaticoduodenal (SPD) venous blood were determined by a high performance liquid chromatography method. SPD venous blood flow was measured with an electromagnetic flowmeter. Pancreatic nerves were directly stimulated for 1 min (2 ms, 12 V) at various frequencies at the level of the SPD artery. Various doses of PACAP1-27 (PACAP27) were locally infused into the pancreas through the SPD artery. Nerve stimulation significantly increased both SPD venous NE concentration and its output from the pancreas in a frequency-dependent manner. With PACAP27 alone, neither SPD venous NE concentration nor its output changed significantly following the local administration of PACAP27 at any dose tested. In the presence of PACAP27, however, the net increases in NE concentration and its output in response to nerve stimulation at 2 Hz were significantly enhanced in a dose-dependent manner. The enhanced NE responses to nerve stimulation by PACAP27 were thus significantly greater than those obtained from the group receiving either PACAP27 or stimulation alone. Increases in NE concentration and its output induced by local administration of tyramine were virtually abolished by desipramine, a neural amine uptake inhibitor. However, the NE response to tyramine was not diminished by PACAP27. The results indicate that PACAP27 enhances the stimulation-induced NE release in the pancreas, and that this facilitatory effect of PACAP27 does not result from an inhibition of the neural amine uptake mechanism. The study suggests that PACAP receptor-mediated mechanisms may be involved either directly or indirectly in the local modulation of neural NE release in the canine pancreas in vivo.Key words: presynaptic, sympathetic nerve, neuropeptide, tyramine, reuptake, anesthetized dog.

Pharmacological evidence for the existence of a neuronal amine uptake mechanism in the dog liver in vivo

1982 ◽  
Vol 60 (6) ◽  
pp. 755-762 ◽  
Author(s):  
Denis Garceau ◽  
Nobuharu Yamaguchi
Keyword(s):  
Hepatic Artery ◽  
Venous Blood ◽  
Neuronal Uptake ◽  
Plasma Catecholamine ◽  
Sodium Pentobarbital ◽  
Uptake Mechanism ◽  
Vascular Conductance ◽  
Duration Of Action ◽  
Plasma Catecholamine Concentrations ◽  
Dog Liver

The possibility of a neuronal uptake mechanism in the liver was studied in dogs anesthetized with sodium pentobarbital. Plasma catecholamine concentrations in hepatic venous blood were determined by a radioenzymatic assay following injections of tyramine (30–1000 μg) into either the common hepatic artery or the portal vein. Concomitant changes in hepatic vascular parameters and aortic catecholamine concentrations were also investigated. The mean basal values for hepatic venous and aortic catecholamine concentrations were found to be 0.081 ± 0.007 ng/mL and 0.433 ± 0.080 ng/mL, respectively. Injections of tyramine (300 and 1000 μg) into the hepatic artery increased hepatic venous catecholamine concentrations significantly to 0.109 ± 0.017 ng/mL and 0.126 ± 0.023 ng/mL (P < 0.05. n = 7), respectively. Hepatic arterial vascular conductance decreased concomitantly by 29.7 and 44.9% (P < 0.05, n = 7), respectively. Intraportal injections of tyramine did not bring about significant changes in either hepatic venous catecholamine concentrations or portal venous vascular conductance at any dose tested. After inhibition of monoamine oxidase with pargyline (10 mg/kg. i.v.), the effects of tyramine (1000 μg) injected into the hepatic artery were potentiated. The duration of action was approximately 10 min after pargyline pretreatment (control duration: 1 min). The effects of tyramine were absent after inhibition of the neuronal uptake mechanism with desipramine (1 mg/kg. i.v.). No drug tested had a significant effect on aortic catecholamine concentrations. The present results support the presence of the neuronal uptake mechanism in the dog liver.

