These endocannabinoids share a polyunsaturated fatty acid moiety
(arachidonic acid) and a polar head group consisting of ethanolamine
or glycerol.
Basavarajappa BS. Mini Rev Med Chem. 2007 Aug;7(8):769-7
The present study was undertaken to investigate the effects of
intravenous (i.v.) administration of rat hemopressin (rHP), 30-1000
microg/kg, on systemic arterial pressure (SAP), cardiac output (CO)
and systemic vascular resistance (SVR) in the anesthetized rat.
Bolus i.v. injections of rHP produced mild decreases in SAP that
were dose-dependent. Since CO was not altered, the decreases in SAP
reflect reductions in SVR. The systemic vasodilator response to rHP
was not subject to tachyphylaxis. The systemic vasodilator response
to rHP was abolished by L-nitro-arginine methylester (L-NAME) but
was not altered by meclofenamate. In addition, rHP lacked direct
contractile and relaxant activity on isolated rat aortic rings (AA)
and pulmonary arterial rings (PA). The present data suggest rHP
dilates the rat systemic vascular bed through the endogenous release
of nitric oxide (NO) independent of the formation of cyclooxygenase
products including prostacyclin. It is possible rHP acts as an
endogenous vasodilator substance to regulate local blood flow during
clinical states of altered red cell turnover, microvascular disease
and hemolysis.
Lippton H et al. Peptides. 2006 Sep;27(9):2284-8. Epub 2006 May 19
Depolarization of
postsynaptic neuron causes the generation and release of
endocannabinoids such as anandamide (AEA). The released
endocannabinoids then activate the CB1 receptors (CB1R) at
presynaptic terminals and suppress the release of glutamate (left)
or GABA (right) by inhibiting Ca2+ channels.
Neural reward circuits important in endocannabinoid action in
modulation of the addiction-related effects of drugs of abuse
including alcohol.
Basavarajappa BS. Mini
Rev Med Chem. 2007 Aug;7(8):769-79
Panel
A shows the responses to various doses of the three peptides.
Note that peptide FDLTADWPL caused little hypotension at the doses
tested. The responses to PVNFKFLSH in the presence of enalapril are
also shown. Panel B shows the potentiation of the responses
to BK, but not to angiotensin II, in rats treated with PVNFKFLSH.
Note that LVVYPWTQRY produced no potentiation. The columns in
panels A and B represent the mean S.E.
of the change in mean arterial blood pressure in three to nine rats.
The mean arterial blood pressure (MABP) of the three groups
of rats after stabilization but before peptide administration were
not significantly different
(138 + 4, 133 + 5, and
142 + 4 mm Hg for rats given peptides PVNFKFLSH,
LVVYPWTQRY, and FDLTADWPL, respectively; analysis of variance
followed by Tukey test). p < 0.05 compared with response without
enalapril.
Hemopressin is an antagonist of the CB1 cannabinoid
receptor. (A) Striatal membranes (10 mg)
were incubated with 3 nM [3H]SR141716 in the absence or presence of
increasing concentrations (0? mM) of
hemopressin (HP), SR141716 (SR), or scrambled peptide (SP) and the
ligand-binding analysis carried out as described (36). (B and C)
Striatal membranes (10 g) were subjected to a GTPS-binding assay
(B) or an adenylyl cyclase assay (C) using increasing concentrations
(0? mM) of Hu-210 (Hu), HP, or SR or
increasing concentrations of Hu in the absence or presence of 10 M
HP or SR, as described (36, 37). (D) HEK-293 cells expressing
Flag-tagged CB1 receptors were treated for 5 min with 100 nM Hu-210
in the absence of presence of 10 mM SR or
HP and levels of phosphorylated MAP kinase determined as
described(36). Values obtained in the absence of drug treatment
were taken as 100%. Results aremeanSE of triplicate experiments. *,
P<0.05; **, P<0.01
Andrea S. Heimann, et al. PNAS published
December 12, 2007, 10.1073/pnas.0706980105
Dale CS, Pagano Rde L, Rioli V. Mem Inst Oswaldo Cruz. 2005 Mar;100 Suppl 1:105-6. Epub 2005 Jun 14
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