Governance of arteriolar oscillation by ryanodine receptors

2003 ◽  
Vol 285 (1) ◽  
pp. R125-R131 ◽  
Author(s):  
Tsuneo Takenaka ◽  
Yoichi Ohno ◽  
Koichi Hayashi ◽  
Takao Saruta ◽  
Hiromichi Suzuki
Keyword(s):  
Calcium Channels ◽  
Calcium Release ◽  
Calcium Influx ◽  
Ryanodine Receptors ◽  
Voltage Dependent ◽  
Fourth Series ◽  
Voltage Dependent Calcium Channels ◽  
Afferent Arterioles ◽  
Series Of Experiments ◽  
Bayk 8644

To investigate the role of ryanodine receptors in glomerular arterioles, experiments were performed using an isolated perfused hydronephrotic kidney model. In the first series of studies, BAYK-8644 (300 nM), a calcium agonist, constricted afferent (19.6 ± 0.6 to 17.6 ± 0.5 μm, n = 6, P < 0.01) but not efferent arterioles. Furthermore, BAYK-8644 elicited afferent arteriolar oscillatory movements. Subsequent administration of nifedipine (1 μM) inhibited both afferent arteriolar oscillation and constriction by BAYK-8644 (to 19.4 ± 0.5 μm). In the second group, although BAYK-8644 constricted afferent arterioles treated with 1 μM of thapsigargin (19.7 ± 0.6 to 16.8 ± 0.6 μm, n = 5, P < 0.05), it failed to induce rhythmic contraction. Removal of extracellular calcium with EGTA (2 mM) reversed BAYK-8644-induced afferent arteriolar constriction (to 20.0 ± 0.5 μm). In the third series of investigations, ryanodine (10 μM) but not 2-aminoethoxyphenyl borate (100 μM) abolished afferent arteriolar vasomotion by BAYK-8644. In the fourth series of experiments, in the presence of caffeine (1 mM), the stronger activation of voltage-dependent calcium channels by higher potassium media resulted in greater afferent arteriolar constriction and faster oscillation. Our results indicate that L-type calcium channels are rich in preglomerular but not postglomerular microvessels. Furthermore, the present findings suggest that either prolonged calcium influx through voltage-dependent calcium channels (BAYK-8644) or sensitized ryanodine receptors (caffeine) is required to trigger periodic calcium release through ryanodine receptors in afferent arterioles.

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.

scholarly journals Integrating multiple paracrine regulators of renal microvascular dynamics

1998 ◽  
Vol 274 (3) ◽  
pp. F433-F444 ◽  
Author(s):  
L. Gabriel Navar
Keyword(s):  
Calcium Channels ◽  
Renal Perfusion ◽  
Calcium Entry ◽  
Tubuloglomerular Feedback ◽  
Fluid Composition ◽  
Control Mechanisms ◽  
Paracrine Factor ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Afferent Arterioles

There has been tremendous growth in our knowledge about the multiple interacting mechanisms that regulate renal microvascular function. Paracrine signals originating from endothelial and epithelial cells exert profound influences on the basal tone and reactivity of the pre- and postglomerular arterioles. Selective responsiveness of these arterioles to various stimuli is possible because of differential activating mechanisms in vascular smooth muscle cells of afferent and efferent arterioles. Afferent arterioles rely predominantly on voltage-dependent calcium channels, while efferent arterioles utilize other mechanisms for calcium entry as well as intracellular calcium mobilization. The autoregulatory responses of preglomerular arterioles exemplify the selectivity of these complex control mechanisms. The myogenic mechanism responds to increases in renal perfusion pressure through “stretch-activated” cation channels that lead to depolarization, calcium entry, and vascular contraction. Autoregulatory efficiency is enhanced by the tubuloglomerular feedback (TGF) mechanism which responds to flow-dependent changes in tubular fluid composition at the level of the macula densa and transmits signals to the afferent arterioles to alter the activation state of voltage-dependent calcium channels. Recent studies have implicated extracellular ATP as one paracrine factor mediating TGF and autoregulatory related signals to the afferent arterioles. Other paracrine agents including nitric oxide, angiotensin II, adenosine, and arachidonic acid metabolites modulate vascular responsiveness in order to maintain an optimal balance between the metabolically determined reabsorptive capabilities of the tubules and the hemodynamically dependent filtered load.

