cannabidiol and Hypertrophy--Left-Ventricular

Cannabidiol (CBD) is suggested to possess cardioprotective properties. We examined the influence of chronic (10 mg/kg once daily for 2 weeks) CBD administration on heart structure (e.g. cardiomyocyte width) and function (e.g. stimulatory and inhibitory responses induced by β-adrenoceptor (isoprenaline) and muscarinic receptor (carbachol) activation, respectively). Experiments were performed on hearts and/or left atria isolated from spontaneously (SHR) and deoxycorticosterone (DOCA-salt) hypertensive rats; Wistar-Kyoto (WKY) and sham-operated rats (SHAM) served as the respective normotensive controls. CBD diminished the width of cardiomyocytes in left ventricle and reduced the carbachol-induced vasoconstriction of coronary arteries both in DOCA-salt and SHR. However, it failed to affect left ventricular hypertrophy and even aggravated the impaired positive and negative lusitropic effects elicited by isoprenaline and carbachol, respectively. In normotensive hearts CBD led to untoward structural and functional effects, which occurred only in WKY or SHAM or, like the decrease in β

Topics: Adrenergic beta-Agonists; Animals; Antihypertensive Agents; Cannabidiol; Carbachol; Cell Size; Coronary Vessels; Disease Models, Animal; Hypertension; Hypertrophy, Left Ventricular; Isolated Heart Preparation; Isoproterenol; Myocytes, Cardiac; Rats, Inbred SHR; Rats, Inbred WKY; Receptors, Adrenergic, beta-1; Receptors, Adrenergic, beta-2; Vasoconstriction; Vasoconstrictor Agents; Ventricular Dysfunction, Left; Ventricular Function, Left