Effects of PACAP1–27 on the canine endocrine pancreas in vivo: interaction with cholinergic mechanism

2003 ◽  
Vol 81 (7) ◽  
pp. 720-729 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Tamar Rita Minassian ◽  
Sanae Yamaguchi
Keyword(s):  
Endocrine Pancreas ◽  
Venous Blood ◽  
Insulin Response ◽  
Glucagon Secretion ◽  
Venous Blood Flow ◽  
Dependent Manner ◽  
Cholinergic Mechanism ◽  
Insulin And Glucagon Secretion ◽  
Anesthetized Dogs

The aim of the present study was to characterize the effects of pituitary adenylate cyclase activating polypeptide (PACAP) on the endocrine pancreas in anesthetized dogs. PACAP1–27 and a PACAP receptor (PAC1) blocker, PACAP6–27, were locally administered to the pancreas. PACAP1–27 (0.005–5 μg) increased basal insulin and glucagon secretion in a dose-dependent manner. PACAP6–27 (200 μg) blocked the glucagon response to PACAP1–27 (0.5 μg) by about 80%, while the insulin response remained unchanged. With a higher dose of PACAP6–27 (500 μg), both responses to PACAP1–27 were inhibited by more than 80%. In the presence of atropine with an equivalent dose (128.2 μg) of PACAP6–27 (500 μg) on a molar basis, the insulin response to PACAP1–27 was diminished by about 20%, while the glucagon response was enhanced by about 80%. The PACAP1–27-induced increase in pancreatic venous blood flow was blocked by PACAP6–27 but not by atropine. The study suggests that the endocrine secretagogue effect of PACAP1–27 is primarily mediated by the PAC1 receptor, and that PACAP1–27 may interact with muscarinic receptor function in PACAP-induced insulin and glucagon secretion in the canine pancreas in vivo.Key words: atropine, PACAP, PAC1, muscarinic, interaction.

Galanin release during pancreatic nerve stimulation is sufficient to influence islet function

1989 ◽  
Vol 256 (1) ◽  
pp. E191-E198 ◽  
Author(s):  
B. E. Dunning ◽  
G. J. Taborsky
Keyword(s):  
Nerve Stimulation ◽  
Venous Blood ◽  
Hormone Secretion ◽  
Immunoreactive Insulin ◽  
Neural Activation ◽  
Venous Blood Flow ◽  
Concentration Difference ◽  
Specific Radioimmunoassay ◽  
Arterial Plasma ◽  
Peripheral Arterial

To determine if galanin is released during pancreatic neural activation, we measured galanin-like immunoreactivity (GLIR) in pancreatic venous and peripheral arterial plasma during 10 min of electrical stimulation of the mixed autonomic pancreatic nerves in halothane-anesthetized dogs, using a sensitive and specific radioimmunoassay. During mixed pancreatic nerve stimulation (MPNS), pancreatic venous GLIR increased by 174 +/- 20 fmol/ml, whereas arterial GLIR did not change. By use of the arteriovenous concentration difference and measurements of pancreatic venous blood flow, pancreatic spillover of GLIR was calculated and found to increase by 640 +/- 90 fmol/min during MPNS. This MPNS inhibited the output of immunoreactive insulin (IRI; delta = -53 +/- 9%) and somatostatin-like immunoreactivity (SLI, delta = -49 +/- 13%) and stimulated that of immunoreactive glucagon (IRG, delta = +600 +/- 200%). To determine if the amount of GLIR released during MPNS was sufficient to elicit these changes of pancreatic hormone secretion, we compared the effect of MPNS on IRI, SLI, and IRG output with the effect of synthetic galanin infused directly into the pancreatic artery at a rate that reproduced the MPNS-induced spillover of GLIR. Exogenous infusion of synthetic galanin (2.7 pmol/min) increased pancreatic venous levels of GLIR by 169 +/- 38 fmol/ml, did not change arterial GLIR levels, and thus increased calculated spillover (appearance) by 550 +/- 160 fmol/min, which was nearly identical to the increment produced by MPNS. This matched infusion of galanin inhibited IRI (delta = -58 +/- 3%) and SLI output (delta = -35 +/- 3%) and modestly stimulated IRG output (delta = +62 +/- 10%).(ABSTRACT TRUNCATED AT 250 WORDS)

