These results demonstrate that the expression of tissue angiotensinogen, AT1 and fibronectin mRNAs is regulated differently in Dahl Iwai salt-sensitive and salt-resistant rats, and indicate that salt-mediated hypertension activates the cardiac fibronectin gene independently of the tissue renin-angiotensin system and stimulates the aortic fibronectin gene with activation of the tissue renin-angiotensin system.

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This study examined whether type 1 angiotensin II receptor (AT 1 ) and angiotensin-converting enzyme (ACE) mRNAs are regulated during dietary salt loading in angiotensinogen gene-knockout (Atg / ) mice which are genetically deficient in endogenous production of angiotensin II. Wild-type (Atg+/+) and Atg / mice were fed a normal-salt (0·3% NaCl) or a high-salt (4% NaCl) diet for 2 weeks. The mRNA levels were measured by Northern blot analysis. In Atg+/+ mice, concentrations of plasma angiotensin peptides were decreased by salt loading, whereas the treatment increased the brainstem, cardiac, pulmonary, renal cortex, gastric and intestinal AT 1 mRNA levels. Salt loading also enhanced renal cortex ACE mRNA levels in Atg+/+ mice. Although plasma angiotensin peptides and urinary aldosterone excretion were not detected in Atg / mice, salt loading increased blood pressure in Atg / mice. In Atg / mice, pulmonary, renal cortex, gastric and intestinal AT 1 , and renal cortex and intestinal ACE mRNA levels were higher than those in Atg+/+ mice. However, salt loading upregulated AT 1 mRNA expression only in the liver of Atg / mice, and the treatment did not affect ACE mRNA levels in Atg / mice. Furthermore, although the levels of ACE enzymatic activity showed the same trend with the ACE mRNA levels in the lung, renal cortex and intestine of both Atg / and Atg+/+ mice, the results of radioligand binding assay showed that cardiac expression of AT 1 protein was regulated differently from AT 1 mRNA expression both in Atg / and Atg+/+ mice. Thus, expression of AT 1 and ACE is regulated by salt loading in a tissue-specific manner that appears to be mediated, at least partly, by a mechanism other than changes in the circulating or tissue levels of angiotensin peptides.

Tumormetastasis to the hypophyseal system has rarely been reported with either clinical or radiographic evidence. A 52-year-old womanpresented with polydipsia, polyuria, and loss of appetite. She was diagnosed as having diabetes insipidus caused by pituitary micrometastasis of lung adenocarcinoma. After she had been treated with radiation therapy to the pituitary gland, the gland size was reduced as confirmed by magnetic resonance imaging, and her urine volume decreased. However,meningitis carcinomatosa appeared later. This was a rare case of secondary diabetes insipidus due to pituitary metastasis of lung cancer. (Internal Medicine 34: 913-918, 1995)

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