Key result
Acute beta-adrenoceptor blockade with metoprolol in conscious hypertensive rats doubled mean sodium excretion at 1 hour and significantly increased mean ANP plasma concentration by 68%.
Why the study?
Does acute beta-blockade with metoprolol increase plasma ANP concentrations and sodium excretion in conscious hypertensive rats?
Does acute beta-blockade with metoprolol increase plasma ANP concentrations and sodium excretion in conscious hypertensive rats?
Acute beta-blockade with metoprolol induces natriuresis in hypertensive rats, likely mediated by an increase in plasma ANP concentrations.
Hypothesis-generating for ANP-mediated natriuresis with acute metoprolol; leaves open human translation in hypertension.
Acute beta-adrenoceptor blockade in rats is known to produce a natriuresis of hitherto uncertain cause. To investigate this phenomenon plasma atrial natriuretic peptide (ANP) concentrations were measured in groups of conscious metoprolol-treated and control rats. In the active treatment group the blood pressure decreased slowly, as expected, settling at a lower level after 2 hours, and the mean sodium excretion doubled 1 hour after metoprolol administration. This natriuretic effect was maximal after 40-60 minutes and thereafter slowly declined towards basal values. The period of enhanced sodium excretion was associated with a significant rise (68%) of the mean ANP plasma concentration. It suggested that this increase in plasma ANP concentration can mediate the acute natriuretic effect beta-adrenoceptor blockade.
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Pettersson et al. (1987) studied Hypertension. Metoprolol vs. Control was evaluated on Plasma atrial natriuretic peptide (ANP) concentrations and sodium excretion. Acute beta-adrenoceptor blockade with metoprolol in conscious hypertensive rats doubled mean sodium excretion at 1 hour and significantly increased mean ANP plasma concentration by 68%.
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