Atrial natriuretic peptide differentially modulates T- and L-type calcium channels

1990 ◽  
Vol 258 (3) ◽  
pp. F473-F478 ◽  
Author(s):  
R. T. McCarthy ◽  
C. M. Isales ◽  
W. B. Bollag ◽  
H. Rasmussen ◽  
P. Q. Barrett
Keyword(s):  
Calcium Channels ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Calcium Influx ◽  
Patch Clamp Technique ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Glomerulosa Cells ◽  
Channel Type ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone stimulated by any of these major physiological agonists: angiotensin II, adrenocorticotropic hormone, or K+. The stimulatory actions of each of these agonists depend on calcium influx through voltage-dependent calcium channels. Because two types of calcium channels have been previously described in bovine glomerulosa cells (T- and L-type), the patch-clamp technique was used to evaluate the effect of ANP on each voltage-dependent calcium channel type. ANP was found to differentially modulate these two channel types, stimulating L-current while inhibiting T-current. Inhibition of T-current resulted from a shift in the voltage dependence of inactivation to more negative potentials within the physiological range. These results indicate that the ANP-induced inhibition of aldosterone secretion may be partially mediated via a reduction of the calcium current through T-type channels.

Effect of intracellular pH on depolarization-evoked calcium influx in human sperm

2004 ◽  
Vol 287 (6) ◽  
pp. C1688-C1696 ◽  
Author(s):  
Juan J. Fraire-Zamora ◽  
Marco T. González-Martínez
Keyword(s):  
Intracellular Ph ◽  
Calcium Release ◽  
Calcium Influx ◽  
Human Sperm ◽  
Calcium Dependent ◽  
Voltage Dependent ◽  
Sigmoid Curve ◽  
Voltage Dependent Calcium Channels ◽  
Calcium Permeability

Human sperm are endowed with putative voltage-dependent calcium channels (VDCC) that produce measurable increases in intracellular calcium concentration ([Ca2+]i) in response to membrane depolarization with potassium. These channels are blocked by nickel, inactivate in 1–2 min in calcium-deprived medium, and are remarkably stimulated by NH4Cl, suggesting a role for intracellular pH (pHi). In a previous work, we showed that calcium permeability through these channels increases approximately onefold during in vitro “capacitation,” a calcium-dependent process that sperm require to fertilize eggs. In this work, we have determined the pHi dependence of sperm VDCC. Simultaneous depolarization and pHi alkalinization with NH4Cl induced an [Ca2+]i increase that depended on the amount of NH4Cl added. VDCC stimulation as a function of pHi showed a sigmoid curve in the 6.6–7.2 pHi range, with a half-maximum stimulation at pH ∼7.00. At higher pHi (≥7.3), a further stimulation occurred. Calcium release from internal stores did not contribute to the stimulating effect of pHi because the [Ca2+]i increase induced by progesterone, which opens a calcium permeability pathway that does not involve gating of VDCC, was unaffected by ammonium. The ratio of pHi-stimulated-to-nonstimulated calcium influx was nearly constant at different test depolarization values. Likewise, depolarization-induced calcium influx in pHi-stimulated and nonstimulated cells was equally blocked by nickel. In our capacitating conditions pHi increased 0.11 pH units, suggesting that the calcium influx stimulation observed during sperm capacitation might be partially caused by pHi alkalinization. Additionally, a calcium permeability pathway triggered exclusively by pHi alkalinization was detected.

