Abstract
We have reported previously that thyroid hormone activates the circulating and tissue renin-angiotensin systems without involving the sympathetic nervous system, which contributes to cardiac hypertrophy in hyperthyroidism. This study examined whether the circulating or tissue renin- angiotensin system plays the principal role in hyperthyroidism-induced cardiac hypertrophy. The circulating renin-angiotensin system in Sprague- Dawley rats was fixed by chronic angiotensin II infusion (40 ng/min, 28 days) via mini-osmotic pumps. Daily J.p. injection of thyroxine (0 · 1 mg/kg per day, 28 days) was used to mimic hyperthyroidism. Serum free tri- iodothyronine, plasma renin activity, plasma angiotensin II, cardiac renin and cardiac angiotensin II were measured with RIAs. The cardiac expression of renin mRNA was evaluated by semiquantitative reverse transcriptase-polymerase chain reaction. Plasma renin activity and plasma angiotensin II were kept constant in the angiotensin II and angiotensin II+thyroxine groups (0 · 12 ± 0 · 03 and 0 · 15 ±0 · 03 μg/h per liter, 126 ± 5 and 130 ± ng/l respectively) (means ± S.E.M.). Despite stabilization of the circulating renin-angiotensin system, thyroid hormone induced cardiac hypertrophy (5 · 0 ± 0 · 5 vs 3 · 5 ± 0 · 1 mg/g) in conjunction with the increases in cardiac expression of renin mRNA, cardiac renin and cardiac angiotensin II (74 ± 2 vs 48 ± 2%, 6 · 5 ± 0 · 8 vs 3 · 8 ± 0 · 4 ng/h per g, 231 ± 30 vs 149 ± 2 pg/g respectively). These results indicate that the local renin-angiotensin system plays the primary role in the development of hyperthyroidism-induced cardiac hypertrophy.
| Original language | English |
|---|---|
| Pages (from-to) | 43-47 |
| Number of pages | 5 |
| Journal | Journal of Endocrinology |
| Volume | 160 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 1999 |
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ASJC Scopus subject areas
- Endocrinology
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Local renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy. / Kobori, H.; Ichihara, A.; Miyashita, Y.; Hayashi, M.; Saruta, T.
In: Journal of Endocrinology, Vol. 160, No. 1, 1999, p. 43-47.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Local renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy
AU - Kobori, H.
AU - Ichihara, A.
AU - Miyashita, Y.
AU - Hayashi, M.
AU - Saruta, T.
PY - 1999
Y1 - 1999
N2 - We have reported previously that thyroid hormone activates the circulating and tissue renin-angiotensin systems without involving the sympathetic nervous system, which contributes to cardiac hypertrophy in hyperthyroidism. This study examined whether the circulating or tissue renin- angiotensin system plays the principal role in hyperthyroidism-induced cardiac hypertrophy. The circulating renin-angiotensin system in Sprague- Dawley rats was fixed by chronic angiotensin II infusion (40 ng/min, 28 days) via mini-osmotic pumps. Daily J.p. injection of thyroxine (0 · 1 mg/kg per day, 28 days) was used to mimic hyperthyroidism. Serum free tri- iodothyronine, plasma renin activity, plasma angiotensin II, cardiac renin and cardiac angiotensin II were measured with RIAs. The cardiac expression of renin mRNA was evaluated by semiquantitative reverse transcriptase-polymerase chain reaction. Plasma renin activity and plasma angiotensin II were kept constant in the angiotensin II and angiotensin II+thyroxine groups (0 · 12 ± 0 · 03 and 0 · 15 ±0 · 03 μg/h per liter, 126 ± 5 and 130 ± ng/l respectively) (means ± S.E.M.). Despite stabilization of the circulating renin-angiotensin system, thyroid hormone induced cardiac hypertrophy (5 · 0 ± 0 · 5 vs 3 · 5 ± 0 · 1 mg/g) in conjunction with the increases in cardiac expression of renin mRNA, cardiac renin and cardiac angiotensin II (74 ± 2 vs 48 ± 2%, 6 · 5 ± 0 · 8 vs 3 · 8 ± 0 · 4 ng/h per g, 231 ± 30 vs 149 ± 2 pg/g respectively). These results indicate that the local renin-angiotensin system plays the primary role in the development of hyperthyroidism-induced cardiac hypertrophy.
AB - We have reported previously that thyroid hormone activates the circulating and tissue renin-angiotensin systems without involving the sympathetic nervous system, which contributes to cardiac hypertrophy in hyperthyroidism. This study examined whether the circulating or tissue renin- angiotensin system plays the principal role in hyperthyroidism-induced cardiac hypertrophy. The circulating renin-angiotensin system in Sprague- Dawley rats was fixed by chronic angiotensin II infusion (40 ng/min, 28 days) via mini-osmotic pumps. Daily J.p. injection of thyroxine (0 · 1 mg/kg per day, 28 days) was used to mimic hyperthyroidism. Serum free tri- iodothyronine, plasma renin activity, plasma angiotensin II, cardiac renin and cardiac angiotensin II were measured with RIAs. The cardiac expression of renin mRNA was evaluated by semiquantitative reverse transcriptase-polymerase chain reaction. Plasma renin activity and plasma angiotensin II were kept constant in the angiotensin II and angiotensin II+thyroxine groups (0 · 12 ± 0 · 03 and 0 · 15 ±0 · 03 μg/h per liter, 126 ± 5 and 130 ± ng/l respectively) (means ± S.E.M.). Despite stabilization of the circulating renin-angiotensin system, thyroid hormone induced cardiac hypertrophy (5 · 0 ± 0 · 5 vs 3 · 5 ± 0 · 1 mg/g) in conjunction with the increases in cardiac expression of renin mRNA, cardiac renin and cardiac angiotensin II (74 ± 2 vs 48 ± 2%, 6 · 5 ± 0 · 8 vs 3 · 8 ± 0 · 4 ng/h per g, 231 ± 30 vs 149 ± 2 pg/g respectively). These results indicate that the local renin-angiotensin system plays the primary role in the development of hyperthyroidism-induced cardiac hypertrophy.
UR - http://www.scopus.com/inward/record.url?scp=0032951933&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032951933&partnerID=8YFLogxK
U2 - 10.1677/joe.0.1600043
DO - 10.1677/joe.0.1600043
M3 - Article
C2 - 9854175
AN - SCOPUS:0032951933
VL - 160
SP - 43
EP - 47
JO - Journal of Endocrinology
JF - Journal of Endocrinology
SN - 0022-0795
IS - 1
ER -