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Developmental changes in systolic blood pressure in male (a) and female (b) controls on standard (CONTc; •) and high salt (CONTs; ○) diet and rats prenatally exposed to angiotensin II on standard (ANGc; ■) and high salt diet (ANGs; □). Measurements were performed during 3-week period. Values are expressed as means ± SEM.
Source publication
Renin angiotensin aldosterone system (RAAS) plays an essential role in the homeostatic control of arterial blood pressure, perfusion of tissues, and control of extracellular fluid. Its components are highly expressed in the developing kidney, general vasculature, brain, and heart. A modified intrauterine environment alters mechanisms controlling bl...
Contexts in source publication
Context 1
... 5-week period, BP showed stable levels in ANG rats and significantly varied in CONT rats (Figure 2). At the age of 14 weeks, ANG and CONT rats were sub- divided into groups with either standard (ANGc and CONTc) or increased salt diet (ANGs and CONTs) and their BP was monitored during the next 3-week period (Figure 3a, b). Three-way repeated measures ANOVA revealed a significant interactions between treatment group and diet (F(1,45) = 5.29; p < 0.05), between week and treatment group (F(2,90) = 4.16; p < 0.05) and between week, diet, and sex (F(2,90) = 3.28; ...
Citations
... Demonstrating the presence of BPA in AH seems to be important from the point of view of many potential threats related to BPs intoxication starting from direct oxidative damage [81], changing the activity of many enzymes [82][83][84][85][86][87][88][89][90][91], deregulation of the gene expression [55,92], up to the increase in pro-inflammatory cytokines [93], and apoptotic proteins [94]. ...
... BPA can work by changing the activity of many enzymes, including the increase in the activity of the angiotensin-converting enzyme (ACE), i.e., the HBP marker [82,83]. It is known that arterial hypertension causes abnormal blood flow and, consequently, visual disturbances and retinal damage, related to the development of hypertensive retinopathy [84], which predisposes to the development of cataracts. ...
Human exposure to BPs is inevitable mostly due to contaminated food. In this preliminary study, for the first time, the presence of bisphenols (BPs) in aqueous humor (AH) collected from 44 patients undergoing cataract surgery was investigated. The measurements were performed using a sensitive ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC–MS/MS). Chromatographic separation was achieved using a reverse-phase column and a gradient elution mode. Multiple reaction monitoring (MRM) was used. The method was validated for bisphenol A (BPA) and bisphenol F (BPF). The limits of quantification (LOQs) of both investigated analytes were 0.25 ng mL−1. The method was linear in the range of 0.25–20.0 ng mL−1 with correlation coefficients (R2) higher than 0.98. Recovery of analytes was in the range of 99.9 to 104.3% and intra-assay and inter-assay precision expressed by relative standard deviations (RSD%) were less than 5%. BPA was detected in 12 AH samples with mean concentrations of 1.41 ng mL−1. BPF was not detected at all. Furthermore, two structural isomers termed BPA-1, and BPA-2 were identified, for the first time, in 40.9% of the AH samples, with almost twice higher mean concentrations of 2.15 ng mL−1, and 2.25 ng mL−1, respectively. The total content of BPs were higher in patients with coexisting ocular pathologies such as glaucoma, age-related macular degeneration (AMD), and diabetes in comparison to cataracts alone. However, the difference between these groups did not reach statistical significance (p > 0.05). Performed investigations indicate the need for further research on a larger population with the aim of knowing the consequences of BPs’ accumulation in AH for visual function.
... Angiotensin-converting enzyme (ACE) catalyzes the conversion of angiotensin I to angiotensin II and also degrades bradykinin and vasoactive peptides [17]. Angiotensin II is an arteriolar vasoconstrictor causing high blood pressure [18,19]. Hence, ACE inhibitors including flavonoids have been effective pharmacological agents to improve endothelial function in a condition of NO deficiency [20]. ...
