Article date: February 1984
By: E. Fritschka, R. Gotzen, R. Kittler, M. Schöneshöfer in Volume 81, Issue 2, pages 245-253
Treatment of fifteen patients with essential hypertension over four weeks using the β‐adrenoceptor blocking agent, metoprolol, resulted in a decrease in 24 h urinary excretion of kallikrein and aldosterone along with a decrease in plasma renin activity.
There was no significant change in 24 h excretion rates of the free adrenal steroids deoxycorticosterone, 18‐OH‐deoxycorticosterone, corticosterone, cortisol or 18‐OH‐corticosterone during treatment, which were not significantly different from excretion rates of normal males, thus excluding inhibitory effects of adrenal steroids on urinary kallikrein activity.
A positive correlation was found between plasma renin activity and urinary excretion of kallikrein during the control period and after 2 weeks on metoprolol, supporting the assumption of a preserved link between the renin‐angiotensin‐aldosterone system and the renal excretion of kallikrein in these patients.
The decrease in kallikrein excretion during β1‐adrenoceptor blockade in patients with essential hypertension may be explained by a reduction in sympathetic tone and by reduced activity of the renin‐aldosterone system.
Treatment of fifteen patients with essential hypertension over four weeks using the β‐adrenoceptor blocking agent, metoprolol, resulted in a decrease in 24 h urinary excretion of kallikrein and aldosterone along with a decrease in plasma renin activity.
There was no significant change in 24 h excretion rates of the free adrenal steroids deoxycorticosterone, 18‐OH‐deoxycorticosterone, corticosterone, cortisol or 18‐OH‐corticosterone during treatment, which were not significantly different from excretion rates of normal males, thus excluding inhibitory effects of adrenal steroids on urinary kallikrein activity.
A positive correlation was found between plasma renin activity and urinary excretion of kallikrein during the control period and after 2 weeks on metoprolol, supporting the assumption of a preserved link between the renin‐angiotensin‐aldosterone system and the renal excretion of kallikrein in these patients.
The decrease in kallikrein excretion during β1‐adrenoceptor blockade in patients with essential hypertension may be explained by a reduction in sympathetic tone and by reduced activity of the renin‐aldosterone system.
DOI: 10.1111/j.1476-5381.1984.tb10071.x
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