Cannabinoids, the active components of Cannabis sativa, and their derivatives produce a wide spectrum of physiological effects mediated by two different types of receptors: G protein coupled cannabinoid receptor CB1 and transient receptor potential vanilloid type 1 (TRPV1). The afferent vagal pathway modulates the cardio-respiratory response to cannabinoids. The present article summarizes the cardio-respiratory effects of selected cannabinoids: endogenous anandamide and a novel drug arvanil, a metabolically stable hybrid between anandamide and capsaicin. An intravenous administration of anandamide in rats induces apnoea coupled with hypotension and evokes the decrease in the tidal volume at the early phase of reinitiated breathing. The inhibition of respiration and depression of blood pressure produced by anandamide are mediated via vagal peripheral input to the respiratory center in the medulla, while the nodose ganglia are essential in the observed phenomena. Post-anandamide apnoea and hypotension are mediated by both TRPV1 and CB1 receptors but the decline of tidal volume evoked by anandamide might depend on receptors of a different type. An administration of arvanil produced an increase of tidal volume and diaphragm activity, hypertension coupled with a fall in respiratory rate. The post-arvanil rise of tidal volume was mediated by both TRPV1 and CB1 receptors. Only vanilloid receptors seemed to be involved in the increase of diaphragm activity and decrease of respiratory frequency. Hypertensive response to arvanil might depend on receptors of a different type. The respiratory effects elicited by arvanil require intact midcervical vagi. Supranodose vagotomy failed to eliminate the hypertension evoked by arvanil. This implies that post-arvanil hypertension could be co-mediated by both vagal and extravagal pathways. The mechanism of cardio-respiratory effects of cannabinoids is worth exploring on account of their anti-tumor and anti-inflammatory actions and the possible usage of cannabinoids and their derivatives as drugs.
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.