Effect of metoprolol on plasma lipids and arterial intimal lipid deposition in spontaneously hypertensive rats

Effects of Diet and Metoprolol on Lípid Levels in the Blood Plasma and Morphology of the Heart and Intramural Branches of Coronary Arteries of Spontaneously Hypertensive Male Rats

“…In this group 2 of the 5 animals also showed lipid deposits in the intramyocardial coro nary arteries intimating fatty streak-like le sions. This incidence of lipid depositions in the coronary arteries is similar to that found (35%) in a separate study using a corre sponding, but larger, group of rats (n = 35) fed on an identical casein-containing pel leted diet for 9 months [23], In the latter study, metoprolol treatment reduced the in cidence of rats with arterial lipid accumu lation to 3%. Therefore, the difference observed between rats not treated with me toprolol (group b: 2 rats of 5 showing intra arterial lipid accumulation) and rats receiv ing metoprolol (group c: no observations of intra-arterial accumulation) fits very well with these other results.…”

“…In addition, me toprolol treatment also affected growth and food consumption in a way that may indi cate some interference with basal metabolic processes. This apparent increase in energy consumption was somewhat surprising, since p-adrenoceptor-blocking agents are currently used in the treatment of hyperthy roid patients [30], However, recent studies in rats have failed to demonstrate effects of Pi-blockade on some of the metabolic altera- tions induced by triiodothyronine treatment [31,32], It is not possible from the available data to decide neither what the type of dis turbance is underlying the effects of metoprolol on growth and food consumption, nor if the effects were due to the drug itself, or to its metabolite(s) [22,23],…”

“…Likewise, it supports the idea suggested by Hadjiisky et al [9] that the development of atherosclerosis-like le sions in the genetically hypertensive rat may be obtained when the arterial hypertension is associated with a second risk factor such as a high plasma LDL level. Accordingly, the ef fect of metoprolol may have been produced, at least to some part, via a reduction of the arterial hypertension [23]. Further details of the importance of different biochemical and hemodynamic factors behind the antiathe rogenic effects of p-blockers have recently been discussed by Ablad et al [37],…”

“…The latter compound is a metabolite of metoprolol, being about 10% as potent (3-blocker as metoprolol [22], It has been shown recently, using an identical way of drug administration, that the dose presently used is effective in reducing the blood pres sure (from 160 ± 21 to 139 ± 11 mm Hg; p < 0.001) and the heart rate (from 417 ± 36 to 383 ± 28 beats/min; p < 0.002) of SHR [23],…”