Abstract
Cannabinoids influence cardiovascular variables in health and disease via multiple mechanisms. The chapter covers the impact of cannabinoids on cardiovascular function in physiology and pathology and presents a critical analysis of the proposed signalling pathways governing regulation of cardiovascular function by endogenously produced and exogenous cannabinoids. We know that endocannabinoid system is overactivated under pathological conditions and plays both a protective compensatory role, such as in some forms of hypertension, atherosclerosis and other inflammatory conditions, and a pathophysiological role, such as in disease states associated with excessive hypotension. This chapter focuses on the mechanisms affecting hemodynamics and vasomotor effects of cannabinoids in health and disease states, highlighting mismatches between some studies. The chapter will first review the effects of marijuana smoking on cardiovascular system and then describe the impact of exogenous cannabinoids on cardiovascular parameters in humans and experimental animals. This will be followed by analysis of the impact of cannabinoids on reactivity of isolated vessels. The article critically reviews current knowledge on cannabinoid induction of vascular relaxation by cannabinoid receptor-dependent and –independent mechanisms and dysregulation of vascular endocannabinoid signaling in disease states.
Keywords
- Cannabis
- Endocacannabinoids
- Cannabinoid receptors
- Endothelial cells
- Vascular
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Abbreviations
- 2-AG:
-
2-Arachidonoylglycerol
- ACPA:
-
arachidonylcyclopropylamide
- BKCa :
-
large conductance calcium-activated potassium channel, KCa1.1
- CB1:
-
cannabinoid receptor type 1
- CB2:
-
cannabinoid receptor type 2
- CBe:
-
endothelial cannabinoid receptor
- CGRP:
-
calcitonin gene-related peptide
- COX:
-
cyclooxygenase, prostaglandin-endoperoxide synthase
- DOC salt hypertension:
-
deoxycorticosterone acetate-induced hypertension
- EDHF:
-
endothelium-derived hyperpolarizing factor
- FAAH:
-
fatty acid amide hydrolase
- IKCa :
-
intermediate conductance calcium-activated potassium channel, KCa3.1
- KATP:
-
ATP-sensitive potassium channel
- NAGly:
-
N-arachidonoyl glycine
- NCX:
-
Na+-Ca2+ exchanger
- NO:
-
nitric oxide
- PPAR:
-
peroxisome proliferator-activated receptor
- SHR:
-
spontaneously hypertensive rats
- TASK:
-
TWIK-related acid-sensitive potassium channel
- THC:
-
Δ9-tetrahydrocannabinol
- TRPA:
-
transient receptor potential cation channel subfamily A (ankyrin)
- TRPV:
-
transient receptor potential cation channel subfamily V (vanniloid)
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The author gratefully acknowledges financial support from the Austrian Science Fund, FWF, grant # P27238-B27.
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Bondarenko, A.I. (2019). Cannabinoids and Cardiovascular System. In: Bukiya, A. (eds) Recent Advances in Cannabinoid Physiology and Pathology. Advances in Experimental Medicine and Biology, vol 1162. Springer, Cham. https://doi.org/10.1007/978-3-030-21737-2_5
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