ANGIOTENSIN-II (AII) AND ADRENAL-GLAND AII RECEPTORS IN RATS WITH CONGENITAL HYPOTHYROIDISM

Plasma angiotensin II (AII) concentration, plasma renin concentration (PRC), lung angiotensin-converting enzyme (ACE) activity and adrenal g land AII receptor isoforms have been evaluated in the postnatal develo pment of the rat, in order to determine the alterations of the renin-a ngiotensin system (RAS) which occur in congenital hypothyroidism. The developmental AII profiles observed in control and hypothyroid rats we re quite similar. Thus, All was elevated at birth and declined at week 5 of life to reach adult values. However, AII levels were lower in hy pothyroid than in euthyroid animals before their stabilization. On the other hand, PRC in newborn hypothyroid and euthyroid animals was high er than in adulthood, being significantly increased immediately after birth in hypothyroid rats. Pulmonary ACE activity in both experimental groups was low at birth and increased with age. This increase was gre ater in euthyroid rats than in congenitally hypothyroid animals from d ay 28 of life. These results confirm that plasma AII levels in rats ar e predominantly controlled by plasma renin activity, although other fa ctors, such as renin substrate availability, may be responsible for th e reduced plasma AII concentration in congenital hypothyroidism during the first weeks of life. The developmental profile of the adrenal gla nd AII receptor showed four isoforms, with pl values of 6.8, 6.7, 6.5 and 6.3. AII receptor-complex expression increased with age but, in co ngenitally hypothyroid rats, a higher induction of AII receptor isofor ms migrating to pl 6-8, 6.5 and 6.3 was observed. These findings show that thyroid hormone deficiency in early life can have an important ro le in the postnatal induction of the RAS components, which may be esse ntial for the regulation of blood pressure, and for fluid and electrol yte balance in developing rats.