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.

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.

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.

Effect of prostaglandins on bradykinin-induced visceral-cardiac reflexes

1985 ◽  
Vol 249 (1) ◽  
pp. H155-H163 ◽  
Author(s):  
C. L. Stebbins ◽  
R. C. Smith ◽  
J. C. Longhurst
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Response ◽  
Serosal Surface ◽  
Abdominal Organs ◽  
Before And After ◽  
Stimulation Of

We examined the effect of prostaglandins on the reflex cardiovascular response to bradykinin applied to the abdominal organs of anesthetized cats. Bradykinin (10 micrograms/ml) was applied to the serosal surface of the stomach, gallbladder, or jejunum before and after injection of indomethacin (2-10 micrograms/ml iv) and after application of 1 microgram/ml of prostaglandins E1, E2, or F2 alpha (PGE1, PGE2, PGF2 alpha) or prostacyclin (PGI2). In six cats, stimulation of the stomach with bradykinin significantly increased mean arterial pressure (MAP) by 37 +/- 5 (SE) mmHg and maximal dP/dt by 633 +/- 101 mmHg/s. Following indomethacin the bradykinin-induced increases in MAP and dP/dt were significantly reduced to 19 +/- 4 mmHg and 191 +/- 58 mmHg/s, respectively. Treatment with PGE1, PGE2, or PGI2, but not PGF2 alpha, restored the initial bradykinin response. The gallbladder and jejunum responded similarly. Also application of exogenous prostaglandins, PGE2 or PGI2, to the stomach, gallbladder, or jejunum significantly augmented the cardiovascular response to bradykinin. Finally, PGE2 restored a portion of the cardiovascular response to bradykinin following the development of tachyphylaxis. We conclude that prostaglandins are necessary for the full manifestation of the cardiovascular response to bradykinin.

Nitric oxide as a regulator of adrenal blood flow

1993 ◽  
Vol 264 (2) ◽  
pp. H464-H469 ◽  
Author(s):  
M. J. Breslow ◽  
J. R. Tobin ◽  
D. S. Bredt ◽  
C. D. Ferris ◽  
S. H. Snyder ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Neural Control ◽  
Splanchnic Nerve ◽  
No Synthase ◽  
Catecholamine Secretion ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Synthase Inhibitor ◽  
Splanchnic Nerve Stimulation

To determine whether nitric oxide (NO) is involved in adrenal medullary vasodilation during splanchnic nerve stimulation (NS)-induced catecholamine secretion, blood flow (Q) and secretory responses were measured in pentobarbital-anesthetized dogs before and after administration of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). L-NAME (40 mg/kg iv over 5 min, followed by 40 mg.kg-1.h-1) reduced NO synthase activity of medullary and cortical homogenates from 5.2 +/- 0.3 to 0.7 +/- 0.1 pmol.min-1.mg protein-1 and from 1.2 +/- 0.2 pmol.min-1.mg protein-1 to undetectable levels, respectively. L-NAME reduced resting medullary and cortical Q by 42 and 60%, respectively. NS before L-NAME increased medullary Q from 181 +/- 16 to 937 +/- 159 ml.min-1.100 g-1 and epinephrine secretion from 1.9 +/- 0.8 to 781 +/- 331 ng/min. NS after L-NAME had no effect on medullary Q (103 +/- 14 vs. 188 +/- 34 ml.min-1.100 g-1), while epinephrine secretion increased to the same extent as in control animals (1.9 +/- 0.7 vs. 576 +/- 250 ng/min). L-NAME also unmasked NS-induced cortical vasoconstriction; cortical Q decreased from 96 +/- 8 to 50 +/- 5 ml.min-1.100 g-1. Administration of hexamethonium (30 mg/kg iv), a nicotinic receptor antagonist, reduced NS-induced epinephrine secretion by 90%. These data suggest independent neural control of medullary Q and catecholamine secretion, the former by NO and the latter by acetylcholine.

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