Cross-Talk between the (Endo)Cannabinoid and Renin-Angiotensin Systems: Basic Evidence and Potential Therapeutic Significance

Mińczuk, Baranowska-Kuczko, Krzyżewska, Schlicker, Malinowska, Krzysztof Mińczuk, Marta Baranowska-Kuczko, Anna Krzyżewska, Eberhard Schlicker, Barbara Malinowska

1 Rs and eCBs is also suggested to be present in the heart ([ 1 Rs (the presence of which was confirmed by immunohistochemistry) by WIN55212-2 and 2-AG increased CF and decreased cardiac contractility in a manner sensitive to the CB 1 R antagonist O2050. A similar mechanism may occur in experiments performed on conscious rats with hypertension induced by infusion of Ang II [ 1 R antagonist AM251 enhanced and the FAAH inhibitor URB597 reduced BP [ 1 R antagonist rimonabant and the FAAH inhibitor URB597 enhanced and reduced BP, respectively [ 1 Rs in the hypotensive action of both compounds [ The question arises whether the protective negative feedback of Ang II—eCBs—CBRs observed in vitro is relevant also under in vivo conditions. Unlike in SHR or hypertension models induced by Ang II [ 19 ] or Ang II with vasopressin infusion [ 46 ], acute or chronic administration of rimonabant decreased BP and body weight in (mRen2)27 rats but not in their normotensive SD controls [ 47 ]. The pressor effects of Ang II and CP55940 given into the PVN result mainly from the activation of facilitatory ATRs on glutamatergic [ 73 74 ] and inhibitory CBRs on GABAergic [ 54 55 ] neurons, respectively ( Figure 5 ). Authors suggested that activation of ATRs by Ang II stimulates 2-AG release, which may act as an autocrine enhancer for CBRs on sweet taste cells ( Table 2 Figure 4 ).

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