scholarly journals Modulation of adrenal catecholamine release by PACAP in vivo

1999 ◽  
Vol 276 (1) ◽  
pp. R162-R170 ◽  
Author(s):  
Stéphane Lamouche ◽  
Daniel Martineau ◽  
Nobuharu Yamaguchi
Keyword(s):  
Adrenal Gland ◽  
High Performance ◽  
Venous Blood ◽  
Splanchnic Nerve ◽  
Venous Blood Flow ◽  
Left Adrenal Gland ◽  
Presynaptic Mechanisms ◽  
Pituitary Adenylate Cyclase ◽  
Anesthetized Dogs

The aim of the present study was to investigate whether pituitary adenylate cyclase-activating polypeptide-(1—27) (PACAP27) can modulate the adrenal catecholamine (CA) secretion induced by splanchnic nerve stimulation (SNS) and by exogenous acetylcholine (ACh) in anesthetized dogs. Plasma CA concentrations in adrenal venous and aortic blood were quantified by a high-performance liquid chromatography coupled with electrochemical detection. Adrenal venous blood flow was measured by gravimetry. Local infusion of PACAP27 (0.5, 5, and 50 ng) to the left adrenal gland via the adrenolumbar artery resulted in an increase in CA output, reaching a significant level at the highest dose tested. Either direct SNS (2 Hz) or local infusion of ACh (0.5 μg) to the left adrenal gland produced significant increases in CA output to an extent similar to that obtained with 50 ng of PACAP27 alone. In the presence of PACAP27 (50 ng), CA responses to either SNS or exogenous ACh were significantly potentiated by approximately four- and sixfold, respectively, compared with those obtained in response to each stimulus alone. However, the enhanced CA responses to ACh were not significantly different from those to SNS. The results indicate that the increase in adrenal CA secretion, induced by either direct SNS or exogenous ACh, is synergistically enhanced by PACAP27. The study suggests that the enhanced CA secretion may result from the activation of a PACAP-mediated facilitatory mechanism(s) localized presumably at the postsynaptic level in the canine adrenal medulla in vivo, although the possible involvement of presynaptic mechanisms cannot completely be ruled out in the present study.

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.

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.

PACAP release from the canine adrenal gland in vivo: its functional role in severe hypotension

2003 ◽  
Vol 284 (2) ◽  
pp. R588-R597 ◽  
Author(s):  
Stéphane Lamouche ◽  
Nobuharu Yamaguchi
Keyword(s):  
Adrenal Gland ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Dependent Manner ◽  
Severe Hypotension ◽  
Pituitary Adenylate Cyclase ◽  
Catecholamine Response ◽  
Splanchnic Nerve Stimulation

This study was to investigate if endogenous pituitary adenylate cyclase-activating polypeptide (PACAP) can be released during direct splanchnic nerve stimulation in vivo and to determine whether PACAP in the adrenal gland can modulate the medullary response to sympathoadrenal reflex. The output of adrenal catecholamine and PACAP-38-like immunoreactivity (PACAP-38-ir) increased in a frequency-dependent manner after direct splanchnic nerve stimulation (0.2–20 Hz). Both responses were highly reproducible, and PACAP-38-ir output closely correlated with catecholamine output. Sodium nitroprusside (SNP; 0.1 mg/kg iv bolus) caused a severe hypotension resulting in marked increases in catecholamine secretion. In the presence of local PACAP-27 (125 ng), the maximum catecholamine response to SNP was significantly potentiated in a synergistic manner compared with that obtained in the group receiving SNP or PACAP-27 alone. The study indicates that endogenous PACAP-38 can be released particularly when the sympathoadrenal system is highly activated and that the local exogenous PACAP-27 enhanced the reflex-induced catecholamine release, suggesting collectively a facilitating role of PACAP as neuromodulator in the sympathoadrenal function in vivo.

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.

