Role of potassium channels in catecholamine secretion in the rat adrenal gland

2000 ◽  
Vol 279 (2) ◽  
pp. R448-R454 ◽  
Author(s):  
Takahiro Nagayama ◽  
Yasuo Fukushima ◽  
Makoto Yoshida ◽  
Mizue Suzuki-Kusaba ◽  
Hiroaki Hisa ◽  
...  
Keyword(s):  
Mast Cell ◽  
Adrenal Gland ◽  
Nicotinic Receptor ◽  
Channel Blocker ◽  
Catecholamine Secretion ◽  
Cholinergic Agonists ◽  
Presynaptic Site ◽  
Mast Cell Degranulating ◽  
Small Conductance

We elucidated the functional contribution of K+ channels to cholinergic control of catecholamine secretion in the perfused rat adrenal gland. The small-conductance Ca2+-activated K+ (SKCa)-channel blocker apamin (10–100 nM) enhanced the transmural electrical stimulation (ES; 1–10 Hz)- and 1,1-dimethyl-4-phenyl-piperazinium (DMPP; 5–40 μM)-induced increases in norepinephrine (NE) output, whereas it did not affect the epinephrine (Epi) responses. Apamin enhanced the catecholamine responses induced by acetylcholine (6–200 μM) and methacholine (10–300 μM). The putative large-conductance Ca2+-activated K+ channel blocker charybdotoxin (10–100 nM) enhanced the catecholamine responses induced by ES, but not the responses induced by cholinergic agonists. Neither the KA channel blocker mast cell degranulating peptide (100–1000 nM) nor the KV channel blocker margatoxin (10–100 nM) affected the catecholamine responses. These results suggest that SKCa channels play an inhibitory role in adrenal catecholamine secretion mediated by muscarinic receptors and also in the nicotinic receptor-mediated secretion of NE, but not of Epi. Charybdotoxin-sensitive Ca2+-activated K+ channels may control the secretion at the presynaptic site.

Role of K+ channels in adrenal catecholamine secretion in anesthetized dogs

1998 ◽  
Vol 274 (4) ◽  
pp. R1125-R1130 ◽  
Author(s):  
Takahiro Nagayama ◽  
Kimiya Masada ◽  
Makoto Yoshida ◽  
Mizue Suzuki-Kusaba ◽  
Hiroaki Hisa ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Splanchnic Nerve ◽  
Channel Blockers ◽  
Cholinergic Agonists ◽  
Voltage Dependent ◽  
Anesthetized Dogs ◽  
Splanchnic Nerve Stimulation ◽  
Mast Cell Degranulating ◽  
Small Conductance

We examined the role of K+ channels in the secretion of adrenal catecholamine (CA) in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. K+ channel blockers and the cholinergic agonists were infused and injected, respectively, into the adrenal gland. The voltage-dependent K+ channel (KA type) blocker mast cell degranulating (MCD) peptide infusion (10–100 ng/min) enhanced increases in CA output induced by SNS (1–3 Hz), but it did not affect increases in CA output induced by ACh (0.75–3 μg), DMPP (0.1–0.4 μg), or muscarine (0.5–2 μg). The small-conductance Ca2+-activated K+(SKCa) channel blocker scyllatoxin infusion (10–100 ng/min) enhanced the ACh-, DMPP-, and muscarine-induced increases in CA output, but it did not affect the SNS-induced increases in CA output. These results suggest that KA channels may play an inhibitory role in the regulation of adrenal CA secretion in response to SNS and that SKCa channels may play the same role in the secretion in response to exogenously applied cholinergic agonists.

scholarly journals Interaction of SKCa channels and L-type Ca2+ channels in catecholamine secretion in the rat adrenal gland

2000 ◽  
Vol 279 (5) ◽  
pp. R1731-R1736 ◽  
Author(s):  
Takahiro Nagayama ◽  
Yasuo Fukushima ◽  
Hirohiko Hikichi ◽  
Makoto Yoshida ◽  
Mizue Suzuki-Kusaba ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Muscarinic Receptor ◽  
Channel Blocker ◽  
Catecholamine Secretion ◽  
Facilitatory Effect ◽  
Muscarinic Agonist ◽  
Receptor Stimulation ◽  
Small Conductance ◽  
Ca2 Channels ◽  
Channel Activator

