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.

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.

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.

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.

In vivo evidence for adrenal catecholamine release mediated by nonnicotinic mechanism: local medullary effect of VIP

1993 ◽  
Vol 265 (4) ◽  
pp. R766-R771 ◽  
Author(s):  
N. Yamaguchi
Keyword(s):  
Adrenal Gland ◽  
Vasoactive Intestinal Peptide ◽  
High Performance ◽  
Physiological Role ◽  
Catecholamine Secretion ◽  
Plasma Catecholamine ◽  
Drug Infusion ◽  
Chromatography Method ◽  
Plasma Catecholamine Concentrations

The aim of the present study was 1) to develop a model in anesthetized dogs in which local infusion of a given substance could be made to the adrenal gland without any systemic effects and 2) to show in this model the potential existence of a nonnicotinic mechanism involved in adrenal catecholamine secretion. Plasma catecholamine concentrations were determined by an high-performance liquid chromatography method. The local infusion into the left adrenolumbar artery (0.5 ml/min for 1 min) of either dimethylphenylpiperazinium (0.3-3.0 micrograms/ml) or vasoactive intestinal peptide (0.1-10.0 micrograms/ml) resulted in dose-dependent increases in both epinephrine and norepinephrine secretions. Neither aortic pressure nor plasma catecholamine levels altered during the drug infusion. The net increases in adrenal catecholamine secretion obtained with dimethylphenylpiperazinium were abolished by the nicotinic blockade with pentolinium (2 mg/ml, 0.5 ml/min for 2 min). However, the net catecholamine responses to vasoactive intestinal peptide remained unaffected in the presence of the same dose of pentolinium. The results suggest that there exists a nonnicotinic mechanism that may be implicated in the local regulation of medullary catecholamine secretion in the dog adrenal gland. This model may be a useful tool for studying local physiological role(s) of various neurotransmitters and neuromodulators in the adrenal secretory function in vivo.

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.

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.

In vivo metabolism of tritiated LHRH by the whole kidney and individual tubules of rats

1983 ◽  
Vol 244 (6) ◽  
pp. F628-F632
Author(s):  
M. A. Stetler-Stevenson ◽  
G. Flouret ◽  
S. Nakamura ◽  
B. Gulczynski ◽  
F. A. Carone
Keyword(s):  
High Performance ◽  
Rat Kidney ◽  
Venous Blood ◽  
Urinary Metabolites ◽  
Proximal Tubules ◽  
Radioactive Label ◽  
Intracellular Degradation ◽  
Contact Digestion ◽  
Distal Tubules

[pyroglutamyl-3,4-3H]Luteinizing hormone-releasing hormone ([3H]LHRH) and [14C]inulin were infused into individual nephrons in Inactin-anesthetized rats and the amount of radioactive label and the identity of the radioactively labeled material in urine were determined. The site of infusion was identified by latex injection and microdissection. [3H]LHRH was microinfused at 1.5 X 10(-5 M (concentration 10(6)-10(7) higher than in plasma) and analysis of urinary metabolites was performed by high-performance liquid chromatography. The urinary recovery of tritium label was 81% when proximal tubules were infused and 94% when distal tubules were infused. For proximal tubules 90% of the label recovered in urine appeared as pGlu-His (metabolite 2), pGlu-His-Trp (metabolite 3), and pGlu-His-Trp-Ser (metabolite 4), and 10% as LHRH. With distal tubules only LHRH was detected in the urine. [3H]LHRH was presented to the renal artery of the filtering rat kidney in vivo, and urine and renal venous blood were analyzed for breakdown products. The urine contained metabolites 2, 3, and 4 and no LHRH, whereas venous blood contained mainly pGlu, metabolite 4, and LHRH. When [3H]LHRH was perfused in vivo through the nonfiltering rat kidney or rat lower limb, renal or femoral venous blood was found to contain only LHRH. These studies suggest that [3H]LHRH undergoes glomerular filtration and contact digestion by brush border enzymes of the proximal tubule to produce metabolites 2, 3, and 4. These metabolites and possibly LHRH are partially reabsorbed and undergo further intracellular degradation to produce pGlu. Endothelial and interstitial cells in the kidney and leg do not appreciably metabolize [3H]LHRH.

Comparative rates of formation, in vivo, of 16-androstenes, testosterone and androstenedione in boar testis

1984 ◽  
Vol 103 (2) ◽  
pp. 179-186 ◽  
Author(s):  
E. L. Hurden ◽  
D. B. Gower ◽  
F. A. Harrison
Keyword(s):  
Binding Sites ◽  
Venous Blood ◽  
Peripheral Circulation ◽  
Total Radioactivity ◽  
Venous Blood Flow ◽  
Large White ◽  
The Third ◽  
Very High ◽  
Venous Plasma

ABSTRACT Three mature Large White boars were anaesthetized and received [7(n)-3H]pregnenolone by continuous infusion into right and left spermatic arteries for up to 180 min. Spermatic venous blood flow was measured by separate timed collections of completely diverted outflow from each testis and blood not sampled was returned to the peripheral circulation. The total radioactivity in plasma from each testis increased markedly during the first 60 min of infusion to reach a plateau from 80 to 180 min. Radiolabelling of 5α-androst-16-en-3-one, 5α-androst-16-en-3β-ol and -3α-ol showed similar patterns with ratios of mean radioactivity of 5:3:1 respectively between 80 and 180 min. In comparison, the amounts of tritiated 4,16-androstadien-3-one formed were very small. The radiolabelling of testosterone and 4-androstenedione occurred more rapidly than that of the 16-androstenes and reached maxima by 30 min. However the amounts were only one-fifth (testosterone) and one-tenth (4-androstenedione) those of the combined quantities of tritiated 16-androstenes. Addition of human chorionic gonadotrophin (hCG) to the infusate to one testis in each animal (so that 5000 i.u. hCG were delivered in 15–20 min) produced no change in the outputs of radiolabelled steroids although radioimmunoassay of spermatic venous plasma in samples from the third experiment showed a transient increase in the concentration of 4-androstene-3,17-dione during the hCG infusion. It is suggested the lack of response to hCG could be produced by saturation and down regulation of binding sites by the very high local concentrations of hCG. J. Endocr. (1984) 103, 179–186

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

Abstract Context Experimental 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. Objective To analyze the testicular microcirculation in KS by contrast-enhanced ultrasonography (CEUS) and correlate vascular parameters with endocrine function. Design and Setting Prospective study. University Setting. Patients 68 testicular scans, 34 testes from 19 T-naïve subjects with KS and 34 testes from age-matched eugonadal men (CNT) who underwent CEUS for incidental nonpalpable testicular lesions. Main Outcomes. CEUS kinetic parameters. Results CEUS revealed slower testicular perfusion kinetics in subjects with KS than in age-matched CNT. Specifically, the wash-in time (Tin, p = 0.018), mean transit time (MTT, p = 0.035), time to peak (TTP, p &lt; 0.001), and washout time (Tout 50%, p = 0.004) 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. Conclusions Testicular venous blood flow is altered in KS and independently predicts T peripheral release.

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