Microscopic Studies of Skin Blood Vessels in Relation to Sympathetic Nerve Stimulation

1957 ◽  
Vol 190 (1) ◽  
pp. 37-40 ◽  
Author(s):  
J. S. Lee ◽  
M. B. Visscher
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Venous Blood ◽  
Vessel Diameter ◽  
Venous Blood Flow ◽  
Sympathetic Nerve Stimulation ◽  
Edema Formation ◽  
Microscopic Studies

Studies have been made of the diameters of microscopic and macroscopic blood vessels in the leg skin of 8 dogs and 13 cats, under pentobarbital anesthesia in parallel with observations on blood pressures in similar vessels, using two techniques, micro-cannulation and a recently described micro-chamber method. During stimulation of the homolateral sympathetic trunk, with or without curarization, there was a rise in venule and small vein pressure, associated with an initial decrease in venous vessel diameter. After cessation of stimulation the venous diameters returned to or exceeded control values while the arteriolar diameters were still markedly reduced. These observations provide direct evidence that even in the absence of mechanical obstruction to venous blood flow the pressures in venules, and therefore necessarily in capillaries when blood is flowing forward, may be elevated by sympathetic nerve stimulation which reduces the blood flow into the vascular bed in question. The possible importance of this mechanism in edema formation and in blood pooling is pointed out.

Functional involvement of angiotensin AT2 receptor in adrenal catecholamine secretion in vivo

1999 ◽  
Vol 77 (5) ◽  
pp. 367-374 ◽  
Author(s):  
Daniel Martineau ◽  
Stéphane Lamouche ◽  
Richard Briand ◽  
Nobuharu Yamaguchi
Keyword(s):  
Adrenal Gland ◽  
High Performance ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Catecholamine Secretion ◽  
Local Administration ◽  
Venous Blood Flow ◽  
Functional Involvement ◽  
Anesthetized Dogs

The aim of the present study was to analyse modulations of adrenal catecholamine secretion from the adrenal gland of anesthetized dogs in response to locally administered angiotensin II (AngII) in the presence of either PD 123319 or CGP 42112, both of which are highly specific and selective ligands to angiotensin AT2 receptor. Plasma concentrations of epinephrine and norepinephrine in adrenal venous and aortic blood were quantified by a high performance liquid chromatography coupled with electrochemical detection (HPLC-EC) method. Adrenal venous blood flow was measured by gravimetry. Local administration of AngII (0.05 µg, 0.1 µM) to the left adrenal gland increased adrenal gland catecholamine output more than 30 times that found in nonstimulated states. Administration of either PD 123319 (0.085 µg (0.23 µM) to 8.5 µg (23 µM)) or CGP 42112 (0.005 µg (0.01 µM) to 5 µg (10 µM)) did not affect the basal catecholamine output significantly. The increase in adrenal catecholamine output in response to AngII was inhibited by ~80% following the largest dose of PD 123319. CGP 42112 significantly attenuated the catecholamine response to AngII by ~70%. PD 123319 and CGP 42112 were devoid of any agonist actions with respect to catecholamine output by the adrenal gland in vivo. Furthermore, both PD 123319 and CGP 42112 inhibited the increase in adrenal catecholamine secretion induced by local administration of AngII. The present study suggests that AT2 receptors play a role in mediating catecholamine secretion by the adrenal medulla in response to AngII receptor agonist administration in vivo.Key words: AT1 and AT2 subtypes, PD 123319, CGP 42112, AT2 antagonist, anesthetized dog.