We elucidated the interaction of small-conductance Ca2+-activated K+ (SKCa) channels and L-type Ca2+ channels in muscarinic receptor-mediated control of catecholamine secretion in the isolated perfused rat adrenal gland. The muscarinic agonist methacholine (10–300 μM) produced concentration-dependent increases in adrenal output of epinephrine and norepinephrine. The SKCachannel blocker apamin (1 μM) enhanced the methacholine-induced catecholamine responses. The facilitatory effect of apamin on the methacholine-induced catecholamine responses was not observed during treatment with the L-type Ca2+ channel blocker nifedipine (3 μM) or Ca2+-free solution. Nifedipine did not affect the methacholine-induced catecholamine responses, but it inhibited the responses during treatment with apamin. The L-type Ca2+channel activator Bay k 8644 (1 μM) enhanced the methacholine-induced catecholamine responses, whereas the enhancement of the methacholine-induced epinephrine and norepinephrine responses were prevented and attenuated by apamin, respectively. These results suggest that SKCa channels are activated by muscarinic receptor stimulation, which inhibits the opening of L-type Ca2+ channels and thereby attenuates adrenal catecholamine secretion.

Role of K+ channels in the PACAP-induced catecholamine secretion from the rat adrenal gland

2002 ◽  
Vol 437 (1-2) ◽  
pp. 69-72 ◽  
Author(s):  
Yasuo Fukushima ◽  
Takahiro Nagayama ◽  
Hirohiko Hikichi ◽  
Kazuhiko Mizukami ◽  
Makoto Yoshida ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Catecholamine Secretion ◽  
K Channels

scholarly journals Role of calcium channel blocker in excessive mast cell degranulation

2021 ◽  
Vol 5 (7) ◽  
Author(s):  
Sagarika Datta
Keyword(s):  
Mast Cell ◽  
Peripheral Neuropathy ◽  
Anxiety Disorder ◽  
Calcium Channel ◽  
Female Patient ◽  
Calcium Channel Blockers ◽  
Channel Blocker ◽  
Mast Cell Degranulation ◽  
Channel Blockers

Here, I present a case of a female patient, age 45 years, for whom the uncontrolled mast cell degranulation created many issues related to allergy like, skin rash, itching, breathing discomfort, frequent throat infection, GERD, migraine, fibromyalgia, peripheral neuropathy, depression, anxiety disorder, constipation etc. For the patient, it was observed that calcium channel blockers seem to control the unnecessary and uncontrolled mast cell degranulation. CCB seemed to have a role to play in mast cell degranulation.

scholarly journals Role of small conductance calcium-activated potassium channels expressed in PVN in regulating sympathetic nerve activity and arterial blood pressure in rats

2012 ◽  
Vol 303 (3) ◽  
pp. R301-R310 ◽  
Author(s):  
Le Gui ◽  
Lila P. LaGrange ◽  
Robert A. Larson ◽  
Mingjun Gu ◽  
Jianhua Zhu ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Channel Blocker ◽  
Dependent Manner ◽  
Sk Channels ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Sk Channel ◽  
Small Conductance

