Canine adrenal catecholamine response to VIP is blocked by PACAP-(6-27) in vivo

1997 ◽  
Vol 272 (5) ◽  
pp. R1606-R1612 ◽  
Author(s):  
R. Gaspo ◽  
L. Lamarche ◽  
J. de Champlain ◽  
N. Yamaguchi
Keyword(s):  
Muscarinic Receptors ◽  
Control Group ◽  
Plasma Catecholamine ◽  
Type I ◽  
Pituitary Adenylate Cyclase ◽  
Catecholamine Response ◽  
Anesthetized Dogs ◽  
Plasma Catecholamine Concentrations ◽  
Ca2 Channels

The goal of the present study was to characterize the adrenal catecholamine response to exogenous vasoactive intestinal peptide (VIP) in anesthetized dogs. We studied the potential involvement of mechanism(s) mediated by muscarinic receptors, L-type Ca2+ channels, VIP-ergic receptors, or pituitary adenylate cyclase-activating peptide (PACAP) receptors. The study consisted of five groups: a vehicle control group receiving VIP (5 micrograms) in the presence of saline and four drug-treated groups receiving VIP (5 micrograms) in the presence of either atropine (500 micrograms), nifedipine (50 micrograms), [Lys1,Pro2,5,Arg3,4,Tyr6]VIP (50 micrograms), or PACAP-(6-27) (50 micrograms). All drugs were locally infused to the left adrenal gland. Plasma catecholamine concentrations were measured in adrenal venous and aortic blood by a high-pressure liquid chromatography-electrochemical method. In the control group, VIP produced a significant increase in adrenal catecholamine output. Neither atropine, nifedipine, nor[Lys1,Pro2,5,Arg3,4,Tyr6]-VIP significantly affected the medullary response to VIP. In the presence of PACAP-(6-27), however, the catecholamine response to VIP was attenuated by approximately 77% (P < 0.05). The present study suggests that adrenal catecholamine secretion induced by exogenous VIP may be mediated by a PACAP-related mechanism, most probably through a PACAP type I receptor, in anesthetized dogs. The data also indicate that neither muscarinic receptors, VIP-ergic receptors, nor dihydropyridine-sensitive L-type Ca2+ channels are operative in the adrenal catecholamine response to exogenous VIP in vivo.

Clonidine Modulation of Hemodynamic and Catecholamine Responses Associated with Hypoxia or Hypercapnia in Dogs

1996 ◽  
Vol 84 (3) ◽  
pp. 672-685 ◽  
Author(s):  
Toshiaki Nishikawa ◽  
Hiroshi Naito
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Bolus Injection ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Anesthetized Dogs ◽  
Plasma Catecholamine Concentrations

