Loss of Basic Fibroblast Growth Factor of Brain Ependyma in Old Spontaneously Hypertensive Rats

1994 ◽  
pp. 161-167 ◽  
Author(s):  
Pedro Cuevas ◽  
Diana Reimers ◽  
Fernando Carceller ◽  
Fu Xiaobing ◽  
Guillermo Giménez-Gallego
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Spontaneously Hypertensive Rats ◽  
Fibroblast Growth ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Basic fibroblast growth factor increases collateral blood flow in spontaneously hypertensive rats

2003 ◽  
Vol 285 (3) ◽  
pp. H1190-H1197 ◽  
Author(s):  
Sunita Srivastava ◽  
Ronald L. Terjung ◽  
H. T. Yang
Keyword(s):  
Nitric Oxide ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Spontaneously Hypertensive Rats ◽  
High Dose ◽  
Fibroblast Growth ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Calf Muscles

Ischemia-induced angiogenic response is reduced in spontaneously hypertensive rats (SHR). To study whether exogenous basic fibroblast growth factor (bFGF) infusion is effective in expanding collateral circulation in frankly hypertensive SHR, femoral arteries of male SHR (weighing ∼250 g) were kept intact (nonoccluded control; n = 9) or occluded for4h( n = 12) or for 16 days with vehicle ( n = 14) or bFGF [0.5 ( n = 17), 5.0 ( n = 13), and 50.0 ( n = 14) μg · kg–1 · day–1 for 14 days] intraarterially. Maximal collateral-dependent blood flows (BF) to the hindlimbs were determined with 85Sr- and 141Ce-labeled microspheres during running at 20 and 25 m/min (15% grade). Preexercise heart rates (∼530 beats/min) and blood pressures (BP; ∼200 mmHg) were similar across groups except in the high-dose bFGF group, where BP was reduced by ∼12% ( P < 0.05). Femoral artery occlusion for 4 h resulted in ∼95% reduction of BF in calf muscles [199 ± 18.7 (nonoccluded group) to 10 ± 1.0 ml · min–1 · 100 g–1; P < 0.001]. BF to calf muscles of the vehicle and low-dose bFGF (0.5 μg · kg–1 · day–1) groups increased to 36 ± 3.2 and 45 ± 2.0 ml · min–1 · 100 g–1, respectively ( P < 0.001). bFGF infusion at 5.0 and 50.0 μg · kg–1 · day–1 further increased ( P < 0.001) BF to calf muscles (62 ± 4.6 and 62 ± 2.2 ml · min–1 · 100 g–1, respectively). Our results show that bFGF can effectively increase BF in hypertensive rats. The reduced hypertension with high-dose bFGF suggests that a critical signal in arteriogenesis (nitric oxide bioavailability) may be restored. These findings suggest that the dulled endothelial nitric oxide synthase of SHR does not preempt collateral vessel remodeling.

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.

Basic fibroblast growth factor inhibits ventricular remodeling in Dahl salt-sensitive hypertensive rats

2008 ◽  
Vol 26 (12) ◽  
pp. 2436-2444 ◽  
Author(s):  
Takeya Suzuki ◽  
Yoshikiyo Akasaka ◽  
Atsushi Namiki ◽  
Kinji Ito ◽  
Yukio Ishikawa ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Ventricular Remodeling ◽  
Fibroblast Growth ◽  
Hypertensive Rats
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