Increased plasma brain natriuretic peptide levels in DOCA-salt hypertensive rats: Relation to blood pressure and cardiac concentration

1990 ◽  
Vol 173 (2) ◽  
pp. 632-638 ◽  
Author(s):  
Naoto Yokota ◽  
Masahito Aburaya ◽  
Yoshitaka Yamamoto ◽  
Johji Kato ◽  
Kazuo Kitamura ◽  
...  
2009 ◽  
Vol 27 (2) ◽  
pp. 425-432 ◽  
Author(s):  
Emmanuel A Andreadis ◽  
Dimitrios X Georgiopoulos ◽  
Chara K Tzavara ◽  
Panagiota M Katsanou ◽  
Eleni G Fragouli ◽  
...  

Hypertension ◽  
2003 ◽  
Vol 41 (4) ◽  
pp. 978-983 ◽  
Author(s):  
Michael H. Freitag ◽  
Martin G. Larson ◽  
Daniel Levy ◽  
Emelia J. Benjamin ◽  
Thomas J. Wang ◽  
...  

1994 ◽  
Vol 266 (2) ◽  
pp. R451-R457 ◽  
Author(s):  
M. Kohno ◽  
T. Fukui ◽  
T. Horio ◽  
K. Yokokawa ◽  
K. Yasunari ◽  
...  

The blood pressure was decreased after chronic treatment with enalapril, MK-954, and hydralazine in deoxycorticosterone acetate (DOCA)-salt-induced malignant hypertension of spontaneously hypertensive rats (SHR); however, ventricular weight and plasma brain natriuretic peptide (BNP) concentration were decreased after enalapril and MK-954 but not after hydralazine. The BNP secretory rates from the ventricle in enalapril- and MK-954-treated DOCA-salt SHR were decreased to approximately 50% of those in untreated DOCA-salt SHR. The BNP secretory rate from the ventricle was positively correlated with ventricular weight in untreated and treated DOCA-salt SHR. In contrast, acute administration of captopril or MK-954 did not decrease the BNP secretory rate from the heart. Results suggest that the decrease in plasma BNP after enalapril and MK-954 is attributed to a decline in the secretion from the ventricle but not from the atrium. The reduction in ventricular mass appeared to be related to this decline.


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.


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