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.

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.

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.

Escape from vasoconstriction in the gastric microcirculation

1975 ◽  
Vol 228 (6) ◽  
pp. 1893-1895 ◽  
Author(s):  
Paul H. Guth ◽  
Esther Smith
Keyword(s):  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
System Response ◽  
In Vivo Microscopy ◽  
Adrenergic Stimulation ◽  
Resistance Vessels ◽  
Autoregulatory Escape ◽  
Splanchnic Nerve Stimulation ◽  
Gastric Microcirculation

Escape of splanchnic resistance vessels from vasoconstriction due to adrenergic stimulation has been attributed to increasing submucosal blood flow due to dilation of submucosal arteriovenous anastomoses (shunts). This postulate, as applied to the rat gastric microcirculation, was studied by in vivo microscopy. Using an image-splitting TV microscope recording system, response of gastric submucosal arterioles (13–33 µm) to 3 min of left splanchnic nerve stimulation, norepinephrine superfusion, and vasopressin superfusion was measured. All stimuli produced initial vasoconstriction. Escape occurred in all rats with nerve stimulation and norepinephrine, but in only one of five with vasopressin. No shunts were seen. The study demonstrates that the gastric submucosal arterioles exhibit an escape phenomenon, suggesting that "autoregulatory escape" in other splanchnic beds also may be due to relaxation of constricted vessels and not to opening of shunts.

Release of galanin from isolated perfused porcine adrenal glands: role of splanchnic nerves

1991 ◽  
Vol 261 (1) ◽  
pp. E31-E40 ◽  
Author(s):  
J. J. Holst ◽  
M. Ehrhart-Bornstein ◽  
T. Messell ◽  
S. S. Poulsen ◽  
H. Harling
Keyword(s):  
Nerve Stimulation ◽  
Adrenal Glands ◽  
Splanchnic Nerve ◽  
High Concentration ◽  
Vitro Model ◽  
Arterial Plasma ◽  
Regulatory Functions ◽  
Splanchnic Nerve Stimulation

We found a high concentration of galanin in extracts of porcine adrenal glands (114 pmol/g). By immunohistochemistry, galanin was localized to groups of medullary cells previously shown to produce norepinephrine. To study mechanisms for the release of galanin, we developed the following in vitro model: isolated perfused porcine adrenals with intact splanchnic nerve supply. When the nerves were electrically stimulated, epinephrine and norepinephrine secretion increased 276- and 291-fold, respectively, and galanin release increased up to 1,300-fold. Acetylcholine at 10(-6) M stimulated galanin release, and hexamethonium almost abolished the response to nerve stimulation. Galanin infusions had no effect on epinephrine and norepinephrine secretion in concentrations of 10(-8) and 10(-7) M, but increased both cortisol and aldosterone secretion (P less than 0.05). Splanchnic nerve stimulation in anesthetized pigs increased the concentration of galanin in the caval vein but not in arterial plasma. It is concluded that galanin, coreleased with catecholamines from the adrenal glands, may have endocrine functions but that galanin may also have local regulatory functions in the adrenals.

Escape from vasoconstriction in the gastric microcirculation

1975 ◽  
Vol 228 (6) ◽  
pp. 1880-1886 ◽  
Author(s):  
PH Guth ◽  
E Smith
Keyword(s):  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
System Response ◽  
In Vivo Microscopy ◽  
Adrenergic Stimulation ◽  
Resistance Vessels ◽  
Autoregulatory Escape ◽  
Splanchnic Nerve Stimulation ◽  
Gastric Microcirculation

Escape of splanchic resistance vessels from vasconstriction due to adrenergic stimulation has been attributed to increasing submucosal blood flow due to dilation of submucosal arteriovenous anastomes (shunts). This postulate, as applied to the rat gastric microcirculation, was studied by in vivo microscopy. Using an image-splittingTV microscope recording system, response of gastric submucosal arterioles (13-33 mum)to 3 min of left splanchnic nerve stimulation, norepinephrine superfision, and vasopressin superfission was measured. All stimuli produced initial vasoconstriction.Escape occurred in all rats with nerve stimulation and norepinephrine, but in onlyone of five with vasopressin. No shunts were seen. The study demonstrates that thegastric submucosal arterioles exhibit an escape phenomenon, suggesting that "autoregulatory escape" in other splanchic beds also may be due to relaxation of constricted vessels and not to opening of shunts.

Effects of clentiazem (TA-3090) and nifedipine on basal circulating catecholamine levels and on stimulation-evoked adrenal catecholamine secretion in anesthetized dogs

1992 ◽  
Vol 70 (7) ◽  
pp. 983-989 ◽  
Author(s):  
Rania Gaspo ◽  
Louis Lamarche ◽  
Nobuharu Yamaguchi ◽  
Jacques de Champlain ◽  
Denis Garceau
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Acute Administration ◽  
Sodium Pentobarbital ◽  
Dependent Manner ◽  
Before And After ◽  
Splanchnic Nerve Stimulation ◽  
Catecholamine Levels

The effects of TA-3090 (clentiazem) and nifedipine on basal sympathoadrenal activity and on the adrenal medullary response during splanchnic nerve stimulation were studied in dogs anesthetized with sodium pentobarbital. Plasma concentrations of epinephrine and norepinephrine were measured in aortic and adrenal venous blood before and after acute administration of the drugs, as well as during left splanchnic nerve stimulation before and after administration of drugs. Following intravenous injections, TA-3090 (30, 100, and 300 μg/kg) did not affect basal circulating catecholamine levels, whereas nifedipine (10, 30, and 100 μg/kg) markedly increased aortic epinephrine and norepinephrine concentrations in a dose-dependent manner in correlation with progressive decreases in mean arterial pressure. The changes in aortic epinephrine and norepinephrine concentrations were inversely related to those in mean arterial pressure (r = 0.603, p < 0.01; r = 0.536, p < 0.01; respectively). In response to direct splanchnic nerve stimulation (2 Hz, 2 ms, 1 min, 12 V), adrenal venous epinephrine and norepinephrine concentrations significantly increased, with a high degree of reproducibility. The catecholamine responses to splanchnic nerve stimulation were not affected by either TA-3090 or nifedipine at any dose tested. The present results suggest that the increases in circulating catecholamine levels following nifedipine administration are due to baroreflex activation secondary to the drug-induced hypotension. The study indicates that both TA-3090 and nifedipine did not significantly affect L-type Ca2+ channels related to catecholamine release in the adrenal medulla under the present experimental conditions.Key words: calcium antagonists, nifedipine, clentiazem, adrenal gland, catecholamines, splanchnic nerve, baroreflex.

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