People who have experienced high blood pressure are at greater risk of susceptibility to other health problems including oculopathy. The patients with these experiences do not have adequate treatment and those who do; spend much funds on the drug purchase. The study examines the protective effect of naringin (NRG) against ocular impairment in L-NAME induced hypertensive rat on exposure to a cellular disruptor. Fifty-six adult male albino rats were randomly distributed into eight (n = 7) groups. Group I: control animals, Group II was treated with Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME), Group III was treated with 50 mg/kg Bisphenol-A, Group IV was treated with L-NAME +50 mg/kg Bisphenol-A. Group V was administered with L-NAME +80 mg/kg NRG. Group VI was administered with 50 Mg/kg BPA + 80 mg/kg NRG. Group VII was administered with L-NAME+50 mg/kg Bisphenol-A +80 mg/kg NRG. Lastly, group VIII was treated with 80 mg/kg NRG alone for 14 days. Naringin prevented hypertension and ocular dysfunction by depleting the activities of angiotensin-converting enzymes, arginase, aldose-reductase and phosphodiesterase-5¹ (PDE-5¹) with corresponding down-regulation of inflammatory markers including TNF-α and IL-B. Moreover, ocular impairment was remarkably reduced by NRG as manifested by the decreased activities of AChE, BuChE, MAO-A and enzymes of ATP hydrolysis (ATPase, ADPase, AMPase) and adenosine deaminase with resultant increased NO level. Also, ocular expression of CD43 transcript, caspaace-9 and tumor suppressor P53 proteins were suppressed on treatment with NRG. This study corroborates the view that NRG may be a useful therapy in alleviating inflammatory markers, apoptosis and metabolic nucleotides disorders via the NOS/cGMP/PKG signaling pathways in hypertensive rat model on exposure to a cellular disruptor.
... Angiotensin II is the most biologically active peptide in the system and exerts its effects on sodium reabsorption and vasoconstriction. Data on the effects on the in utero fetal development of angiotensin II are scarce during pregnancy (Svitok et al. 2017). In this study, there was no appreciable relation between salt and water intake across pregnancy trimesters, on the one side, and the maternal serum angiotensin II and aldosterone content, on the other side. ...
Birth weight is a key determinant of perinatal outcomes which affect physical development and metabolic function. In this study, we evaluated the potential role of maternal body composition and nutritional status in programing fetal birth weight. This was a longitudinal study that included 29 pregnant women and their full-term newborns. Maternal dietary energy and fluid intake and body adipose tissue were assessed. In addition, we measured the serum content of copeptin, aldosterone, and angiotensin II in maternal and umbilical cord blood. The measurements were done across the three trimesters of pregnancy, on average, at 11.6 weeks, 18.3 weeks, and 30.2 weeks. Each newborn’s birth weight was determined at the percentile line, using the World Health Organization (WHO) standards based on the gestational age, gender, and weight. We found no appreciable relation of fetal birth weight to the maternal dietary and fluid intakes, and the content of angiotensin II, aldosterone, or copeptin. However, birth weight correlated with increases in body adipose tissue in early pregnancy stages. Further, birth weight correlated positively with copeptin and adversely with angiotensin II in cord blood. We conclude that the present findings may be helpful in the assessment of a critical level of body adipose tissue in women of child-bearing age, above which the potential risk of macrosomia appears. The female population of child-bearing age needs a continual update on the nutritional knowledge to prevent modifiable maternal and fetal perinatal complications.
... Increased BP in offspring prenatally exposed to enhanced angiotensin 2 (Ang2) concentrations was previously documented. This increase was abolished following exposure to a high-salt diet and was not accompanied by heart hypertrophy; however, decreased relative left-ventricle weight and relative kidney weight were observed (11). ...
... Moreover, Ang2 influences also the ionic composition of blood serum (36). Increased Na,K-ATPase activity in rats exposed prenatally to increased Ang2 levels corresponds to increased BP in these animals (11). These results are in line with the role of Na,K-ATPase in renal proximal tubules, as the basolateral membrane-localised enzyme is the key element involved in Na + reabsorption (37). ...
