scholarly journals A synthetic peptide from transforming growth factor- 1 type III receptor prevents myocardial fibrosis in spontaneously hypertensive rats

2008 ◽  
Vol 81 (3) ◽  
pp. 601-609 ◽  
Author(s):  
N. Hermida ◽  
B. Lopez ◽  
A. Gonzalez ◽  
J. Dotor ◽  
J. J. Lasarte ◽  
...  
Keyword(s):  
Growth Factor ◽  
Myocardial Fibrosis ◽  
Synthetic Peptide ◽  
Spontaneously Hypertensive Rats ◽  
Transforming Growth Factor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Type Iii

scholarly journals THE EFFECTS OF LEPTIN ADMINISTRATION ON RENAL FUNCTION IN SPONTANEOUSLY HYPERTENSIVE RATS

2016 ◽  
Vol 10 (1) ◽  
pp. 108
Author(s):  
Brinnell Annette Caszo ◽  
Azdayanti Muslim ◽  
Zanariah Awang ◽  
Effat Omar ◽  
Effendi Ibrahim ◽  
...  
Keyword(s):  
Renal Function ◽  
Growth Factor ◽  
Mrna Expression ◽  
Spontaneously Hypertensive Rats ◽  
Transforming Growth Factor ◽  
Morphological Changes ◽  
Transforming Growth Factor Β1 ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Tgf Β1

ABSTRACTObjective: Elevated levels of leptin may be responsible directly for progression and severity of renal disease in obesity and hypertension. It may exertits effects by promoting fibrosis through the actions of transforming growth factor-β1 (TGF-β1) and the Smad pathway. This study determines theeffect of leptin administration on the development of renal fibrosis in nonobese spontaneously hypertensive rats (SHRs).Methods: Male SHRs, aged 12-14 weeks, were injected with either leptin (60 µg/kg/day) or saline (for the control group) subcutaneously daily for42 days. At the end of the experimental period, animals were euthanized and their kidneys were removed. The right kidney was harvested for thedetermination of messenger ribonucleic acid (mRNA) expression of TGF-β1, Smad2, Smad3, and bone morphogenic protein 7 (BMP7). The left kidneyswere stored in neutral buffered 10% formalin until they were processed and stained with hematoxylin and eosin. Prepared slides were examinedunder light microscopy. 30 consecutive glomeruli were examined for the cell counts based on the number of nuclei seen and the total area of glomeruli.Results: No significant difference was evident in renal function between control and leptin-treated rats. Cellularity and area of glomeruli were also notdifferent between the two groups. mRNA expression of TGF-β1, Smad2, and BMP7 were, however, higher in leptin-treated rats.Conclusion: It appears that 6 weeks of leptin administration increases renal TGF-β1 and Smad2 levels but with little morphological changes in thekidney. Whether the elevated BMP7 expression was responsible for lack of effect of leptin on renal morphological changes remains unclear.Keywords: Leptin, Renal function, Hypertension, Glomerulus, Transforming growth factor-β1, Smad, Spontaneously hypertensive rats.

Prophylactic effects of an N- and L-type Ca2+ antagonist, cilnidipine, against cardiac hypertrophy and dysfunction in stroke-prone, spontaneously hypertensive rats

2005 ◽  
Vol 83 (8-9) ◽  
pp. 785-790 ◽  
Author(s):  
Kumiko Takemori ◽  
Hiroyuki Ishida ◽  
Kensaku Dote ◽  
Kazuo Yamamoto ◽  
Hiroyuki Ito
Keyword(s):  
Growth Factor ◽  
Cardiac Remodeling ◽  
Cardiac Dysfunction ◽  
Spontaneously Hypertensive Rats ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Fibroblast Growth ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Beneficial Effects

To clarify the beneficial effects of cilnidipine, an L- and N-type calcium channel blocker, which were clinically observed against diastolic dysfunction in hypertrophied hearts of hypertensive patients, we investigated the effects of cilnidipine on cardiac remodeling and enhanced gene expression in stroke-prone, spontaneously hypertensive rats in comparison with that of captopril, a well-known angiotensin-converting enzyme inhibitor, at threshold doses with little blood pressure lowering effect. The expression of type III collagen and β/α-myosin heavy chain as well as transforming growth factor-β, and basic fibroblast growth factor were suppressed by both treatments, indicating the prevention or amelioration of cardiac dysfunction. Such beneficial effects were much more intense with cilnidipine treatment than in captopril. These results indicate that Ca2+ is a key factor in the pathogenesis of cardiac remodeling in hypertension. One possible beneficial effect of cilnidipine in the prevention of cardiac dysfunction may be due to the decreased amount of growth factors such as transforming growth factor-β and basic fibroblast growth factor via direct action for Ca2+ influx and also via inhibition of local renin-angiotensin system in the myocardium.Key words: hypertension, cardiac hypertrophy, Ca2+-blocker, growth factor.

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