The aim of the present study was to examine whether endocannabinoidscause PPARγ-mediated vascular actions.
In the present study, we have examined whether endocannabinoidscause time-dependent, PPARγ-mediated
vascular effects as previously shown for the phytocannabinoid, THC [, ].
In these studies, we demonstrate for the
first time that the endocannabinoidsanandamide and NADAcause PPARγ-mediated,
time-dependent vasorelaxation of rat aortae, which is dependent on de novo protein synthesis, nitric oxide
production and superoxide dismutase activity.
On the basis that PPARγ
agonists cause time-dependent vasorelaxation of isolated aortae [, ], and
that endocannabinoids activate PPARγ [–],
we investigated whether endocannabinoidsproduce time-dependent
vasorelaxation.
In addition, noladin ethercaused a delay in wound healing of confluent trabecular meshwork monolayers and this effect of noladin ether was antagonized by SR141716A.
Collectively, in MDCK cells, anandamide induced [Ca(2+)](i) rises by causing Ca(2+) release from endoplasmic reticulum and Ca(2+) influx from extracellular space.
This study examined whether anandamidealtered Ca(2+) levels and caused Ca(2+)-dependent cell death in Madin-Darby canine kidney (MDCK) cells. [Ca(2+)](i) and cell death were measured using the fluorescent dyes fura-2 and WST-1 respectively.
However, the details of the mechanisms for the regulation of cough sensitivity by anandamide are not yet well known.
These results suggest that anandamide, an endogenous cannabinoid ligand, may modulate cough sensitivity and that anandamide transporters play an important role in this modulation.
In conclusion, the present results suggest that anandamide, an endogenous cannabinoid ligand, may modulate cough sensitivity and anandamide transporters play an important role in this modulation.
Furthermore, it is possible that higher doses of anandamide may cause the activation of the cytosolic domain of TRPV1 receptors, since anandamide-induced enhancement of the number of coughs was abolished by pretreatment with either capsazepine, a selective TRPV1 receptor antagonist, or VDM11.
This review focuses on the results of recent studies indicating that beyond their receptor-mediated effects, endocannabinoidsalter the functions of ion channels and other integral membrane proteins directly.
Furthermore, functional properties of G-protein-coupled receptors for different types of neurotransmitters and neuropeptides are altered by direct actions of endocannabinoids.
These data show that: 1) Ca2+ and anandamidecause hyperpolarization-mediated relaxation of mesenteric branch arteries, which is dependent on an iberiotoxin-sensitive Ca2+-activated K+ channel, 2) relaxation induced by both Ca2+ and anandamide is inhibited by CB receptor blockade, and 3) relaxation induced by anandamide is not dependent on its breakdown to arachidonic acid and subsequent metabolism.
Although several pieces of evidence indicate that the endocannabinoid system modulates anxiety-like behaviors and stress adaptation, few studies have investigated the brain sites of these effects.
These results suggest that facilitation of endocannabinoid system neurotransmission in the ventral hippocampus modulates anxiety-like behaviors and that this effect depends on previous stress experience.
This conditional release of endocannabinoids can transform motoneurons and crossing interneurons into modulatory neurons by enabling them to regulate their inhibitory synaptic inputs and thus contribute to the modulation of the locomotor burst frequency.
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