Vascular tone regulation in renal interlobar arteries of male rats is dysfunctional after intrauterine growth restriction

Author(s):  
Jenny Voggel ◽  
Lubomir Lubomirov ◽  
Felix Lechner ◽  
Gregor Fink ◽  
Eva Nüsken ◽  
...  

Intrauterine growth restriction (IUGR) due to an adverse intrauterine environment predisposes to arterial hypertension and loss of kidney function. Here we investigated whether vascular dysregulation in renal interlobar arteries (RIA) may contribute to hypertensive glomerular damage after IUGR. In rats, IUGR was induced by bilateral uterine vessel ligation. Offspring of non-operated rats served as controls (C). From postnatal day (PND) 49, blood pressure was telemetrically recorded. On PND 70, we evaluated contractile function in RIA and mesenteric arteries (MA). Additionally, blood, urine and glomerular parameters and renal collagen deposition were analyzed. IUGR-RIA not only showed loss of stretch activation in 9/11 arteries and reduced stretch-induced myogenic tone, but also a shift of the concentration-response relation of acetylcholine-induced relaxation towards lower concentrations. However, IUGR-RIA also exhibited augmented contractions through phenylephrine (PE). Systemic mean arterial pressure [mean differences 4.8 (daytime) and 5.7 mmHg (night)], mean glomerular area (IUGR, 9754 ± 338; C, 8395 ± 227 µm2) and urinary protein/creatinine ratio (IUGR, 1.67 ± 0.13; C, 1.26 ± 0.10 g/g) were elevated after IUGR. We conclude that male IUGR rat offspring may have increased vulnerability towards hypertensive glomerular damage due to loss of myogenic tone and augmented endothelium-dependent relaxation in RIA.

2014 ◽  
Vol 12 (1) ◽  
pp. 62 ◽  
Author(s):  
Mathilde Janot ◽  
Marie-Laure Cortes-Dubly ◽  
Stéphane Rodriguez ◽  
Uyen Huynh-Do

2016 ◽  
Vol 80 (4) ◽  
pp. 547-553 ◽  
Author(s):  
Michael Keenaghan ◽  
Lena Sun ◽  
Aili Wang ◽  
Eiichi Hyodo ◽  
Sinichi Homma ◽  
...  

2017 ◽  
Vol 16 (4) ◽  
pp. 1515-1525 ◽  
Author(s):  
Amanda P. Pedroso ◽  
Adriana P. Souza ◽  
Ana P. S. Dornellas ◽  
Lila M. Oyama ◽  
Cláudia M. O. Nascimento ◽  
...  

2009 ◽  
Vol 297 (3) ◽  
pp. R813-R824 ◽  
Author(s):  
Bérengère Coupé ◽  
Isabelle Grit ◽  
Dominique Darmaun ◽  
Patricia Parnet

Epidemiological studies demonstrated a relationship between low birth weight mainly caused by intrauterine growth restriction (IUGR) and adult metabolic disorders. The concept of metabolic programming centers on the idea that nutritional and hormonal status during the key period of development determines the long-term control of energy balance by programming future feeding behavior and energy expenditure. The present study examined the consequence of early or late “catch-up growth” after IUGR on feeding behavior and metabolic cues of male offspring of rat dams exposed to protein restriction during gestation and/or lactation. Our results suggest that early catch-up growth may be favorable for fasting metabolic parameters at weaning, as no differences were observed on plasma leptin, triglyceride, glucose, and insulin levels compared with controls. In contrast, if pups remained malnourished until weaning, low insulin concentration was detected and was accompanied by hyperphagia associated with a large increase in hypothalamic NPY and AgRP mRNA expression. At adult age, on a regular chow diet, only the meal structure was modified by fetal programming. The two IUGR groups demonstrated a reduced meal duration that enhanced the speed of food ingestion and consequently increased the rest period associated to the satiety state without changes in the hypothalamic expression of appetite neuropeptides. Our findings demonstrate that in IUGR, regardless of postnatal growth magnitude, metabolic programming occurred in utero and was responsible for both feeding behavior alteration and postprandial higher insulin level in adults. Additionally, catch-up growth immediately after early malnutrition could be a key point for the programming of postprandial hyperleptinemia.


2018 ◽  
Vol 9 (3) ◽  
pp. 315-328 ◽  
Author(s):  
E. K. Zinkhan ◽  
B. Yu ◽  
C. W. Callaway ◽  
R. A. McKnight

AbstractIntrauterine growth restriction (IUGR) and fetal exposure to a maternal high-fat diet (HFD) independently increase the risk of developing obesity in adulthood. Excess glucocorticoids increase obesity. We hypothesized that surgically induced IUGR combined with an HFD would increase adiposity and glucocorticoids more than in non-IUGR offspring combined with the same HFD, findings that would persist despite weaning to a regular diet. Non-IUGR (N) and IUGR (I) rat offspring from dams fed either regular rat chow (R) or an HFD (H) were weaned to either a regular rat chow or an HFD. For non-IUGR and IUGR rats, this study design resulted in three diet groups: offspring from dams fed a regular diet and weaned to a regular diet (NRR and IRR), offspring rats from dams fed an HFD and weaned to a regular diet (NHR and IHR) and offspring from dams fed an HFD and weaned to an HFD (NHH and IHH). Magnetic resonance imaging or fasting visceral and subcutaneous adipose tissue collection occurred at postnatal day 60. IHH male rats had greater adiposity than NHH males, findings that were only partly normalized by weaning to a regular chow. IHH male rats had a 10-fold increase in serum corticosterone levels. IHH female rats had increased adiposity and serum triglycerides. We conclude that IUGR combined with an HFD throughout life increased adiposity, glucocorticoids and triglycerides in a sex-specific manner. Our data suggest that one mechanism through which the perinatal environment programs increased adiposity in IHH male rats may be via increased systemic glucocorticoids.


2021 ◽  
Author(s):  
Ekaterina Selivanova ◽  
Anastasia Shvetsova ◽  
Lyubov Shilova ◽  
Olga Tarasova ◽  
Dina Gaynullina

Abstract Intrauterine growth restriction (IUGR) is one of the most common pathologies of pregnancy. The cardiovascular consequences of IUGR do not disappear in adulthood and can manifest themselves in pathological alterations of vasomotor control. The hypothesis was tested that IUGR weakens anticontractile influence of NO and augments procontractile influence of Rho-kinase in arteries of adult offspring. To model IUGR in the rat, dams were 50% food restricted starting from the gestational day 11 till delivery. Mesenteric and coronary arteries of male offspring were studied at the age of 3 months using wire myography, qPCR, and Western Blotting. Contractile responses of mesenteric arteries to α1-adrenoceptor agonist methoxamine as well as influences of NO and Rho-kinase did not differ between control and IUGR rats. However, coronary arteries of IUGR rats demonstrated elevated contraction to thromboxane A2 receptor agonist U46619 due to weakened anticontractile influence of NO and enhanced role of Rho-kinase in the endothelium. This was accompanied by reduced abundance of SODI protein and elevated content of RhoA protein in coronary arteries of IUGR rats. IUGR considerably changes the regulation of coronary vascular tone in adulthood and, therefore, can serve as a risk factor for the development of cardiac disorders.


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