scholarly journals Renal NOS isoforms and splicing in 13 week obese female Zucker rats on antioxidant vs regular diet

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Sharon R Inman ◽  
Yuriy Slyvka ◽  
Yelena Feldman ◽  
Felicia V Nowak
2021 ◽  
Vol 113 ◽  
pp. 101919
Author(s):  
Dolores Adriana Bravo Durán ◽  
Selina Jocelyn Barreda Guzmán ◽  
Angélica Trujillo Hernández ◽  
Adriana Berenice Silva Gómez

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Masato Tsutsui ◽  
Yasuko Yatera ◽  
Hiroaki Shimokawa ◽  
Sei Nakata ◽  
Kiyoko Shibata ◽  
...  

We have recently developed mice lacking all three nitric oxide synthase (NOS) isoforms: nNOS, iNOS, and eNOS ( PNAS 2005). In this study, we examined the effects of a high-cholesterol (HC) diet on lipid metabolism and vascular lesion formation in those mice. Experiments were performed in 2-month-old male wild-type (WT) and singly, doubly, and triply NOS −/− mice (n=6–9). They were maintained on either a regular diet or a HC diet for 3 months. The HC feeding significantly increased plasma levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL) in all the genotypes studied as compared on the regular diet (all P <0.05). These serum levels of TC and LDL on the HC diet (mg/dl) were both significantly higher in all the singly, doubly, and triply NOS −/− genotypes as compared with the WT genotype (singly nNOS −/− [371±61 and 205±65], iNOS −/− [559±62 and 350±62], eNOS −/− [619±22 and 395±25], doubly n/iNOS −/− [518±77 and 328±72], n/eNOS −/− [635±56 and 458.8±42], e/iNOS −/− [480±38 and 260±40], triply n/i/eNOS −/− [2316±704 and 1588±715], and WT [326±43 and 244±54]) (all P <0.05). Notably, the extent of the dyslipidemia was by far severest in the triply n/i/eNOS −/− genotype among the NOS −/− genotypes, and intriguingly, the serum levels of TC and LDL in the triply n/i/eNOS −/− genotype were equivalent to those in apolipoprotein E −/− mice that exhibit severe hypercholesterolemia. Lipid accumulation in the aorta on the HC diet (lipid area, %, oil red O staining) was also significantly more accelerated in all the NOS −/− genotypes than in the WT genotype (singly nNOS −/− [6.6±1.5], iNOS −/− [6.7±2.2], eNOS −/− [5.5±2.3], doubly n/iNOS −/− [4.7±1.7], n/eNOS −/− [6.4±1.4], i/eNOS −/− [6.8±1.3], triply n/i/eNOS −/− [20.6±1.0], and WT [3.6±1.2]), while the extent of the aortic atherosclerosis was again by far severest in the triply n/i/eNOS −/− genotype (all P <0.05). These results demonstrate that mice deficient in all NOSs manifest severe hypercholesterolemia and lipid-rich atherosclerotic lesion formation in response to a HC diet, indicating a pivotal role of the whole NOS system in preventing those disorders. Our triply NOS −/− mouse is a new experimental model of human hypercholesterolemia and atherosclerosis.


1987 ◽  
Vol 117 (7) ◽  
pp. 1291-1297 ◽  
Author(s):  
Sam J. Bhathena ◽  
Patricia Aparicio ◽  
Kenneth Revett ◽  
Nancy Voyles ◽  
Lillian Recant

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Yuriy Slyvka ◽  
Sharon R Inman ◽  
Felicia V Nowak
Keyword(s):  

2000 ◽  
Vol 37 (4) ◽  
pp. 377-387 ◽  
Author(s):  
Adam S. Fox ◽  
Arielle Foorman ◽  
Deborah H. Olster

1985 ◽  
Vol 248 (4) ◽  
pp. H438-H444 ◽  
Author(s):  
N. F. Paradise ◽  
C. F. Pilati ◽  
W. R. Payne ◽  
J. A. Finkelstein

We sought to determine if left ventricular (LV) function of the heart from the adult, chronically obese animal is impaired. Hearts from 50 wk-old genetically obese female Zucker rats (624 +/- 13 g) and their lean littermate controls (275 +/- 5 g) were isolated during ether anesthesia, supported metabolically by retrograde aortic perfusion (6 ml/min, 35 degrees C) with physiological solution containing suspended canine erythrocytes (hematocrit, 20%), and the ventricles were paced at 180 beats/min. A distensible, fluid-filled balloon was placed in the LV, and pressure-volume (PV) relationships were obtained. The obese and lean end-diastolic PV curves were not different, and therefore the obese and lean LV chamber compliances were similar. Comparison of the systolic PV relationships demonstrated that the obese rat's heart had a greater pressure-generating capability, which probably was a reflection of its increased LV mass (0.96 +/- 0.03 vs. 0.72 +/- 0.02 g). The calculated average meridional (or circumferential) peak systolic wall stress in the LV of the obese rat's heart, however, was significantly reduced compared with control. This diminished ability to develop systolic stress from the same end-diastolic volumes suggests that the hypertrophied LV of the middle-aged obese rat's heart is dilated or that its contractility is depressed, or both.


Biomedicines ◽  
2018 ◽  
Vol 6 (2) ◽  
pp. 55 ◽  
Author(s):  
Reza Hakkak ◽  
Clinton Gauss ◽  
Andrea Bell ◽  
Soheila Korourian

Sign in / Sign up

Export Citation Format

Share Document