Background Hypoxia or hypercapnia elicits cardiovascular responses associated with increased plasma catecholamine concentrations, whereas clonidine, an alpha(2)- adrenergic agonist, decreases plasma catecholamine concentrations. The authors examined whether systemic clonidine administration would alter the hemodynamic and catecholamine responses to hypoxia or hypercapnia in anesthetized dogs. Methods Pentobarbital-anesthetized dogs whose lungs were mechanically ventilated were instrumented for measurement of mean arterial pressure, heart rate, mean pulmonary artery pressure, right atrial pressure, cardiac output, left ventricular end-diastolic pressure, and the peak of first derivative of left ventricular pressure. The dogs were randomly assigned to receive an intravenous bolus injection of 10 microg/kg clonidine followed by continous infusion at a rate of 1 microg. kg (-1). min (-1)(clonidine-10 group, n = 7), an intravenous bolus injection of microg/kg clonidine followed by continuous infusion at a rate of 0.5 micro.kg(-).min(-1)(clonidine-5 group, n = 7), or an equivalent volume of 0.9% saline (control group = 7). Each dog underwent random challenges of hypoxia (PaO2 30, 40, and 50 mmHg) and hypercapnia (PaCO2 60, 80, and 120 mmHg). Measurements of hemodynamic and plasma norepinephrine and epinephrine concentrations were made after the loading dose of clonidine and the first and the second exposure of hypoxia or hypercapnia. Results Although significant increases from prehypoxic values in mean arterial pressure (39 +/- 10 mmHg) and plasma norepinephrine (291 +/- 66 pg/ml) and epinephrine (45 +/- 22 pg/ml) concentrations were noted during hypoxia of PaO2 30, mmHg in the control group (P&lt;0.05), such changes were absent in both clonidine groups. During hypercapnia of PaCo2 120 mmHg, changes from prehypercapnic values in mean arterial pressure, mean pulmonary artery pressure, the peak of first derivative of left ventricular pressure, and plasma norepinephrine and epinephrine concentrations in the clonidine-10 and clonidine-5 groups were significantly less than those in the control group. Plasma clonidine concentrations in the clonidine-10 and clonidine-5 groups were 16.8 +/- 1.7 and 8.9 =/- 1.0, 42.5 =/- 2.9 and 21.5 +/- 1.5, and 51.1 +/- 3.2 and 26.7 +/- 1.0 ng/ml after the loading dose of clonidine and the first and the second exposure of hypoxia or hypercapnia, respectively. Conclusions Systemic clonidine administration alter the hemodynamic changes associated with hypoxia or hypercapnia and suppresses plasma catecholamine responses in anesthetized dogs when a larger dose of clonidine is administered. catecholamines: epinephrine; norepinephrine.)

Inhibition by BMS 186295, a selective nonpeptide AT1 antagonist, of adrenal catecholamine release induced by angiotensin II in the dog in vivo

1995 ◽  
Vol 73 (4) ◽  
pp. 459-464 ◽  
Author(s):  
Daniel Martineau ◽  
Nobuharu Yamaguchi ◽  
Richard Briand
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Catecholamine Release ◽  
Catecholamine Secretion ◽  
Control Group ◽  
Plasma Catecholamine ◽  
Dose Dependency ◽  
At1 Antagonist ◽  
Plasma Catecholamine Concentrations

The aim of the present study was to investigate whether a novel nonpeptide AT1 selective antagonist, BMS 186295 (BMS), can antagonize adrenal catecholamine release induced by local administration of angiotensin II (AII) in anesthetized dogs. Plasma catecholamine concentrations in adrenal venous and aortic blood were determined by an HPLC–electrochemical method. AII was locally administered to the left adrenal gland in the absence and presence of BMS. In the first group (n = 7), local infusion (0.5 mL/min, 1 min) of AII (0.001 – 1.0 μg/mL) resulted in a significant dose-dependent increase in the basal secretion of adrenal catecholamines. Aortic catecholamine levels and mean aortic pressure remained unchanged at all doses tested. In the second group (control, n = 10), four repeated infusions (at intervals of 15 min) of AII at 0.1 μg/mL resulted in significant increases of adrenal catecholamine secretion compared with the baseline. In the third group receiving BMS given locally to the gland (n = 8), the basal adrenal catecholamine secretion was not significantly altered by BMS itself at any dose tested. However, the net catecholamine response to AII (0.1 μg/mL) was significantly and dose dependency attenuated by approximately 40, 60, and 80% in the presence of BMS at doses of 0.1, 1.0, and 10 μg/mL, respectively, compared with the control group. The study indicates that BMS dose dependency blocks AII-induced catecholamine secretion in the dog adrenal gland in vivo.Key words: adrenal gland, angiotensin II, AT1 antagonist, BMS 186295, catecholamine, dog, in vivo.

