Mechanism of hyperosmolality stimulation of ANP secretion: its dependency on calcium and sodium

1995 ◽  
Vol 268 (3) ◽  
pp. E476-E483 ◽  
Author(s):  
R. J. Schiebinger ◽  
C. M. Joseph ◽  
Y. Li ◽  
E. J. Cragoe
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Channel Blocker ◽  
Calcium Influx ◽  
Voltage Dependent Calcium Channel ◽  
Sodium Dependent ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Sodium Dependency ◽  
Sarcoplasmic Reticulum Calcium ◽  
Stimulation Of

The calcium dependency of hyperosmolality stimulation of atrial natriuretic peptide (ANP) secretion was determined using isolated superfused nonbeating rat left atrium. Increasing osmolality by 65, 85, and 100 mosmol/kgH2O by superfusion with sucrose produced a peak rise in ANP secretion of 1.8-, 2.0-, and 2.7-fold. To determine whether calcium influx played a role in osmolality (osm)-stimulated ANP secretion, atria were superfused with 2 mM lanthanum, a calcium antagonist. Lanthanum inhibited by 85% the response to a 100 mosmol/kgH2O increase in osm. The voltage-dependent calcium channel blocker isradipine had no effect on osm-stimulated ANP secretion, suggesting that calcium influx via voltage-dependent calcium channels was not playing a significant role. Likewise, depleting sarcoplasmic reticulum calcium with 1 microM ryanodine did not block the response to osm, suggesting that calcium influx was not adequate to induce consequential release of calcium from the sarcoplasmic reticulum. To determine whether calcium influx was via Na(+)-Ca2+ exchange, we determined the sodium dependency of osm-stimulated ANP secretion. Replacement of sodium with lithium or choline blocked the secretory response to 100 mosmol/kgH2O. We conclude that osm-stimulated ANP secretion is calcium and sodium dependent. Calcium influx via Na(+)-Ca2+ exchange is highly implicated as the mechanism of cellular calcium entry.

scholarly journals Agatoxin-IVA-Sensitive Calcium Channels Mediate the Presynaptic and Postsynaptic Nicotinic Activation of Cardiac Vagal Neurons

2001 ◽  
Vol 85 (1) ◽  
pp. 164-168 ◽  
Author(s):  
Jijiang Wang ◽  
Mustapha Irnaten ◽  
David Mendelowitz
Keyword(s):  
Calcium Channels ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Patch Clamp Technique ◽  
Current Increase ◽  
Inward Current ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

Whole cell currents and miniature glutamatergic synaptic events (minis) were recorded in vitro from cardiac vagal neurons in the nucleus ambiguus using the patch-clamp technique. We examined whether voltage-dependent calcium channels were involved in the nicotinic excitation of cardiac vagal neurons. Nicotine evoked an inward current, increase in mini amplitude, and increase in mini frequency in cardiac vagal neurons. These responses were inhibited by the nonselective voltage-dependent calcium channel blocker Cd (100 μM). The P-type voltage-dependent calcium channel blocker agatoxin IVA (100 nM) abolished the nicotine-evoked responses. Nimodipine (2 μM), an antagonist of L-type calcium channels, inhibited the increase in mini amplitude and frequency but did not block the ligand gated inward current. The N- and Q-type voltage-dependent calcium channel antagonists conotoxin GVIA (1 μM) and conotoxin MVIIC (5 μM) had no effect. We conclude that the presynaptic and postsynaptic facilitation of glutamatergic neurotransmission to cardiac vagal neurons by nicotine involves activation of agatoxin-IVA-sensitive and possibly L-type voltage-dependent calcium channels. The postsynaptic inward current elicited by nicotine is dependent on activation of agatoxin-IVA-sensitive voltage-dependent calcium channels.

scholarly journals Voltage-Dependent Calcium Channel CaV1.3 Subunits Regulate the Light Peak of the Electroretinogram

2007 ◽  
Vol 97 (5) ◽  
pp. 3731-3735 ◽  
Author(s):  
Jiang Wu ◽  
Alan D. Marmorstein ◽  
Jörg Striessnig ◽  
Neal S. Peachey
Keyword(s):  
Calcium Channel ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Rod Photoreceptor ◽  
Wild Type ◽  
Fast Oscillation ◽  
Light Peak ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

In response to light, the mouse retinal pigment epithelium (RPE) generates a series of slow changes in potential that are referred to as the c-wave, fast oscillation (FO), and light peak (LP) of the electroretinogram (ERG). The LP is generated by a depolarization of the basolateral RPE plasma membrane by the activation of a calcium-sensitive chloride conductance. We have previously shown that the LP is reduced in both mice and rats by nimodipine, which blocks voltage-dependent calcium channels (VDCCs) and is abnormal in lethargic mice, carrying a null mutation in the calcium channel β4 subunit. To define the α1 subunit involved in this process, we examined mice lacking CaV1.3. In comparison with wild-type (WT) control littermates, LPs were reduced in CaV1.3−/− mice. This pattern matched closely with that previously noted in lethargic mice, confirming a role for VDCCs in regulating the signaling pathway that culminates in LP generation. These abnormalities do not reflect a defect in rod photoreceptor activity, which provides the input to the RPE to generate the c-wave, FO, and LP, because ERG a-waves were comparable in WT and CaV1.3−/− littermates. Our results identify CaV1.3 as the principal pore-forming subunit of VDCCs involved in stimulating the ERG LP.

