scholarly journals Calcium current modulation in frog sympathetic neurones: multiple neurotransmitters and G proteins.

1992 ◽  
Vol 451 (1) ◽  
pp. 229-246 ◽  
Author(s):  
K S Elmslie
Keyword(s):  
G Proteins ◽  
Calcium Current ◽  
Current Modulation ◽  
Sympathetic Neurones

Molecular mechanisms underlying calcium current modulation by nociceptin

Neuroreport ◽  
2004 ◽  
Vol 15 (14) ◽  
pp. 2205-2209 ◽  
Author(s):  
Kyu-Young Yeon ◽  
Mi-Young Sim ◽  
Se-Young Choi ◽  
Sung Joong Lee ◽  
Kyungpyo Park ◽  
...  
Keyword(s):  
Calcium Current ◽  
Molecular Mechanisms ◽  
Current Modulation

scholarly journals Altered Neural and Vascular Mechanisms in Hypertension

2011 ◽  
pp. 381-402 ◽  
Author(s):  
M. PINTÉROVÁ ◽  
J. KUNEŠ ◽  
J. ZICHA
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
G Proteins ◽  
High Blood Pressure ◽  
Calcium Current ◽  
Calcium Influx ◽  
Dominant Role ◽  
Cardiovascular Complications ◽  
Sympathetic Nervous

Essential hypertension is a multifactorial disorder which belongs to the main risk factors responsible for renal and cardiovascular complications. This review is focused on the experimental research of neural and vascular mechanisms involved in the high blood pressure control. The attention is paid to the abnormalities in the regulation of sympathetic nervous system activity and adrenoceptor alterations as well as the changes of membrane and intracellular processes in the vascular smooth muscle cells of spontaneously hypertensive rats. These abnormalities lead to increased vascular tone arising from altered regulation of calcium influx through L-VDCC channels, which has a crucial role for excitation-contraction coupling, as well as for so-called “calcium sensitization” mediated by the RhoA/Rho-kinase pathway. Regulation of both pathways is dependent on the complex interplay of various vasodilator and vasoconstrictor stimuli. Two major antagonistic players in the regulation of blood pressure, i.e. sympathetic nervous system (by stimulation of adrenoceptors coupled to stimulatory and inhibitory G proteins) and nitric oxide (by cGMP signaling pathway), elicit their actions via the control of calcium influx through L-VDCC. However, L-type calcium current can also be regulated by the changes in membrane potential elicited by the activation of potassium channels, the impaired function of which was detected in hypertensive animals. The dominant role of enhanced calcium influx in the pathogenesis of high blood pressure of genetically hypertensive animals is confirmed not only by therapeutic efficacy of calcium antagonists but especially by the absence of hypertension in animals in which L-type calcium current was diminished by pertussis toxin-induced inactivation of inhibitory G proteins. Although there is considerable information on the complex neural and vascular alterations in rats with established hypertension, the detailed description of their appearance during the induction of hypertension is still missing.

scholarly journals The Monomeric G-Proteins Rac1 and/or Cdc42 Are Required for the Inhibition of Voltage-Dependent Calcium Current by Bradykinin

1997 ◽  
Vol 17 (11) ◽  
pp. 4094-4100 ◽  
Author(s):  
Malgorzata A. Wilk-Blaszczak ◽  
William D. Singer ◽  
Timothy Quill ◽  
Billy Miller ◽  
Jeffrey A. Frost ◽  
...  
Keyword(s):  
G Proteins ◽  
Calcium Current ◽  
Voltage Dependent

Presynaptic Calcium Current Modulation by a Metabotropic Glutamate Receptor

Science ◽  
1996 ◽  
Vol 274 (5287) ◽  
pp. 594-597 ◽  
Author(s):  
T. Takahashi ◽  
I. D. Forsythe ◽  
T. Tsujimoto ◽  
M. Barnes-Davies ◽  
K. Onodera
Keyword(s):  
Glutamate Receptor ◽  
Calcium Current ◽  
Metabotropic Glutamate Receptor ◽  
Current Modulation ◽  
Metabotropic Glutamate ◽  
Presynaptic Calcium
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