Nitric Oxide Suppresses Cerebral Vasomotion by sGC-Independent Effects on Ryanodine Receptors and Voltage-Gated Calcium Channels

The influence of ryanodine channels on the cytosole Ca2+ dynamics was studied. We added the equations for ryanodine receptors and voltage-gated calcium channels into the original De Pitta et al. model of Ca2+. The derived model was shown to have significantly wider range of predictions: we derived the frequency of cytosole calcium spontaneous oscillations (which are absent in the original De Pitta et al. model) for various existing models of Ca2+ signalling in astrocytes. Particularly, the initial De Pitta et al. results can be converted to either Lavrentovich and Hemkin model or in the Dupont et al model predictions. The absence of the Ca2+ oscillations in astrocytes with the active ryanodine channels only was recently reported. This behaviour can be achieved in our model predictions for the certain values of parameters, which are supposedly responsible for the bifurcation landscape between the oscillatory and non-oscillatory dynamics of cytosol Ca2+ in astrocytes. We also investigated the interplay between the spontaneous and glutamate-triggered oscillations.

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Verapamil abolishes the preglomerular response to ANG II during intrarenal nitric oxide synthesis inhibition

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1997.272.5.r1670 ◽

1997 ◽

Vol 272 (5) ◽

pp. R1670-R1676

Author(s):

C. G. Schnackenberg ◽

J. P. Granger

Keyword(s):

Nitric Oxide ◽

Calcium Channels ◽

Hemodynamic Response ◽

Treated Group ◽

Ang Ii ◽

Synthesis Inhibition ◽

Voltage Gated ◽

Voltage Gated Calcium Channels ◽

Renal Hemodynamic ◽

Vasoconstrictor Response

We have recently reported that intrarenal nitric oxide (NO) synthesis inhibition exaggerates the preglomerular vasoconstrictor response more than the postglomerular response to angiotensin II (ANG II) in dogs. Previous studies have suggested that preglomerular vasoconstriction may be more dependent on extracellular calcium than postglomerular vasoconstriction. The purpose of this study is to determine whether the enhanced preglomerular response to ANG II during intrarenal NO synthesis inhibition occurs through voltage-gated calcium channels. In three groups of anesthetized dogs with stop-flow kidneys, the renal hemodynamic response to intrarenal ANG II infusion (2.0 ng.kg-1.min-1) was determined. Renal artery pressure was servo-controlled at 80 +/- 1 mmHg, and glomerular filtration rate was zero. In vehicle-treated dogs, ANG II decreased renal blood flow (RBF) by 29% and increased glomerular hydrostatic pressure (Pg) by 2.7 +/- 1.9 mmHg. Postglomerular vascular resistance increased by 51%, whereas preglomerular resistance was unchanged in response to ANG II. In dogs pretreated with an intrarenal infusion of NG-nitro-L-arginine methyl ester (L-NAME; 5 micrograms.kg-1.min-1) for 60 min, ANG II decreased RBF by 36% and decreased Pg 4.4 +/- 2.9 mmHg. In contrast to the vehicle-treated group, preglomerular resistance increased by 261% and postglomerular resistance increased by 48% after ANG II infusion in the L-NAME-treated group. In dogs pretreated with an intrarenal infusion of L-NAME and verapamil (50 micrograms/min) for 60 min, the renal hemodynamic response to ANG II was similar to the response in the vehicle-treated dogs. ANG II decreased RBF by 25% and decreased Pg by 5.3 +/- 1.2 mmHg. Postglomerular resistance increased by 51%, whereas preglomerular resistance was unchanged in response to ANG II infusion in dogs with intrarenal NO synthesis and voltage-gated calcium channel blockade. These data indicate that the preglomerular response to ANG II under conditions of reduced NO synthesis within the kidney is dependent on voltage-gated calcium channels.

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Effects of nitric oxide on apoptosis and voltage‐gated calcium channels in human cardiac myofibroblasts

Clinical and Experimental Pharmacology and Physiology ◽

10.1111/1440-1681.13178 ◽

2019 ◽

Vol 47 (1) ◽

pp. 16-26

Author(s):

Hyemi Bae ◽

Taeho Kim ◽

Inja Lim

Keyword(s):

Nitric Oxide ◽

Calcium Channels ◽

Voltage Gated ◽

Voltage Gated Calcium Channels ◽

Cardiac Myofibroblasts

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Ryanodine receptors, voltage-gated calcium channels and their relationship with protein kinase A in the myocardium

Physiological Research ◽

10.33549/physiolres.931171 ◽

2008 ◽

pp. 141-149

Author(s):

MM Petrovic ◽

K Vales ◽

B Putnikovic ◽

V Djulejic ◽

DM Mitrovic

Keyword(s):

Protein Kinase ◽

Calcium Channels ◽

Cardiac Muscle ◽

Protein Kinase A ◽

Ryanodine Receptor ◽

Ryanodine Receptors ◽

Physiological Role ◽

Voltage Gated ◽

Voltage Gated Calcium Channels ◽

Kinase A

We present a review about the relationship between ryanodine receptors and voltage-gated calcium channels in myocardium, and also how both of them are related to protein kinase A. Ryanodine receptors, which have three subtypes (RyR1-3), are located on the membrane of sarcoplasmic reticulum. Different subtypes of voltage-gated calcium channels interact with ryanodine receptors in skeletal and cardiac muscle tissue. The mechanism of excitation-contraction coupling is therefore different in the skeletal and cardiac muscle. However, in both tissues ryanodine receptors and voltage-gated calcium channels seem to be physically connected. FK-506 binding proteins (FKBPs) are bound to ryanodine receptors, thus allowing their concerted activity, called coupled gating. The activity of both ryanodine receptors and voltage-gated calcium channels is positively regulated by protein kinase A. These effects are, therefore, components of the mechanism of sympathetic stimulation of myocytes. The specificity of this enzyme’s targeting is achieved by using different A kinase adapting proteins. Different diseases are related to inborn or acquired changes in ryanodine receptor activity in cardiac myocytes. Mutations in the cardiac ryanodine receptor gene can cause catecholamineprovoked ventricular tachycardia. Changes in phosphorylation state of ryanodine receptors can provide a credible explanation for the development of heart failure. The restoration of their normal level of phosphorylation could explain the positive effect of beta-blockers in the treatment of this disease. In conclusion, molecular interactions of ryanodine receptors and voltage-gated calcium channels with PKA have a significant physiological role. However, their defects and alterations can result in serious disturbances.

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