Functional evidence for L-type Ca2+ channels controlling ANG II-induced adrenal catecholamine release in vivo

1996 ◽  
Vol 271 (6) ◽  
pp. R1713-R1719
Author(s):  
D. Martineau ◽  
R. Briand ◽  
N. Yamaguchi
Keyword(s):  
Catecholamine Release ◽  
Bay K 8644 ◽  
Catecholamine Secretion ◽  
Dependent Manner ◽  
Ang Ii ◽  
Catecholamine Response ◽  
Series Of Experiments ◽  
Plasma Catecholamine Concentrations ◽  
Ca2 Channels

The aim of the present study was to investigate the functional involvement of L- and/or N-type Ca2+ channels in adrenal catecholamine secretion in response to exogenous angiotensin II (ANG II) in anesthetized dogs. Plasma catecholamine concentrations in adrenal venous and aortic blood were determined by a high-performance liquid chromatography-electrochemical method. In the first series of experiments, repeated infusions of BAY K 8644 locally into the left adrenal gland at 15-min intervals resulted in significant and reproducible increases in adrenal catecholamine secretion. Nifedipine, similarly administered 5 min before BAY K 8644, diminished BAY K 8644-induced catecholamine secretion in a dose-dependent manner and completely blocked the catecholamine response at the highest dose tested. In the second series of experiments, local infusion of ANG II resulted in a significant increase in adrenal catecholamine secretion. The maximum catecholamine response to ANG II was attenuated by approximately 65% in the presence of nifedipine at the dose that abolished the BAY K 8644-induced catecholamine release. This inhibition by nifedipine remained unchanged in the presence of omega-conotoxin. The present study shows that dihydropyridine-sensitive L-type Ca2+ channels are operative in the adrenal medulla of the dog in vivo. The results indicate that the L-type Ca2+ channels are only partially implicated in the local regulation of ANG II-induced adrenal catecholamine secretion, suggesting the existence of another mechanism. However, omega-conotoxin-sensitive N-type Ca2+ channels are unlikely to be functionally involved in postsynaptic mechanisms mediating adrenal catecholamine secretion in response to exogenous ANG II under in vivo conditions.

Enhanced reactivity of the adrenal medulla in response to pituitary adenylate cyclase activating polypeptide1-27 (PACAP) during insulin-induced hypoglycemia in anesthetized dogs

1999 ◽  
Vol 77 (10) ◽  
pp. 819-826 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Stéphane Lamouche
Keyword(s):  
Adenylate Cyclase ◽  
Adrenal Medulla ◽  
Maximum Level ◽  
Experimental Period ◽  
Insulin Injection ◽  
Control Group ◽  
Plasma Catecholamine ◽  
Aortic Blood ◽  
Pituitary Adenylate Cyclase ◽  
Anesthetized Dogs

The present study was to test the hypothesis that the reactivity of the adrenal medulla to pituitary adenylate cyclase activating polypeptide1-27 (PACAP27) is enhanced during insulin-induced hypoglycemia (IIH) in anesthetized dogs. Plasma catecholamine (CA) concentrations in adrenal venous and aortic blood were determined by an HPLC method coupled with electrochemical detection, and the plasma glucose concentration in aortic blood was measured using a glucometer. PACAP27 (25 ng) was administered locally via the adrenolumbar artery to the left adrenal gland. The resulting CA responses were compared before and during IIH following an intravenous bolus injection of insulin (0.15 IU/kg, iv). In the first group with normal adrenal innervation, the basal adrenal CA secretion gradually increased, reaching a maximum level 45 min after the insulin injection. The net increase in PACAP27-induced CA secretion was significantly greater 30, 45, and 60 min after the induction of hypoglycemia, compared with the initial net response to PACAP27 observed before insulin injection. In the second group receiving local adrenal denervation, neither the basal CA secretion nor the net CA response to PACAP27 significantly increased despite the presence of IIH, which developed to an extent similar to that found in the first group. In the third group, which was the normoglycemic control group, both the basal CA secretion and the net CA response to PACAP27 remained unchanged during the experimental period. The results indicate that the adrenomedullary reactivity to PACAP27 was significantly enhanced during IIH only when the sympathoadrenal system was activated. The present study suggests that PACAP27 may play a beneficial role in glucose counterregulatory mechanisms in the adrenal medulla during hypoglycemia.Key words: catecholamine, counterregulation, denervation, secretion, splanchnic, sympathoadrenal.