Correlation between neural release of VIP and adrenomedullary catecholamine secretion in vivo

1995 ◽  
Vol 268 (6) ◽  
pp. R1449-R1455 ◽  
Author(s):  
R. Gaspo ◽  
N. Yamaguchi ◽  
J. de Champlain
Keyword(s):  
Adrenal Gland ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Dependent Manner ◽  
Strongly Correlated ◽  
Anesthetized Dogs ◽  
Supramaximal Stimulation ◽  
Dose Dependent ◽  
Splanchnic Nerve Stimulation

The aim of the present study was to determine whether vasoactive intestinal peptide (VIP) can be released along with catecholamines from the adrenal gland in response to direct splanchnic nerve stimulation in anesthetized dogs. An attempt was made to verify whether VIP was released mainly from chromaffin cells or from the splanchnic nerve terminals. The first group received a supramaximal stimulation (12 V) given on the left splanchnic nerve at three successive frequencies of 0.2, 2, and 20 Hz. The second group received increasing doses of 1,1-dimethyl-4-phenylpiperazinium (DMPP) locally infused into the denervated left adrenal gland. In response to nerve stimulation, adrenal venous catecholamine concentration significantly increased in a frequency-dependent manner, whereas VIP-like immunoreactive substance (VIP-ir) reached a significant level only at the highest frequency. The multiple linear regression analyses revealed that the net increases in adrenal venous catecholamine concentrations were strongly correlated with combined variables of VIP-ir concentration and frequencies, indicating r = 0.915 and 0.949 (n = 42, P < 0.0001) for epinephrine and norepinephrine concentrations, respectively. In response to local DMPP infusion, adrenal venous catecholamines increased in a dose-dependent manner, whereas VIP-ir remained unchanged. The results indicate that VIP-ir is released along with catecholamines from the dog adrenal gland in response to direct splanchnic nerve stimulation in vivo. The study also suggests that VIP is mainly released from splanchnic nerve endings.

Functional role of local angiotensin-converting enzyme (ACE) in adrenal catecholamine secretion in vivo

1999 ◽  
Vol 77 (11) ◽  
pp. 878-885 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Daniel Martineau ◽  
Stéphane Lamouche ◽  
Richard Briand
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Angiotensin Converting Enzyme ◽  
Venous Blood Flow ◽  
Dependent Manner ◽  
Converting Enzyme ◽  
Left Adrenal Gland ◽  
Angiotensin I ◽  
Aortic Blood

The aim of the present study was to investigate whether exogenous angiotensin I (AngI) is locally converted to angiotensin II (AngII), which in turn results in an increase in the adrenal catecholamine (CA) secretion in the adrenal gland in anesthetized dogs. Plasma CA concentrations in adrenal venous and aortic blood were determined by an HPLC-electrochemical method. Adrenal venous blood flow was measured by gravimetry. Local administration of AngI (0.0062 to 6.2 µg, 0.0096 to 9.6 µM) to the left adrenal gland resulted in significant increases in CA output in a dose-dependent manner. Following administration of 0.62 µg (0.96 µM) of AngI, adrenal epinephrine and norepinephrine outputs increased from 20.8 ± 13.6 to 250.9 ± 96.4 ng·min-1·g-1 (p < 0.05, n = 5) and from 2.8 ± 1.7 to 29.6 ± 11.1 ng·min-1·g-1 (p < 0.05, n = 5), respectively. From the same left adrenal gland, the output of AngII increased from -0.02 ± 0.04 to 26.39 ± 11.38 ng·min-1·g-1 (p < 0.05, n = 5), while plasma concentrations of AngII in aortic blood remained unchanged. In dogs receiving captopril (12.5 µg, 0.5 mM) 10 min prior to AngI, the net amounts of CA and AngII secreted during the first 3 min after AngI were diminished by about 80% (p < 0.05, n = 5) compared with those obtained from the control group. There was a close correlation (r2 = 0.91, n = 6) between the net increases in AngII and CA outputs induced by AngI. The results indicate that the local angiotensin converting enzyme is functionally involved in regional AngII formation in the canine adrenal gland in vivo. The study suggests that AngII thus generated may play a role in the local regulation of adrenal CA secretion.Key words: angiotensin I, angiotensin II, captopril, adrenal gland, anesthetized dog.

