Aim To study the effect of high salt diet during pregnancy on the development of renal vessels in offspring rats and its mechanism.Methods Natural pregnant Sprague-Dawley rats were randomly divided into high-salt group and control group.The pregnant rats in the high-salt group were given high-salt diet of 8% NaCl content , while the control group normal diet with 1% NaCl content.In both groups, pregnant rats were given normal drinking water.After delivery, all mothers returned to normal diet and all neonatal rats were breast-fed until one month old.The adult male off springs were used as experimental animals.The vessel tone of renal interlobar arteries and electrophysiological behavior of single vascular smooth muscle cells (VSMCs) were detected respectively.Results The contractile response of renal arteries to phenylephrine(Phe) in high-salt group was stronger than that in the control group(P<0.05).The effect of protein kinase C(PKC) non selective blocker GF109203X on Phe-induced contraction in two groups also showed significant difference(P<0.05).In electrophysiology experiments, Phe inhibited high-conductance Ca2+-activated K+ channel(BK channel) currents in renal arteriolar smooth muscle cells in two groups, and the inhibitory effect was more pronounced in high-salt offsprings (P<0.05).GF109203X could eliminate the response of Phe on BK currents in both groups(P>0.05).Conclusions High-salt diet during pregnancy could increase the sensitivity of renal interlobar arterial contractile response to Phe in adult male offsprings, which is associated with PKC-mediated BK channels pathway.Maternal high-salt diet during pregnancy may increase the risk of renal vascular diseases in adult offsprings.

Objective To determine the effects of β-estradiol on vasoconstriction in human umbilical artery and vein and its potential mechanisms.Methods Human umbilical cord samples were obtained from 96 term neonates of healthy singleton pregnant women born in the First Hospital of Soochow University between December 2013 and June 2015 (multiple pregnancy,pregnancy complications,cesarean delivery and low birth weight were excluded).Human umbilical arteries and veins were isolated and suspended in 37 2 organ baths containing 5 ml Krebs solution and exposed to β-estradiol followed by phenylephrine (PE) for vasoconstriction test.The subjects were divided into β-estradiol group and control group according to the presence or absence of β-estradiol incubation.To determine the effects and the possible underlying mechanisms of β-estradiol on PE-induced vasoconstriction,human umbilical artery and vein rings were pretreated with N ω-nitro-L-arginine (L-NMMA,nitric oxide synthesis inhibitor),fulvestrant (ICI182780,estradiol receptor antagonist),indomethacin (prostaglandin synthesis blocker),and removal of endothelium,then incubated with β-estradiol for 60 min followed by PE,and the concentration-response curves to PE were recorded.The concentrationresponse curves to phorbol 12,13-dibutyrate (PDBU,protein kinase C agonist) in Krebs solution in the presence or absence of β-estradiol were also obtained.Nonlinear regression and fitting curve were performed,and the two-sample ANOVA was used for analysis.Results (1) β-estradiol suppressed PE-induced vasoconstriction of human umbilical vein and artery.In human umbilical vein and artery of the control group,the maximum contraction intensity induced by PE was (59.17± 5.98)％ and (43.35± 5.02)％ of that induced by potassium chloride,respectively.The maximum contraction induced by PE in β-estradiol group was (5.87± 1.32)％and (4.52±1.22)％ of that induced by potassium chloride.(2) In both groups,incubation with L-NMMA or endothelium removal enhanced the vasoconstriction of human umbilical artery and vein,indicating that the inhibitory effect of β-estradiol was not influenced by the endothelium.(3) The suppression of β-estradiol on PE-induced vasoconstriction in human umbilical artery and vein was not significantly decreased by estrogen receptor antagonist.(4) β-estradiol did not affect human umbilical artery and vein vasoconstriction induced by PDBU.(5) In the control group,incubation with indomethacin did not affect human umbilical artery and vein vasoconstriction induced by PE.In the β-estradiol group,indomethacin significantly enhanced the contraction response induced by PE,suggesting that prostacycline synthesis was partly involved in β-estradiol-suppressed contractility in human umbilical artery and vein.The contractile response induced by phenylephrine was still lower in the β-estradiol group than in the control group,which was induced by indomethacin.Conclusions (1) β-estradiol can suppress vasoconstriction in human umbilical artery and vein,which is not dependent on endothelium and estrogen receptors,or protein kinase C activity,(2) Prostacycline synthesis is partly involved in β-estradiol-suppressed vasoconstriction in human umbilical artery and vein.

Objective To explore the effects and mechanisms of prenatal hypoxia on vasomotor functions of fetal rats.Methods Sixteen pregnant Sprague-Dawley rats were randomly divided into two groups:control and hypoxia groups (eight in each group).Rats in the hypoxia group were provided with 10.5％ of oxygen from gestation day 5 to 21,while those in the control group were exposed to normoxic condition.Fetuses were removed from the pregnant rats by cesarean section on gestational day 21.Fetal body weight,blood gas and electrolyte levels were measured.Thoracic aorta rings were separated from fetal rats and used in different vascular function tests.Effects of hypoxia during pregnancy on angiotensin Ⅱ (Ang Ⅱ)-mediated vasoconstrictions and acetylcholine (Ach)-mediated vasodilatations in fetal thoracic aortas were measured.Changes in vasomotor functions were observed after both endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methyl ester (L-Name) and L-type calcium channel (LTCC) inhibitor nifedipine were administered.T-test and two-way analysis of variance were used for statistical analysis.Results (1) Compared with the control group,fetal body weight [(4.40±0.23) vs (3.33±0.42) g,t=2.871],blood partial pressure of oxygen [(50.64±2.17) vs (42.50-±-2.32) mmHg (1 mmHg=0.133 kPa),t=-2.618] and blood oxygen saturation [(58.95±1.97)％ vs (47.73±2.24)％,t=3.564] in the hypoxia group were significantly reduced (all P＜0.05).(2) Compared with the control group,Ang Ⅱ-mediated vasoconstrictions increased,but Ach-mediated vasodilatations in fetal thoracic aortas decreased in the hypoxia group (both P＜0.05).L Name induced stronger Ang Ⅱ-mediated contractions in thoracic aortas in the control group than that in the hypoxia group (P＜0.05).However,nifedipine decreased Ang Ⅱ-induced contractions,especially in the hypoxia group (P＜0.05).Conclusions Maternal hypoxia during pregnancy not only affects the growth and development of fetuses but also changes their blood vessel functions,which may be related to the change of LTCC and the impairment of eNOS.