Why the study?
Does ACE inhibition with MK 421, SA 446, or captopril affect blood pressure and urinary kallikrein/kinin excretion differently in normotensive rats on a low vs regular sodium diet?
Does ACE inhibition with MK 421, SA 446, or captopril affect blood pressure and urinary kallikrein/kinin excretion differently in normotensive rats on a low vs regular sodium diet?
In normotensive rats, the augmented hypotensive response to ACE inhibitors on a low sodium diet may be mediated by an enhanced renal kallikrein-kinin system in addition to renin-angiotensin system suppression.
Hypothesis-generating for sodium-ACE inhibitor synergy via kallikrein-kinin in rats; no basis for clinical practice change.
Responses in urinary kallikrein and kinin excretion and systolic blood pressure to MK 421, SA 446 or captopril were studied in normotensive rats fed on a regular or a low sodium diet to assess the role of renal kallikrein-kinin system in their hypotensive effect. MK 421, SA 446 or captopril were infused at a rate of 6 mg/kg/day by osmotic minipump implanted intraperitoneally for up to 6 days. The magnitude of fall in systolic blood pressure was greater on a low sodium diet when compared to on a regular diet, whereas the pattern of the fall was similar on both diets. The magnitude of falls in plasma angiotensin II and aldosterone concentration induced by MK 421, SA 446 and captopril was not significantly different between both regular and low sodium diets. Urinary kallikrein and kinin excretion and sodium excretion were increased during infusion of MK 421, SA 446 or captopril on a low sodium diet, however any significant changes were not found in each of them on a regular diet. The present results suggest that on a low sodium diet the augmented hypotensive response to angiotensin converting enzyme inhibitors in the rats might be due to the enhanced renal kallikrein-kinin system in addition to suppressed renin-angiotensin system.
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Yasujima et al. (1984) studied this question.
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