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Upregulation of rho A and rho kinase messenger RNAs in the basilar artery of a rat model of subarachnoid hemorrhage.
OBJECT Rho A, a small guanosine triphosphate-binding protein, and rho kinases have been suggested to play an important role in the agonist-induced myofilament Ca++ sensitization and cytoskeletal
Dual regulation of cerebrovascular tone by UTP: P2U receptor‐mediated contraction and endothelium‐dependent relaxation
TLDR
In the presence of an intact endothelium, UTP‐induced relaxation of pre‐constricted middle cerebral artery is mainly mediated indirectly, by the production of an endothelia‐derived relaxing factor, but at high doses of UTP, vascular smooth muscle contraction is mediated directly via activation of P2U purinoceptor and [Ca2+]i elevation without Ca2+‐sensitization of the contractile apparatus.
The mechanisms of the relaxation induced by vasoactive intestinal peptide in the porcine coronary artery
TLDR
It is concluded that VIP relaxes the coronary artery via three mechanisms: (1) a decrease in [Ca2+]i by inhibiting the Ca2+ influx presumably through the membrane hyperpolarization mediated by the activation of the large conductance Ca2-‐activated (charybdotoxin‐sensitive) K+ channels and voltage‐dependent (4‐AP‐ sensitive) K+.
Resting load regulates cytosolic calcium‐force relationship of the contraction of bovine cerebrovascular smooth muscle.
TLDR
At a given degree of [Ca2+]i elevation, the developed force induced by U‐46619 was greater than that induced by high K+ depolarization, and preload, or resting load, regulates contractile responsiveness of cerebrovascular smooth muscle to various stimulations, mainly by modulating the [Ca(2+)‐force relationship.
P2U receptor is linked to cytosolic Ca2+ transient and release of vasorelaxing factor in bovine endothelial cells in situ.
TLDR
The activation of the nucleotide receptor, P2U, induces [Ca2+]i elevation in endothelial cells in situ, and thus leads to the release of vasorelaxing factors, and the peak elevation of the Ca2+i transient induced by these nucleotides is independent of extracellular Ca2+.
P2UPurinergic Activation Leads to the Cell Cycle Progression from the G1to the S and M Phases but Not from the G0to G1Phase in Vascular Smooth Muscle Cells in Primary Culture
TLDR
Results indicate that P 2U purinergic activation mediates a [Ca 2+ ]i transient and a progression growth factor effect of nucleotides in VSMCs.
Altered Expression of P2 Receptor mRNAs in the Basilar Artery in a Rat Double Hemorrhage Model
TLDR
The differential expression of the P2 receptors indicates that P2X1 subtype might not play an important role in vasospasm, and the upregulation of P2Y1 and P2y2 receptors might enable ATP to produce contraction at low levels of concentration.
Resting load regulates vascular sensitivity by a cytosolic Ca(2+)-insensitive mechanism.
TLDR
It is concluded that the resting load regulates the sensitivity of vascular smooth muscles, irrespective of types of stimuli, through a [Ca2+]i-insensitive mechanism.
P2U purinergic activation leads to the cell cycle progression from the G1 to the S and M phases but not from the G0 to G1 phase in vascular smooth muscle cells in primary culture.
TLDR
Results indicate that P2U purinergic activation mediates a [Ca2+]i transient and a progression growth factor effect of nucleotides in VSMCs.
Cytotoxicity of ventricular cerebrospinal fluid from Parkinson patients: Correlation with clinical profiles and neurochemistry
TLDR
The cytotoxic effect of PD-vCSF did not directly correlate with any clinical profiles studied or energy metabolism of PD brain, except for a slight correlation between vCSF and disease progression rate in heat treated samples from female patients.
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