scholarly journals Characteristic of the vasorlaxant action of the talatisamine alkaloid and its derivatives

2021 ◽  
Vol 4 (2) ◽  
pp. 01-05
Author(s):  
Mirzayeva Yu.T.
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Channel Blocker ◽  
Aortic Ring ◽  
Diterpenoid Alkaloids ◽  
Relaxant Effect ◽  
Ring Contraction ◽  
Voltage Dependent ◽  
Ca2 Channels ◽  
Isolated Rat

The aim of our research is to study the effect relaxant action of diterpenoid alkaloids talatisamine, 14-O-benzoylthalatisamine and 14-O-acetylthalatisamine was studied using isolated rat aortic rings. Alkaloids significantly and dose-dependently inhibited contraction of the aortic rings caused by high KCl content. At the same time, under these conditions, alkaloids significantly reduced Ca2+-induced contraction of the aortic rings. The relaxing effects of alkaloids are significantly suppressed by verapamil, a potent potentiometer-dependent Ca2+ channel blocker. The alkaloids also significantly reduced norepinephrine-induced aortic ring contraction in normal as well as Ca2+ free Krebs solutions. The data obtained indicate that talatisamine, 14-benzoylthalatisamine and 14-O-acetylthalatisamine exhibit a pronounced relaxant effect in almost the same way in the case of contraction induced by a high content of KCl and norepinephrine. The mechanism of the relaxant action of alkaloids is probably complex and may include suppression of Ca2+influx through voltage-dependent and receptor-driven Ca2+ channels, as well as inhibition of Ca2+transport in the sarcoplasmic reticulum.

5-Hydroxytryptamine potentiates vasoconstrictor effect of endothelin-1

1992 ◽  
Vol 262 (4) ◽  
pp. H931-H936
Author(s):  
B. C. Yang ◽  
W. W. Nichols ◽  
D. L. Lawson ◽  
J. L. Mehta
Keyword(s):  
Receptor Antagonist ◽  
Channel Blocker ◽  
Contractile Response ◽  
Thromboxane A2 ◽  
Threshold Concentration ◽  
Endothelin 1 ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Ly 53857 ◽  
A2 Receptors

Interactions between 5-hydroxytryptamine (5-HT) and endothelin-1 (ET-1) relative to contraction of rat aortic rings were examined in this study. Pretreatment of rings with threshold concentration of 5-HT potentiated the subsequent contractile response to ET-1. However, pretreatment with threshold concentration of ET-1 did not potentiate the contractile response to 5-HT. The 5-HT receptor antagonist LY 53857 blocked the synergistic contractile effects of 5-HT and ET-1 on rat aortic rings. Indomethacin and the thromboxane A2/endoperoxide receptor antagonist SQ 29548 also attenuated (P less than 0.05) the synergistic contractile effects of 5-HT and ET-1, suggesting release of thromboxane A2 or expression of thromboxane A2 receptors during this interaction. The calcium channel blocker verapamil also decreased the synergistic contractile effects of 5-HT and ET-1. Contraction of aortic rings by 5-HT alone was abolished by LY 53857 and attenuated by verapamil, diltiazem, and SQ 29548. Decrease in the force of contraction by verapamil as well as diltiazem indicates activation of voltage-dependent calcium channels during 5-HT-mediated contraction and perhaps during amplification of the vasoconstrictor activity of ET-1 by 5-HT.

Initial and sustained phases of myogenic response of rat mesenteric small arteries

2001 ◽  
Vol 281 (5) ◽  
pp. H2176-H2183 ◽  
Author(s):  
S. Chlopicki ◽  
H. Nilsson ◽  
M. J. Mulvany
Keyword(s):  
Calcium Channels ◽  
Neuropeptide Y ◽  
Initial Phase ◽  
Calcium Influx ◽  
Myogenic Response ◽  
Octadecanoic Acid ◽  
Small Arteries ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Cytochrome P 450

A possible role for a metabolite of cytochrome P-450 ω-hydroxylase in the initial and sustained phases of the myogenic response in cannulated rat mesenteric small arteries was studied. With slight preconstriction (norepinephrine and neuropeptide Y), pressure was raised from 60 to 100 mmHg, and both initial (within 2 min) and sustained phases (at 10 min) of the myogenic response were quantified. The myogenic response was fully inhibited by D600 (methoxyverapamil). Ketoconazole and 17-octadecanoic acid did not affect the initial phase but inhibited the sustained phase. In contrast, miconazole did not affect either phase. Charybdotoxin and iberiotoxin potentiated the initial phase but eliminated the sustained phase. Apamin, glibenclamide, 4-aminopyridine, and barium had no effect on either phase. The results demonstrate different mechanisms for the initial and sustained phases of the myogenic response of rat mesenteric small arteries. Only the sustained phase appears mediated through a cytochrome P-450 ω-hydroxylase metabolite and calcium-activated K+ channels. However, both phases of the response are dependent on calcium influx through voltage-dependent calcium channels.

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