Role of L-type Ca2+ channel in PACAP-induced adrenal catecholamine release in vivo

1997 ◽  
Vol 273 (4) ◽  
pp. R1339-R1345 ◽  
Author(s):  
Guoju Geng ◽  
Rania Gaspo ◽  
Fethi Trabelsi ◽  
Nobuharu Yamaguchi
Keyword(s):  
Adrenal Medulla ◽  
High Performance ◽  
Dependent Manner ◽  
Amino Acid Residues ◽  
Chromatography Method ◽  
Pituitary Adenylate Cyclase ◽  
Group A ◽  
Anesthetized Dogs ◽  
Liquid Chromatography Method

The aim of the present study was to investigate whether the dihydropyridine-sensitive L-type Ca2+ channel is operative in adrenal catecholamine (CA) secretion induced by a novel neuropeptide, pituitary adenylate cyclase-activating polypeptide (PACAP), in anesthetized dogs. Plasma CA concentrations in adrenal venous and aortic blood were determined by a high-performance liquid chromatography method. All drugs tested were locally infused into the left adrenal gland via the left adrenolumbar artery. PACAP, with the isoform consisting of 27 (PACAP-27) and 38 (PACAP-38) amino acid residues, significantly increased CA output in a dose-dependent manner, with doses ranging from 5 to 500 ng and 7 to 700 ng, respectively. However, the amplitude of epinephrine response to PACAP-27 was three times greater than that obtained with PACAP-38 at the highest dose tested. In a separate group, a single dose of PACAP-27 (50 ng) induced highly reproducible CA responses when the same dose was repeated with an interval of 35 min. In dogs treated with nifedipine (50 μg), 5 min before the second administration of PACAP-27, the net CA response was significantly inhibited by ∼50% compared with that obtained in the presence of vehicle. A similar CA response to BAY K 8644 (5 μg) was completely abolished by the same dose of nifedipine. The present results indicate that both PACAP-27 and PACAP-38 have the direct local secretagogue effect on the adrenal medulla in vivo and that CA responses to PACAP-27 were greater than those observed with PACAP-38 at equivalent mole doses. The study suggests that the dihydropyridine-sensitive L-type Ca2+ channel is functionally involved in PACAP-induced adrenal CA secretion in the canine adrenal medulla in vivo.

scholarly journals Testicular microvascular flow is altered in Klinefelter syndrome and predicts circulating testosterone

2021 ◽  
Author(s):  
Francesco Carlomagno ◽  
Carlotta Pozza ◽  
Marta Tenuta ◽  
Riccardo Pofi ◽  
Luigi Tarani ◽  
...  
Keyword(s):  
Blood Flow ◽  
Klinefelter Syndrome ◽  
Mean Transit Time ◽  
Venous Blood ◽  
Experimental Studies ◽  
Principal Component ◽  
Endocrine Function ◽  
Venous Blood Flow ◽  
Testicular Blood Flow

ABSTRACTContextExperimental studies on Klinefelter syndrome (KS) reported increased intratesticular testosterone (T) levels coexisting with reduced circulating levels. Abnormalities in testicular microcirculation have been claimed; however, no studies investigated in vivo testicular blood flow dynamics in humans with KS.ObjectiveTo analyze the testicular microcirculation in KS by contrast-enhanced ultrasonography (CEUS) and correlate vascular parameters with endocrine function.Design and SettingProspective study. University Settings.Patients51 testicular scans, 17 testes from 10 T-naïve subjects with KS and 34 testes from age-matched eugonadal men (CNT) who underwent CEUS for incidental nonpalpable testicular lesions.Main OutcomesCEUS kinetic parameters.ResultsCEUS revealed slower testicular perfusion kinetics in subjects with KS than in age-matched CNT. Specifically, the wash-in time (Tin, p = 0.008), mean transit time (MTT, p = 0.008), time to peak (TTP, p < 0.001), and washout time (Tout 50%, p = 0.008) were all prolonged. Faster testicular blood flow was associated with higher total T levels. Principal component analysis and multiple linear regression analyses confirmed the findings, and supported a role for reduced venous blood flow as independent predictor of total T levels.ConclusionsTesticular venous blood flow is altered in KS and independently predicts T peripheral release.

