| First Author | Kai T | Year | 1998 |
| Journal | J Hypertens | Volume | 16 |
| Issue | 12 Pt 2 | Pages | 2045-9 |
| PubMed ID | 9886895 | Mgi Jnum | J:286506 |
| Mgi Id | MGI:6404258 | Doi | 10.1097/00004872-199816121-00028 |
| Citation | Kai T, et al. (1998) Tissue-localized angiotensin II enhances cardiac and renal disorders in Tsukuba hypertensive mice. J Hypertens 16(12 Pt 2):2045-9 |
| abstractText | OBJECTIVE: To evaluate the relation of tissue-localized angiotensin II (Ang II) concentration with cardiac hypertrophy and glomerulosclerosis in Tsukuba hypertensive mice (THM) carrying both human renin and angiotensinogen genes. DESIGN: Thirty THM aged 12 weeks were distributed equally to a lisinopril dosage group, a hydralazine dosage group, and an untreated group. Ten age-matched C57BL/6 mice were used as normal controls. Administration was performed for 8 weeks from 12 weeks of age. All mice were euthanized at 20 week of age, and the heart-to-body weight ratio, the renal glomerulosclerosis score, tissue Ang II concentration and tissue catecholamine concentration were measured. RESULTS: In the untreated group, a significant increase in every examination item was found as compared with that in C57BL/6 mice. In the lisinopril group, the observed value of every item was significantly lower than that in the untreated group. In the hydralazine group, tissue Ang II and catecholamine concentrations and the heart-to-body weight ratio were not different from those in the untreated group. Although the glomerulosclerosis score in the hydralazine group was significantly less than that in the untreated group, this was significantly higher than that in the lisinopril group. CONCLUSION: Tissue Ang II concentration is more important than hypertension in causing cardiac hypertrophy, and both tissue Ang II level and hypertension are important in causing glomerulosclerosis in THM. |