Nifedipine inhibits adrenal but not circulating catecholamine response to nicotinic stimulation in dogs

1994 ◽  
Vol 267 (6) ◽  
pp. R1545-R1551 ◽  
Author(s):  
R. Gaspo ◽  
N. Yamaguchi ◽  
J. de Champlain
Keyword(s):  
High Performance ◽  
Vehicle Control ◽  
Control Group ◽  
Vehicle Control Group ◽  
Aortic Blood ◽  
Catecholamine Response ◽  
Ca2 Channels ◽  
Sodium Plasma ◽  
Catecholamine Concentration

We investigated whether dihydropyridine-sensitive L-type Ca2+ channels are implicated in adrenal and sympathetic neural catecholamine release in response to nicotinic stimulation by 1,1-dimethyl-4-phenylpiperazinium (DMPP), a selective cholinergic nicotinic agonist, in dogs anesthetized with pentobarbital sodium. Plasma epinephrine and norepinephrine concentrations were measured in adrenal venous and aortic blood by a high-performance liquid chromatography-electrochemical method. In the vehicle control group, intravenous injection of DMPP (15 micrograms/kg iv) produced a significant increase in adrenal venous catecholamine output and aortic catecholamine concentration. These increasing responses were highly reproducible on the repetition of DMPP injection given 30 min after the first injection. In dogs receiving nifedipine (100 micrograms/kg iv), the net increase in adrenal venous epinephrine and norepinephrine output in response to DMPP was attenuated by 42% (P < 0.05), while no significant changes were observed in the aortic catecholamine response to DMPP. In dogs treated with pentolinium (1 mg/kg iv), both adrenal epinephrine and norepinephrine responses to DMPP were inhibited by 67% (P < 0.05) and 84% (P < 0.05), respectively. Furthermore, pentolinium inhibited aortic catecholamine response to DMPP by > 95% (P < 0.05). The present study suggests that DMPP-induced release of adrenal catecholamines was mediated, at least in part, through mechanisms involving dihydropyridine-sensitive L-type Ca2+ channels under in vivo conditions. By contrast, however, the results also suggest that dihydropyridine-sensitive L-type Ca2+ channels were not implicated in the neurotransmission at the level of sympathetic ganglions.

scholarly journals Gender difference in the glucagon response to glucopenic stress in mice

2002 ◽  
Vol 282 (1) ◽  
pp. R281-R288 ◽  
Author(s):  
Sven Karlsson ◽  
Anton J. W. Scheurink ◽  
Bo Ahrén
Keyword(s):  
Gender Difference ◽  
Cell Mass ◽  
Plasma Catecholamine ◽  
Plasma Glucagon ◽  
Male Mice ◽  
Female Mice ◽  
Autonomic Activation ◽  
Catecholamine Response ◽  
Increased Sensitivity

A gender difference in the glucagon response to insulin-induced hypoglycemia was previously demonstrated in humans. Whether this reflects a gender difference in autonomic activation or in pancreatic α-cell regulation is not known. We investigated the glucagon, epinephrine, and norepinephrine responses to neuroglycopenic stress induced by 2-deoxy-d-glucose (2-DG) or insulin in female and male mice. 2-DG increased plasma glucagon levels by 559 ± 68% in females versus 281 ± 46% in males ( P< 0.01). Plasma levels of epinephrine or norepinephrine after 2-DG administration did not differ between genders. During insulin-induced hypoglycemia, the glucagon response was similarly higher in females ( P < 0.001), whereas the plasma catecholamine response was higher in males ( P < 0.05). In vivo, the glucagon response to carbachol or clonidine was higher in females ( P < 0.05). In isolated islets, the glucagon response to carbachol (100 μM; P = 0.003) but not to clonidine (1 μM) was larger in females. We conclude that in addition to a larger α-cell mass (previously described in female mice), an increased sensitivity of the glucagon-producing α-cell to cholinergic activation contributes to the larger glucagon response to glucopenic stress in female mice.