Small conductance Ca2+-activated K+ (SK) channels regulate membrane properties of rostral ventrolateral medulla (RVLM) projecting hypothalamic paraventricular nucleus (PVN) neurons and inhibition of SK channels increases in vitro excitability. Here, we determined in vivo the role of PVN SK channels in regulating sympathetic nerve activity (SNA) and mean arterial pressure (MAP). In anesthetized rats, bilateral PVN microinjection of SK channel blocker with peptide apamin (0, 0.125, 1.25, 3.75, 12.5, and 25 pmol) increased splanchnic SNA (SSNA), renal SNA (RSNA), MAP, and heart rate (HR) in a dose-dependent manner. Maximum increases in SSNA, RSNA, MAP, and HR elicited by apamin (12.5 pmol, n = 7) were 330 ± 40% ( P < 0.01), 271 ± 40% ( P < 0.01), 29 ± 4 mmHg ( P < 0.01), and 34 ± 9 beats/min ( P < 0.01), respectively. PVN injection of the nonpeptide SK channel blocker UCL1684 (250 pmol, n = 7) significantly increased SSNA ( P < 0.05), RSNA ( P < 0.05), MAP ( P < 0.05), and HR ( P < 0.05). Neither apamin injected outside the PVN (12.5 pmol, n = 6) nor peripheral administration of the same dose of apamin (12.5 pmol, n = 5) evoked any significant changes in the recorded variables. PVN-injected SK channel enhancer 5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one (DCEBIO, 5 nmol, n = 4) or N-cyclohexyl- N-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-4-pyrimidin]amine (CyPPA, 5 nmol, n = 6) did not significantly alter the SSNA, RSNA, MAP, and HR. Western blot and RT-PCR analysis of punched PVN tissue showed abundant expression of SK1-3 channels. We conclude that SK channels expressed in the PVN play an important role in the regulation of sympathetic outflow and cardiovascular function.

scholarly journals Role of endogenous PACAP in catecholamine secretion from the rat adrenal gland

2001 ◽  
Vol 281 (5) ◽  
pp. R1562-R1567 ◽  
Author(s):  
Yasuo Fukushima ◽  
Hirohiko Hikichi ◽  
Kazuhiko Mizukami ◽  
Takahiro Nagayama ◽  
Makoto Yoshida ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Adrenal Gland ◽  
Adenylate Cyclase ◽  
Receptor Antagonist ◽  
Catecholamine Secretion ◽  
Type I ◽  
Type Ii ◽  
Low Concentrations ◽  
Pituitary Adenylate Cyclase

We elucidated the contribution of endogenous pituitary adenylate cyclase-activating polypeptide (PACAP) to neurally evoked catecholamine secretion from the isolated perfused rat adrenal gland. Infusion of PACAP (100 nM) increased adrenal epinephrine and norepinephrine output. The PACAP-induced catecholamine output responses were inhibited by the PACAP type I receptor antagonist PACAP- (6-38) (30–3,000 nM) but were resistant to the PACAP type II receptor antagonist [Lys1,Pro2,5,Ara3,4,Tyr6]-vasoactive intestinal peptide (LPAT-VIP; 30–3,000 nM). Transmural electrical stimulation (ES; 1–10 Hz) or infusion of ACh (6–200 nM) increased adrenal epinephrine and norepinephrine output. PACAP-(6–38) (3,000 nM), but not LPAT-VIP, also inhibited the ES-induced catecholamine output responses. However, PACAP-(6–38) did not affect the ACh-induced catecholamine output responses. PACAP at low concentrations (0.3–3 nM), which had no influence on catecholamine output, enhanced the ACh-induced catecholamine output responses, but not the ES-induced catecholamine output responses. These results suggest that PACAP is released from the nerve endings to facilitate the neurally evoked catecholamine secretion through PACAP type I receptors in the rat adrenal gland.

Role of calcium channels and adenylate cyclase in the PACAP-induced adrenal catecholamine secretion

2001 ◽  
Vol 281 (2) ◽  
pp. R495-R501 ◽  
Author(s):  
Yasuo Fukushima ◽  
Takahiro Nagayama ◽  
Hisako Kawashima ◽  
Hirohiko Hikichi ◽  
Makoto Yoshida ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Adenylate Cyclase ◽  
Calcium Channels ◽  
Catecholamine Secretion ◽  
Induced Responses ◽  
Free Solution ◽  
Pituitary Adenylate Cyclase ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

We elucidated the functional contribution of voltage-dependent calcium channels (VDCCs) and adenylate cyclase to epinephrine (Epi) and norepinephrine (NE) secretion induced by pituitary adenylate cyclase-activating polypeptide (PACAP) in the isolated perfused rat adrenal gland. PACAP increased Epi and NE output, which was inhibited by perfusion with calcium-free solution or by nifedipine, an L-type VDCC blocker. However, the PACAP-induced responses were resistant to ω-conotoxin GVIA, an N-type VDCC blocker, or ω-conotoxin MVIIC, a P/Q-type VDCC blocker. MDL-12330A, an adenylate cyclase inhibitor, inhibited the PACAP-induced increase in Epi, but not NE, output. Treatment with nifedipine and MDL-12330A caused additive inhibition of the PACAP-induced catecholamine responses. These results suggest that opening of L-type VDCCs is responsible for adrenal catecholamine secretion induced by PACAP and that activation of adenylate cyclase is involved in the PACAP-induced Epi, but not NE, secretion. These pathways may act independently of each other.

