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Identification of the vasodilatory endothelial cannabinoid receptor in the human pulmonary artery.
J Hypertens. 2007 Nov; 25(11):2240-8.JH

Abstract

BACKGROUND

The endocannabinoid anandamide is implicated in the pathogenesis of hypotension in haemorrhagic, endotoxic, and cardiogenic shock. It has been demonstrated in animal, but not in human, vessels that the vasodilatory effects of anandamide and abnormal cannabidiol are partially mediated by an as yet unidentified endothelial cannabinoid receptor. Our study was performed to examine the influence of abnormal cannabidiol on the human pulmonary artery.

METHODS

Isolated human pulmonary arteries were obtained from patients without clinical evidence of pulmonary hypertension during resection of lung carcinoma. Vasodilatory effects of abnormal cannabidiol were examined on endothelium-intact vessels preconstricted with serotonin or potassium chloride.

RESULTS

Anandamide and abnormal cannabidiol relaxed serotonin-preconstricted vessels concentration-dependently. The effect of abnormal cannabidiol was reduced by endothelium denudation, pertussis toxin and two antagonists of the novel endothelial receptor, cannabidiol and O-1918, but not by the nitric oxide synthase inhibitor L-NAME given together with the cyclooxygenase inhibitor indomethacin. It was also diminished by blockade of calcium-activated potassium channels by the nonselective blocker tetraethylammonium or by combination of selective blockers of small (apamin) and intermediate and large (charybdotoxin) conductance calcium-activated potassium channels. The potency of abnormal cannabidiol to relax vessels was lower in potassium chloride than in serotonin-preconstriced preparations.

CONCLUSIONS

Abnormal cannabidiol relaxes human pulmonary arteries in an endothelium-independent and endothelium-dependent manner. The latter component is probably mediated via the putative endothelial cannabinoid receptor, activation of which may release endothelium-derived hyperpolarizing factor, which in turn acts via calcium-activated potassium channels. Abnormal cannabidiol is behaviourally inactive; it may have a therapeutic implication in vascular diseases, especially in the treatment of pulmonary hypertension.

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Authors+Show Affiliations

Kozłowska H
Department of Experimental Physiology, Medical University of Białystok, Białystok, Poland. hkozl@amb.edu.pl
Baranowska M
No affiliation info available
Schlicker E
No affiliation info available
Kozłowski M
No affiliation info available
Laudański J
No affiliation info available
Malinowska B
No affiliation info available

MeSH

Arachidonic AcidsDose-Response Relationship, DrugEndocannabinoidsEndothelium, VascularFemaleHumansIn Vitro TechniquesIndomethacinMaleMiddle AgedNG-Nitroarginine Methyl EsterPertussis ToxinPolyunsaturated AlkamidesPotassium Channel BlockersPotassium ChloridePulmonary ArteryReceptors, CannabinoidResorcinolsSerotoninVasodilation

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17921818

Citation

Kozłowska, Hanna, et al. "Identification of the Vasodilatory Endothelial Cannabinoid Receptor in the Human Pulmonary Artery." Journal of Hypertension, vol. 25, no. 11, 2007, pp. 2240-8.
Kozłowska H, Baranowska M, Schlicker E, et al. Identification of the vasodilatory endothelial cannabinoid receptor in the human pulmonary artery. J Hypertens. 2007;25(11):2240-8.
Kozłowska, H., Baranowska, M., Schlicker, E., Kozłowski, M., Laudański, J., & Malinowska, B. (2007). Identification of the vasodilatory endothelial cannabinoid receptor in the human pulmonary artery. Journal of Hypertension, 25(11), 2240-8.
Kozłowska H, et al. Identification of the Vasodilatory Endothelial Cannabinoid Receptor in the Human Pulmonary Artery. J Hypertens. 2007;25(11):2240-8. PubMed PMID: 17921818.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Identification of the vasodilatory endothelial cannabinoid receptor in the human pulmonary artery. AU - Kozłowska,Hanna, AU - Baranowska,Marta, AU - Schlicker,Eberhard, AU - Kozłowski,Mirosław, AU - Laudański,Jerzy, AU - Malinowska,Barbara, PY - 2007/10/9/pubmed PY - 2008/1/11/medline PY - 2007/10/9/entrez SP - 2240 EP - 8 JF - Journal of hypertension JO - J Hypertens VL - 25 IS - 11 N2 - BACKGROUND: The endocannabinoid anandamide is implicated in the pathogenesis of hypotension in haemorrhagic, endotoxic, and cardiogenic shock. It has been demonstrated in animal, but not in human, vessels that the vasodilatory effects of anandamide and abnormal cannabidiol are partially mediated by an as yet unidentified endothelial cannabinoid receptor. Our study was performed to examine the influence of abnormal cannabidiol on the human pulmonary artery. METHODS: Isolated human pulmonary arteries were obtained from patients without clinical evidence of pulmonary hypertension during resection of lung carcinoma. Vasodilatory effects of abnormal cannabidiol were examined on endothelium-intact vessels preconstricted with serotonin or potassium chloride. RESULTS: Anandamide and abnormal cannabidiol relaxed serotonin-preconstricted vessels concentration-dependently. The effect of abnormal cannabidiol was reduced by endothelium denudation, pertussis toxin and two antagonists of the novel endothelial receptor, cannabidiol and O-1918, but not by the nitric oxide synthase inhibitor L-NAME given together with the cyclooxygenase inhibitor indomethacin. It was also diminished by blockade of calcium-activated potassium channels by the nonselective blocker tetraethylammonium or by combination of selective blockers of small (apamin) and intermediate and large (charybdotoxin) conductance calcium-activated potassium channels. The potency of abnormal cannabidiol to relax vessels was lower in potassium chloride than in serotonin-preconstriced preparations. CONCLUSIONS: Abnormal cannabidiol relaxes human pulmonary arteries in an endothelium-independent and endothelium-dependent manner. The latter component is probably mediated via the putative endothelial cannabinoid receptor, activation of which may release endothelium-derived hyperpolarizing factor, which in turn acts via calcium-activated potassium channels. Abnormal cannabidiol is behaviourally inactive; it may have a therapeutic implication in vascular diseases, especially in the treatment of pulmonary hypertension. SN - 0263-6352 UR - https://www.unboundmedicine.com/medline/citation/17921818/Identification_of_the_vasodilatory_endothelial_cannabinoid_receptor_in_the_human_pulmonary_artery_ L2 - https://doi.org/10.1097/HJH.0b013e3282ef7a0a DB - PRIME DP - Unbound Medicine ER -