Augmented expression of cardiac atrial natriuretic peptide system in hypertensive rats

The present study was aimed at investigating the regulation of atrial natriuretic peptide (ANP) system in association with either enhanced or attenuated activity of the renin-angiotensin system (RAS). The cardiac tissue mRNA and peptide levels of ANP were measured in rats with two-kidney, one clip (2K1C) or deoxycorticosterone acetate (DOCA)-salt hypertension. Plasma renin concentration was increased in 2K1C hypertension along with increases of renin mRNA and protein contents in the clipped kidney. On the contrary, it was suppressed in DOCA-salt hypertension along with decreases of renin mRNA and protein contents in the remaining kidney. The plasma ANP concentration was similarly increased in both models of hypertension. The cardiac tissue ANP contents were not significantly changed, but the tissue ANP mRNA levels were upregulated in the hypertrophied heart in these two models of hypertension. It is suggested that the cardiac ANP system is transcriptionally enhanced by cardiac hypertrophy associated with hypertension, independent of the systemic RAS.

Tissue-specific regulation of angiotensinogen and angiotensin II receptor gene expression in deoxycorticosterone acetate-salt hypertensive rats

Molecular regulation of the renin-angiotensin system (RAS) was investigated in deoxycorticosterone acetate (DOCA)-salt hypertension. The expression of renin, angiotensinogen and angiotensin II receptor genes in the kidney and liver was determined by Northern blot analysis in rats which were made DOCA-salt hypertensive over the period of 2 or 4 weeks. Along with the hypertension, renin mRNA was decreased in the remnant kidney. The expression of angiotensinogen gene was not significantly altered in the kidney, but was significantly decreased in the liver. The expression of angiotensin II receptor gene was increased in the kidney, while it remained unaltered in the liver. The duration of hypertension did not affect the altered gene expression. It is suggested that the components of RAS are transcriptionally regulated in DOCA-salt hypertension in a tissue-specific manner.

Tissue-Specific Regulation of Angiotensinogen and Angiotensin II Receptor Genes in Two-Kidney, One Clip Hypertensive Rats / 대한신장학회잡지

The present study was aimed at investigating the molecular regulation of the renin- angiotensin system (RAS) in two-kidney, one clip (2K1C) hypertension. The expression of renin, angiotensinogen and angiotensin II receptor genes was determined by Northern blot analysis in rats made 2K1C hypertensive for 2 or 4 weeks. The expression of renin gene was increased in the clipped kidney and decreased in the contralateral non-clipped kidney at weeks 2 and 4. The expression of angiotensinogen gene was not significantly altered at week 2, but increased at week 4 in the clipped kidney. However, it was not significantly altered in the contralateral kidney either at week 2 or 4. Nor was the expression of angiotensinogen gene significantly altered in the liver either at week 2 or 4. On the other hand, the expression of angiotensin II receptor gene was decreased at week 2, and increased at week 4 in the clipped kidney, whereas it was not significantly changed in the contralateral kidney either at week 2 or 4. In the liver, the expression of angiotensin II receptor gene was not significantly altered at week 2, but decreased at week 4. These results suggest that the components of RAS are transcriptionally regulated in 2K1C hypertension in a manner dependent on tissues and duration of hypertension.

Effects of Cyclosporine on the Intrarenal Renin-Angiotensin System / 대한신장학회잡지

The present study was aimed at investigating the effect of cyclosporine A (CsA) on the renal renin-angiotensin systems. In rats chronically treated with CsA, the intrarenal expression of various genes of the renin-angiotensin system was assessed by Northern blot analysis. Along with the increases in plasma and renal renin activities, chronic CsA-treatment differentially affected the renal expression of renin-angiotensin system. The treatment with CsA for one week did not significantly alter the expression of either type 1 angiotensin II receptor (AT1A) or angiotensinogen gene, but increased the renin mRNA level. The three-week-treatment caused increases in the expression not only of renin but also of AT1A and angiotensinogen genes. Supplementation with L-arginine kept the expression of renin mRNA normal in the one-week-treated, but failed to prevent the alterations of the gene expression in the three-week-treated. Feedback control among components of the renin-angiotensin system also influences angiotesinogen. In the liver, the expression of angiotensinogen mRNA was decreased by the CsA-treatment for either one- or three-weeks. In conclusion, chronic CsA-treatment is associated with a differential expression of various genes for the renin-angiotensin system. L-Arginine may be effective in maintaining the normality of renin-angiotensin system only during early period after beginning the use of CsA.