Hemodynamics and metabolism of the in vivo vascularly isolated canine pancreas.

1979 ◽  
Vol 236 (6) ◽  
pp. E626
Author(s):  
R J Alteveer ◽  
M J Jaffe ◽  
J Van Dam
Keyword(s):  
Blood Flow ◽  
Glucose Uptake ◽  
Venous Blood ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Anesthetized Dogs ◽  
Metabolic Variables ◽  
The Stability ◽  
First Time

Surgical procedures are detailed that have yielded for the first time an in vivo vascularly isolated, autoperfused preparation of the entire pancreas in anesthetized dogs. Previous studies had isolated only part of the pancreas or had resorted to blood-flow techniques not requiring pooled pancreatic venous blood, necessary for metabolic studies of the organ. Pancreatic blood flow (48 ml/min), O2 uptake (180 mumol/min), glucose uptake (51.0 mumol/min), lactate output (6.6 mumol/min), net free fatty acid uptake (2.23 mumol/min), all per 100 g tissue, and various other measured and calculated hemodynamic and metabolic variables were determined on the preparation during control conditions. The stability of the preparation was verified by serial determinations of these parameters and of blood alpha-amylase and beta-glucuronidase levels from 1 to 2.5 h postsurgery. Metabolic rate and glucose uptake were both found to be much higher than in intestinal tissues and approached values characteristic of liver tissue.

Effects of adrenomedullin and PAMP on adrenal catecholamine release in dogs

1999 ◽  
Vol 276 (4) ◽  
pp. R1118-R1124
Author(s):  
Kimiya Masada ◽  
Takahiro Nagayama ◽  
Akio Hosokawa ◽  
Makoto Yoshida ◽  
Mizue Suzuki-Kusaba ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Catecholamine Release ◽  
Induced Response ◽  
Dependent Manner ◽  
Pentobarbital Sodium ◽  
Anesthetized Dogs ◽  
Dose Dependent ◽  
Splanchnic Nerve Stimulation

We examined the effects of proadrenomedullin-derived peptides on the release of adrenal catecholamines in response to cholinergic stimuli in pentobarbital sodium-anesthetized dogs. Drugs were administered into the adrenal gland through the phrenicoabdominal artery. Splanchnic nerve stimulation (1, 2, and 3 Hz) and ACh injection (0.75, 1.5, and 3 μg) produced frequency- or dose-dependent increases in adrenal catecholamine output. These responses were unaffected by infusion of adrenomedullin (1, 3, and 10 ng ⋅ kg−1 ⋅ min−1) or its selective antagonist adrenomedullin-(22—52) (5, 15, and 50 ng ⋅ kg−1 ⋅ min−1). Proadrenomedullin NH2-terminal 20 peptide (PAMP; 5, 15, and 50 ng ⋅ kg−1 ⋅ min−1) suppressed both the splanchnic nerve stimulation- and ACh-induced increases in catecholamine output in a dose-dependent manner. PAMP also suppressed the catecholamine release responses to the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (0.5, 1, and 2 μg) and to muscarine (0.5, 1, and 2 μg), although the muscarine-induced response was relatively resistant to PAMP. These results suggest that PAMP, but not adrenomedullin, can act as an inhibitory regulator of adrenal catecholamine release in vivo.

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