scholarly journals Mechanisms Responsible for Genetic Hypertension in Schlager BPH/2 Mice

2019 ◽  
Vol 10 ◽  
Author(s):  
Kristy L. Jackson ◽  
Geoffrey A. Head ◽  
Cindy Gueguen ◽  
Emily R. Stevenson ◽  
Kyungjoon Lim ◽  
...  
Keyword(s):  
Genetic Hypertension

Influence of the Thymus in the Development of Genetic Hypertension in the Rats of the Lyon Strain

1986 ◽  
Vol 4 (5) ◽  
pp. 639-640 ◽  
Author(s):  
A Bataillard ◽  
J L Touraine ◽  
M Vincent ◽  
J Sassard
Keyword(s):  
Genetic Hypertension

Effects of genetic hypertension and nutritional anaemia on ventricular remodelling and myocardial damage in rats

1993 ◽  
Vol 27 (7) ◽  
pp. 1316-1325 ◽  
Author(s):  
G. Olivetti ◽  
F. Quaini ◽  
C. Lagrasta ◽  
R. Ricci ◽  
P. Tosini ◽  
...  
Keyword(s):  
Myocardial Damage ◽  
Ventricular Remodelling ◽  
Genetic Hypertension

Rat Brain Regional Preproenkephalin A Messenger RNA Levels Are Altered in Genetic Hypertension

1989 ◽  
Vol 2 (7) ◽  
pp. 542-548 ◽  
Author(s):  
David B. Hoegler ◽  
Michael J. Sole ◽  
Choong-Chin Liew
Keyword(s):  
Rat Brain ◽  
Messenger Rna ◽  
Genetic Hypertension ◽  
Rna Levels

Enalapril attenuates cardiorenal damage in nitric-oxide-deficient spontaneously hypertensive rats

2004 ◽  
Vol 106 (3) ◽  
pp. 337-343 ◽  
Author(s):  
Leila M. M. PEREIRA ◽  
Daniele G. BEZERRA ◽  
Denise L. MACHADO ◽  
Carlos A. MANDARIM-DE-LACERDA
Keyword(s):  
Nitric Oxide ◽  
Body Mass ◽  
Structural Damage ◽  
Spontaneously Hypertensive Rats ◽  
Left Ventricular ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Genetic Hypertension ◽  
Lv Mass ◽  
Significant Difference

Stereological structural alterations of the heart and kidney were studied in four groups (n=5) of spontaneously hypertensive rats (SHRs) treated for 30 days: (i) control, (ii) NG-nitro-L-arginine methyl ester [L-NAME; nitric oxide (NO) synthesis inhibitor] alone, (iii) enalapril alone and (iv) L-NAME plus enalapril. Blood pressure (BP) was elevated significantly in NO-deficient SHRs (rats receiving L-NAME) or significantly lower in enalapril-treated SHRs. Co-administration of L-NAME and enalapril caused a 20% decrease in BP compared with untreated SHRs. NO-deficient SHRs had a decrease in body mass, but this loss of body mass was prevented efficiently in the enalapril-treated group. Enalapril treatment decreased the left ventricular (LV) mass index in SHRs, even in animals with NO synthesis blocked. NO deficiency in SHRs caused a larger decrease in the number of LV cardiomyocyte nuclei, which had a negative correlation with both LV mass index and BP. The volume-weighted glomerular volume (VWGV) separated the SHRs into two groupings: (i) control and NO-deficient SHRs, and (ii) enalapril- and L-NAME plus enalapril-treated SHRs. There was a significant difference between these two groupings, with VWGV being more than 15% smaller in the latter compared with the former grouping. The present findings reinforce the evidence that enalapril efficiently treats genetic hypertension, and demonstrate that this effect is observed even when NO synthesis is inhibited. Enalapril administration also decreases cardiac and renal structural damage caused by genetic hypertension, as well as by the interaction between genetic hypertension and NO deficiency.

Circulating Natriuretic Factor in the Pathogenesis of Genetic Hypertension of Renal Origin

1987 ◽  
pp. 174-176
Author(s):  
P. Ferrari ◽  
H. E. de Wardener ◽  
J. A. Millet ◽  
L. Torielli ◽  
M. Ferrandi ◽  
...  
Keyword(s):  
Genetic Hypertension ◽  
Natriuretic Factor ◽  
Renal Origin

scholarly journals ROLE OF DOPAMINE D3 RECEPTORS IN THE PATHOGENESIS OF GENETIC HYPERTENSION• 1635

1997 ◽  
Vol 41 ◽  
pp. 275-275 ◽  
Author(s):  
Laureano D Asico ◽  
Sara Fuchs ◽  
Domenico Accili ◽  
Gilbert M Eisner ◽  
Pedro A Jose
Keyword(s):  
Dopamine D3 Receptors ◽  
D3 Receptors ◽  
Genetic Hypertension ◽  
Dopamine D3

Resistance artery phosphoinositide metabolism in genetic hypertension

1990 ◽  
Vol 8 (6) ◽  
pp. 557-563 ◽  
Author(s):  
Helen Durkin ◽  
Jeremy D. Ollerenshaw ◽  
Anthony M. Heagerty
Keyword(s):  
Phosphoinositide Metabolism ◽  
Resistance Artery ◽  
Genetic Hypertension
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