... These results suggest that prenatal exposure to Ang2 desensitises the enzyme so that it fails to respond to the increased salt intake. These results are in accordance with the increased BP observed after high salt intake in the offspring of sham-operated but not Ang2-treated mothers (11). The salt insensitivity observed in rats prenatally treated with Ang2 resembles the results obtained in Dahl salt-sensitive and saltresistant rats, where salt-resistant rats did not exhibit increased BP in response to a high-salt diet (2). ...
In rodents, increased angiotensin 2 (Ang2) during pregnancy increases blood pressure and decreases salt sensitivity in the offspring. To explore the underlying mechanisms, this study evaluated the effects of prenatal Ang2 exposure on the activity of renal Na,K-ATPase, which is one of the main systems that maintains sodium ion homeostasis in an organism. Moreover, this study also investigated the impact of a higher-salt diet on the enzyme activity in the offspring in a sex-dependent manner. Pregnant Wistar rats were implanted with osmotic minipumps that continuously released Ang2 (2 μg/kg/h) for 2 weeks. Male and female offspring of treated and control females were allocated to groups fed with normal or high-salt diets. In the offspring prenatally treated with Ang2, a significant Vmax increase (23 - 36%) was observed in females fed with both a normal and high-salt diet. In addition, a significant increase in Km (20 - 26%) was also observed in the female groups, compared to respective male groups, independently of their diet. Evaluation of KNa showed significantly lower values (13 - 17%) in female offspring fed with a high-salt diet, independent of the prenatal treatment. In conclusion, these data suggest that increased prenatal Ang2 has a predominant impact on the properties of renal Na,K-ATPase in both sexes. Moreover, the enzyme is resistant to higher salt intake in offspring prenatally exposed to Ang2.
Impact statement:
Suboptimal prenatal conditions can contribute to development of cardiovascular diseases and an altered renin-angiotensin-aldosterone system (RAAS) can be involved in the process. In our study, increased angiotensin II in pregnant female rats resulted in renal cortical interstitial damage, and renal ultrastructural changes in the glomeruli, the brush border of proximal tubules and mitochondria in mature male offspring. The treatment promoted infiltration of T cells and macrophages in the kidneys and primed an oxidative burst of circulating neutrophils, indicating a pro-inflammatory state in the progeny of angiotensin II-treated mothers. Deregulated RAAS of mothers is involved in developmental programming of hypertension in adult male offspring via damaging kidney morphology and function. These findings suggest that preventing the activation of RAAS and oxidative stress during perinatal development might protect against hypertension development in adult male progeny.
Suboptimal conditions during prenatal and early postnatal development can increase risk of hypertension later in life. We studied consequences of a changed perinatal environment by initiating the cross-fostering of homozygous Ren-2 transgenic rat (TGR) offspring to normotensive, transgene-negative control mothers, and vice versa. We hypothesized that cross-fostering to a normotensive female can attenuate the development of malignant hypertension in TGR offspring (TGRx) and change their salt-sensitive response. Blood pressure (BP) was monitored by the telemetry system under normal salt intake, and BP responses to increased salt intake in the phase of established hypertension. Under normal salt conditions, BP was not markedly different in cross-fostered animals compared with controls. However, BP responses to 2% salt intake led to a stronger BP response in TGRx during the active phase when compared with the control TGR group. The TGRx also exhibited increased albuminuria, lower sodium excretion, and creatinine clearance under higher salt intake compared with control salt intake. Higher salt intake resulted in a significant increase of aldosterone concentrations only in the TGRx group; moreover, TGRx rats exhibited more pronounced renal injury compared with controls. In conclusion, our data indicate that cross-fostering in TGR not only did not attenuate the development of hypertension but, on the contrary, led to the deterioration of BP regulation, particularly due to exaggerated salt sensitivity and sodium retention in TGRx. Results underline the important role of the mother during lactation in postnatal development of the offspring, since these changes reflected different ion content in milk of a particular strain of rats.