Role of endogenous endothelins in catecholamine secretion in the rat adrenal gland

2000 ◽  
Vol 406 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Takahiro Nagayama ◽  
Fumiyo Kuwakubo ◽  
Takayuki Matsumoto ◽  
Yasuo Fukushima ◽  
Makoto Yoshida ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Catecholamine Secretion

Ventricular tachyarrhythmias in rats with acute myocardial infarction involves activation of small-conductance Ca2+-activated K+ channels

2013 ◽  
Vol 304 (1) ◽  
pp. H118-H130 ◽  
Author(s):  
Le Gui ◽  
Zhiwei Bao ◽  
Yinyu Jia ◽  
Xiaotong Qin ◽  
Zixi (Jack) Cheng ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Channel Blocker ◽  
Left Ventricular ◽  
Dependent Manner ◽  
Ventricular Tachyarrhythmias ◽  
Sk Channels ◽  
Sk Channel ◽  
Small Conductance

In vitro experiments have shown that the upregulation of small-conductance Ca2+-activated K+ (SK) channels in ventricular epicardial myocytes is responsible for spontaneous ventricular fibrillation (VF) in failing ventricles. However, the role of SK channels in regulating VF has not yet been described in in vivo acute myocardial infarction (AMI) animals. The present study determined the role of SK channels in regulating spontaneous sustained ventricular tachycardia (SVT) and VF, the inducibility of ventricular tachyarrhythmias, and the effect of inhibition of SK channels on spontaneous SVT/VF and electrical ventricular instability in AMI rats. AMI was induced by ligation of the left anterior descending coronary artery in anesthetized rats. Spontaneous SVT/VF was analyzed, and programmed electrical stimulation was performed to evaluate the inducibility of ventricular tachyarrhythmias, ventricular effective refractory period (VERP), and VF threshold (VFT). In AMI, the duration and episodes of spontaneous SVT/VF were increased, and the inducibility of ventricular tachyarrhythmias was elevated. Pretreatment in the AMI group with the SK channel blocker apamin or UCL-1684 significantly reduced SVT/VF and inducibility of ventricular tachyarrhythmias ( P < 0.05). Various doses of apamin (7.5, 22.5, 37.5, and 75.0 μg/kg iv) inhibited SVT/VF and the inducibility of ventricular tachyarrhythmias in a dose-dependent manner. Notably, no effects were observed in sham-operated controls. Additionally, VERP was shortened in AMI animals. Pretreatment in AMI animals with the SK channel blocker significantly prolonged VERP ( P < 0.05). No effects were observed in sham-operated controls. Furthermore, VFT was reduced in AMI animals, and block of SK channels increased VFT in AMI animals, but, again, this was without effect in sham-operated controls. Finally, the monophasic action potential duration at 90% repolarization (MAPD90) was examined in the myocardial infarcted (MI) and nonmyocardial infarcted areas (NMI) of the left ventricular epicardium. Electrophysiology recordings showed that MAPD90 in the MI area was shortened in AMI animals, and pretreatment with SK channel blocker apamin or UCL-1684 significantly prolonged MAPD90 ( P < 0.05) in the MI area but was without effect in the NMI area or in sham-operated controls. We conclude that the activation of SK channels may underlie the mechanisms of spontaneous SVT/VF and suseptibility to ventricular tachyarrhythmias in AMI. Inhibition of SK channels normalized the shortening of MAPD90 in the MI area, which may contribute to the inhibitory effect on spontaneous SVT/VF and inducibility of ventricular tachyarrhythmias in AMI.

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