Atrial Natriuretic Peptide Gene Expression within Invertebrate Hearts

1995 ◽  
Vol 100 (1) ◽  
pp. 61-68 ◽  
Author(s):  
John E. Poulos ◽  
William R. Gower ◽  
Frank E. Friedl ◽  
David L. Vesely
1996 ◽  
Vol 90 (3) ◽  
pp. 197-204 ◽  
Author(s):  
Hideo Kawakami ◽  
Hideki Okayama ◽  
Mareomi Hamada ◽  
Kunio Hiwada

1. We assessed the changes of atrial natriuretic peptide and brain natriuretic peptide gene expression associated with progression and regression of cardiac hypertrophy in renovascular hypertensive rats (RHR). 2. Two-kidney, one-clip hypertensive rats (6-week-old male Wistar) were made and studied 6 (RHR-1) and 10 weeks (RHR-2) after the procedure. Regression of cardiac hypertrophy was induced by nephrectomy at 6 weeks after constriction, and the nephrectomized rats were maintained further for 4 weeks (nephrectomized rat: NEP). Sham operation was performed, and the rats were studied after 6 (Sham-1) and 10 weeks (Sham-2). Atrial natriuretic peptide and brain natriuretic peptide gene expression in the left ventricle was analysed by Northern blotting. 3. Plasma atrial natriuretic peptide and brain natriuretic peptide were significantly higher in RHR-1 and RHR-2 than in Sham-1, Sham-2 and NEP. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels in RHR-1 were approximately 7.2-fold and 1.8-fold higher than those in Sham-1, respectively, and the corresponding levels in RHR-2 were 13.0-fold and 2.4-fold higher than those in Sham-2, respectively. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels of NEP were normalized. Levels of atrial natriuretic peptide and brain natriuretic peptide mRNA were well correlated positively with left ventricular weight/body weight ratios. There was a significant positive correlation between the levels of atrial natriuretic peptide and brain natriuretic peptide mRNA (r = 0.86, P<0.01). 4. We conclude that the expression of atrial natriuretic peptide and brain natriuretic peptide genes is regulated in accordance with the degree of myocardial hypertrophy and that the augmented expression of these two natriuretic peptides may play an important role in the maintenance of cardiovascular haemodynamics in renovascular hypertension.


1994 ◽  
Vol 202 (1) ◽  
pp. 562-570 ◽  
Author(s):  
W.R. Gower ◽  
J.R. Dietz ◽  
D.L. Vesely ◽  
C.L. Finley ◽  
K.A. Skolnick ◽  
...  

1997 ◽  
Vol 29 (Supplement) ◽  
pp. 227
Author(s):  
M. Perhonen ◽  
T. E.S. Takala ◽  
O. Vuolteenaho ◽  
P. M??ntymaa ◽  
J. Lepp??luoto ◽  
...  

1998 ◽  
Vol 274 (6) ◽  
pp. R1511-R1517 ◽  
Author(s):  
Songcang Chen ◽  
Jinzi Su ◽  
Kegui Wu ◽  
Wenyang Hu ◽  
David G. Gardner ◽  
...  

Treatment of spontaneously hypertensive rats (SHR) with captopril (100 mg ⋅ kg−1 ⋅ day−1) throughout development and during the first 16 wk of life leads to a reduction in blood pressure and left ventricular hypertrophy. Blood pressures and hypertrophy are reduced in these animals (vs. untreated SHR) for up to 24 wk after discontinuation of the drug. We used conventional blot hybridization and Western analysis to examine hypertrophy-dependent gene expression during this period. Ventricular expression of the atrial natriuretic peptide gene was reduced by >90% at 16 wk of age in the captopril-treated SHR. Expression increased in the 24 wk after discontinuation of treatment, but remained well below that of the untreated SHR. A similar reduction in ventricular c- myc gene expression was seen with captopril treatment. Neither renal expression of the atrial natriuretic peptide gene nor ventricular expression of the c- fos gene was affected by captopril. This study demonstrates that captopril treatment during a critical period of development in the SHR leads to a sustained reduction in hypertrophy-dependent myocardial gene expression, which does not revert to levels seen in the untreated SHR after discontinuation of the drug.


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