Search

A 19-month-old boy presented with failure to thrive and polydipsia. Low-renin hypertension was diagnosed by the presence of hypertension, hypokalaemic alkalosis, suppressed plasma renin activity and low plasma aldosterone. Plasma levels and urinary excretion of other mineralocorticoids and glucocorticosteroids were low or normal. Urinary tetrahydrocortisol (THF) was increased relative to tetrahydrocortisone (THE) and also the plasma cortisol to cortisone ratio was elevated. These findings are suggestive of a decreased activity of cortisol-11 beta-hydroxysteroid dehydrogenase. Hypertension and hypokalaemia were not influenced by spironolactone and dexamethasone. Triamterene normalised serum potassium, but addition of furosemide was required for lowering blood pressure. With this treatment catch-up growth was observed.

Basal plasma renin activity (PRA), angiotensin I and II (AI, AII), angiotensin-converting enzyme (ACE) activity and plasma aldosterone (PA) and sodium and potassium concentration were simultaneously measured in 55 healthy recumbent children aged between 1 week and 13 years. A significant (P less than 0.001) age-related decrease for PRA (r = -0.73), AI (r = -0.72), AII (r = -0.51) and PA (r = -0.71) was observed but not for ACE (r = 0.26, P = 0.06). After correction for age the correlation between PRA or PA and AI or AII was still significant (P less than 0.005). The strong correlation between AI and AII in the group as a whole (r = 0.82, P less than 0.001) and also in separate age groups, and an AI to AII ratio which was not different between the various age groups suggest that ACE activity in this age range is not rate-limiting for AII generation.

The objective of this study was to investigate the relationship between the high activity of the renin-angiotensin-aldosterone system (RAAS) and the control of blood pressure and aldosterone in the canine puppy. The effect of the angiotensin II analog saralasin on arterial pressure (MAP), plasma renin activity (PRA), plasma renin concentration (PRC), and aldosterone (PA) was studied in unanesthetized normal, salt-loaded and salt-depleted puppies aged 9 to 30 days. Salt-loading was performed by daily intraperitoneal administration of 10 mEq sodium/kg body weight for 5 days and salt-depletion by furosemide injections. Saralasin infusion, 6 micrograms/kg/min, during 60 min significantly decreased MAP and increased PRC not only in salt-depleted puppies, as has been observed in adult salt-depleted dogs, but also in normal puppies (mean fall, 6.6 mm Hg). Although any developmental changes in the RAAS and MAP and in their relationship could not be ascertained, the fall in MAP during saralasin in normal puppies was significantly correlated to presaralasin renin values (r = 0.76, P less than 0.01, N = 11). PA did not change in both groups of puppies. In salt-loaded puppies saralasin caused no change of MAP, PRC, and PA. We conclude that the high renin levels at young age contribute to the basal arterial pressure in puppies.