Implication of L-type Ca2+ channels in noncholinergic adrenal catecholamine secretion by endothelin-1 in vivo

1995 ◽  
Vol 269 (2) ◽  
pp. R287-R293 ◽  
Author(s):  
N. Yamaguchi
Keyword(s):  
High Performance ◽  
Cholinergic Receptor ◽  
Secondary Response ◽  
Control Group ◽  
Rapid Decline ◽  
Chromatography Method ◽  
Endothelin 1 ◽  
Liquid Chromatography Method ◽  
Ca2 Channels

The aim of the present study was to investigate if either dihydropyridine-sensitive L-type Ca2+ channels or cholinergic receptor-mediated mechanisms are implicated in endothelin-1 (ET)-induced adrenal catecholamine (CA) secretion in anesthetized dogs. ET was locally administered to the left adrenal gland via the left adrenolumbar artery. Plasma CA concentrations in adrenal venous and aortic blood were determined by a high-performance liquid chromatography method. In the control group, local infusion (1 min, 0.5 ml/min) of ET (the fixed total dose of 0.5 microgram given to the gland or approximately 0.0197 microgram/kg of body weight) resulted in a sharp increase in the basal CA output, followed by a rapid decline, and a relatively slow secondary response lasted over a period of 15-30 min. In the second group treated with nifedipine (5 micrograms or approximately 0.207 microgram/kg) similarly administered 10 min before ET infusion, the ET-induced first steep increase in CA output was significantly attenuated by approximately 75% (P < 0.05, n = 6). In dogs similarly receiving either pentolinium (1 mg or approximately 0.041 mg/kg) or atropine (0.5 mg or approximately 0.018 mg/kg), the ET-induced CA response remained unchanged. The results indicate that ET-induced adrenal CA release was largely mediated by the activation of dihydropyridine-sensitive L-type Ca2+ channels. Furthermore, neither nicotinic nor muscarinic receptors were functionally implicated in the CA response to ET. The study suggests the existence of noncholinergic mechanisms involved in the secretory action of ET on the adrenal medulla in the dog in vivo.

scholarly journals In Vivo Antiviral Effects of U18666A Against Type I Feline Infectious Peritonitis Virus

Pathogens ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 67 ◽  
Author(s):  
Tomoyoshi Doki ◽  
Tomoyo Tarusawa ◽  
Tsutomu Hohdatsu ◽  
Tomomi Takano
Keyword(s):  
Clinical Symptoms ◽  
Treated Group ◽  
Control Group ◽  
Type I ◽  
Feline Infectious Peritonitis Virus ◽  
Feline Infectious Peritonitis ◽  
Amphiphilic Drug ◽  
Antiviral Effects

Background: The cationic amphiphilic drug U18666A inhibits the proliferation of type I FIPV in vitro. In this study, we evaluated the in vivo antiviral effects of U18666A by administering it to SPF cats challenged with type I FIPV. Methods: Ten SPF cats were randomly assigned to two experimental groups. FIPV KU-2 were inoculated intraperitoneally to cats. The control group was administered PBS, and the U18666A-treated group was administered U18666A subcutaneously at 2.5 mg/kg on day 0, and 1.25 mg/kg on days 2 and 4 after viral inoculation. Results: Two of the five control cats administered PBS alone developed FIP. Four of the five cats administered U18666A developed no signs of FIP. One cat that temporarily developed fever, had no other clinical symptoms, and no gross lesion was noted on an autopsy after the end of the experiment. The FIPV gene was detected intermittently in feces and saliva regardless of the development of FIP or administration of U18666A. Conclusions: When U18666A was administered to cats experimentally infected with type I FIPV, the development of FIP might be suppressed compared with the control group. However, the number of animals with FIP is too low to establish anti-viral effect of U18666A in cats.

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.

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