Sigma-1 receptors do not regulate calcium influx through voltage-dependent calcium channels in mouse brain synaptosomes

2012 ◽  
Vol 677 (1-3) ◽  
pp. 102-106 ◽  
Author(s):  
Luis G. González ◽  
Cristina Sánchez-Fernández ◽  
Enrique J. Cobos ◽  
José M. Baeyens ◽  
Esperanza del Pozo
Keyword(s):  
Calcium Channels ◽  
Mouse Brain ◽  
Calcium Influx ◽  
Brain Synaptosomes ◽  
Voltage Dependent ◽  
Sigma 1 ◽  
Voltage Dependent Calcium Channels

Calcium influx in rat thalamic relay neurons through voltage-dependent calcium channels is inhibited by enkephalin

1995 ◽  
Vol 201 (1) ◽  
pp. 21-24 ◽  
Author(s):  
Alessandro Formenti ◽  
Elda Arrigoni ◽  
Marzia Martina ◽  
Stefano Taverna ◽  
Giuliano Avanzini ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Calcium Influx ◽  
Thalamic Relay ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Thalamic Relay Neurons ◽  
Relay Neurons

scholarly journals 8-Oxo-9-Dihydromakomakine Isolated from Aristotelia chilensis Induces Vasodilation in Rat Aorta: Role of the Extracellular Calcium Influx

Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 3050 ◽  
Author(s):  
Fredi Cifuentes ◽  
Javier Palacios ◽  
Adrián Paredes ◽  
Chukwuemeka Nwokocha ◽  
Cristian Paz
Keyword(s):  
Calcium Channels ◽  
Contractile Response ◽  
Calcium Influx ◽  
Folk Medicine ◽  
Indole Alkaloid ◽  
Rat Aorta ◽  
Inward Rectifier Potassium Channel ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Aristotelia Chilensis

8-Oxo-9-dihydromakomakine is a tetracyclic indole alkaloid extracted from leaves of the Chilean tree Aristotelia chilensis. The present study investigated the effects of this alkaloid on vascular response in tissues isolated from aortic segments obtained from normotensive rats. Our results showed that 8-oxo-9-dihydromakomakine induced a dose-dependent relaxation of aortic rings pre-contracted with phenylephrine (PE; 10−6 M). The vasorelaxation induced by 8-oxo-9-dihydromakomakine in rat aortic rings is independent of endothelium. The pre-incubation of aortic rings with 8-oxo-9-dehydromakomakine (10−4 M) significantly reduced the contractile response to KCl (p < 0.001) more than PE (p < 0.05). The highest dose of 8-oxo-9-dehydromakomakine (10−4 M) drastically reduced the contraction to KCl (6·10−2 M), but after that, PE (10−6 M) caused contraction (p < 0.05) in the same aortic rings. The addition of 8-oxo-9-dihydromakomakine (10−5 M) decreased the contractile response to tetraethylammonium (a voltage-dependent potassium channels blocker; TEA; 5 × 10−3 M; p < 0.01) and BaCl2 (a non-selective inward rectifier potassium channel blocker; 5 × 10−3 M; p < 0.001) in rat aorta. 8-oxo-9-dihydromakomakine (10−5 M) decreased the contractile response to PE in rat aorta in the presence or absence of ouabain (an inhibitor of Na,K-ATPase; 10−3 M; p < 0.05). These results could indicate that 8-oxo-9-dihydromakomakine partially reduces plasma membrane depolarization-induced contraction. In aortic rings depolarized by PE, 8-oxo-9-dihydromakomakine inhibited the contraction induced by the influx of extracellular Ca2+ in a Ca2+ free solution (p < 0.01). 8-oxo-9-dihydromakomakine reduced the contractile response to agonists of voltage-dependent calcium channels type L (Bay K6844; 10−8 M; p < 0.01), likely decreasing the influx of extracellular Ca2+ through the voltage-dependent calcium channels. This study provides the first qualitative analysis indicating that traditional folk medicine Aristotelia chilensis may be protective in the treatment of cardiovascular pathologies.

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