The present investigation was undertaken to elucidate the possible interplay between the circulating kinin (s) and the renin angiotensin axis in hyperthyroidism.
The responsiveness of plasma aldosterone (p-Ald), kinin (p-BK), plasma renin activity (PRA) and serum angiotensin converting enzyme activity (ACEA) to infusion of angiotensin II at a dose of 4, 8 and 16 ng/kg.min. was asessed in 15 hyperthyroid pateints and 10 euthyroid controls. There was impaired angiotensin II induced response of blood pressure in hyper-thyroid pateints, and basal concentrations of p-Ald were 7.7±3.8 ng/dl in euthyroid controls and 12.6±3.1 ng/dl in hyperthyroid patients (p<0.05).
As compared to the euthyroid controls, the hyperthyroid patients showed a reduced response of plasma aldosterone to angiotensin II infusion. Angiotensin II infusion increased p-BK from basal levels of 19.1±8.2 pg/ml to 31.0±7.8 pg/ml (p<0.05) only in hyperthyroid patients and did not increase ACEA in either group.
Next, the effects of a single administration of captopril (50 mg p.o.) on blood pressure and p-BK in hyperthyroid patients and euthyroid controls were studied. In the two groups blood pressure was not changed by captopril, but p-BK increased significantly.
The present results do not support the view that there may be a direct linkage between the kallikrein kinin system and the renin angiotensin axis mediated by kininase II or angiotensin converting enzyme in human peripheral blood. Also it is unlikely that kinin may play a role in the mechanism of reduced responsiveness of aldosterone and blood pressure to angiotensin II in hyperthyroidism.