Role of PAC1 receptor in adrenal catecholamine secretion induced by PACAP and VIP in vivo

2001 ◽  
Vol 280 (2) ◽  
pp. R510-R518 ◽  
Author(s):  
Stéphane Lamouche ◽  
Nobuharu Yamaguchi
Keyword(s):  
Receptor Antagonist ◽  
Venous Blood ◽  
Partial Sequence ◽  
Type I ◽  
Venous Blood Flow ◽  
Dependent Manner ◽  
Pac1 Receptor ◽  
Electrochemical Detector ◽  
Liquid Chromatograph

The present study was conducted to investigate the functional implication of the pituitary adenylate cyclase-activating polypeptide (PACAP) type I (PAC1) receptor in the adrenal catecholamine (CA) secretion induced by either PACAP-27 or vasoactive intestinal polypeptide (VIP) in anesthetized dogs. PACAP-27, VIP, and their respective antagonists were locally infused to the left adrenal gland via the left adrenolumbar artery. Plasma CA concentrations in adrenal venous and aortic blood were determined by means of a high-performance liquid chromatograph coupled with an electrochemical detector. Adrenal venous blood flow was measured by gravimetry. The administration of PACAP-27 (50 ng) resulted in a significant increase in adrenal CA output. VIP (5 μg) also increased the basal CA secretion to an extent comparable to that observed with PACAP-27. In the presence of PACAP partial sequence 6–27 [PACAP-(6–27); a PAC1 receptor antagonist] at the doses of 7.5 and 15 μg, the CA response to PACAP-27 was attenuated by ∼50 and ∼95%, respectively. Although the CA secretagogue effect of VIP was blocked by ∼85% in the presence of PACAP-(6–27) (15 μg), it remained unaffected by VIP partial sequence 10–28 [VIP-(10–28); a VIP receptor antagonist] at the dose of 15 μg. Furthermore, the CA response to PACAP-27 did not change in the presence of the same dose of VIP-(10–28). The results indicate that PACAP-(6–27) diminished, in a dose-dependent manner, the increase in adrenal CA secretion induced by PACAP-27. The results also indicate that the CA response to either PACAP-27 or VIP was selectively inhibited by PACAP-(6–27) but not by VIP-(10–28). It is concluded that PAC1receptor is primarily involved in the CA secretion induced by both PACAP-27 and VIP in the canine adrenal medulla in vivo.

Decreased Platelet-Free Dopamine and Unchanged Noradrenaline and Adrenaline in Essential Hypertension

1988 ◽  
Vol 60 (02) ◽  
pp. 251-254 ◽  
Author(s):  
S E Kjeldsen ◽  
K Gjesdal ◽  
P Leren ◽  
I K Eide
Keyword(s):  
Body Weight ◽  
Essential Hypertension ◽  
Blood Platelets ◽  
Plasma Catecholamine ◽  
Catecholamine Synthesis ◽  
Hypertensive Group ◽  
Plasma Catecholamine Concentrations ◽  
Noradrenaline And Adrenaline ◽  
Over Time ◽  
Normotensive Control

SummaryThe content of free-catecholamines in blood platelets is much higher than in plasma and platelet catecholamines must be taken up from plasma, since platelets lack the enzymes for catecholamine synthesis. There is some evidence that platelet catecholamine content under certain circumstances may be an integrated measure of plasma catecholamine concentrations over time. Platelet-free catecholamines were therefore assayed in 18 untreated patients with essential hypertension and in 16 normotensive control subjects. Mean platelet-free dopamine in the hypertensive group was 3.7 ± 0.4 pg/mg platelet weight, i.e. significantly less than the 6.5 ± 0.9 pg/mg found in the normotensive (p <0.005). Platelet contents of noradrenaline and adrenaline did not differ. Decreased platelet-free dopamine and unchanged platelet noradrenaline and adrenaline persisted after adjustment for increased body weight in the hypertensive group. Although the reasons for decreased platelet-free dopamine in the hypertensive group remain unknown, this finding may add to previous result showing facilitated release of granular contents from blood platelets in patients with essential hypertension. Our data do not support platelet levels of free-catecholamines to be a marker of increased sympathetic tone in essential hypertension.

Norethynodrel with mestranol and venous blood flow

JAMA ◽  
1966 ◽  
Vol 198 (7) ◽  
pp. 784-785 ◽  
Author(s):  
A. Neistadt
Keyword(s):  
Blood Flow ◽  
Venous Blood ◽  
Venous Blood Flow
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