Fatty acids of the pregnant rat uterus

1971 ◽  
Vol 27 (10) ◽  
pp. 1151-1151 ◽  
Author(s):  
J. R. Beall
Keyword(s):  
2017 ◽  
Vol 58 (2) ◽  
pp. 141-148 ◽  
Author(s):  
Kálmán F. Szűcs ◽  
György Grosz ◽  
Miklós Süle ◽  
Anikó Nagy ◽  
Zita Tiszai ◽  
...  

2002 ◽  
Vol 283 (2) ◽  
pp. L310-L318 ◽  
Author(s):  
Alan J. Ryan ◽  
Jheem D. Medh ◽  
Diann M. McCoy ◽  
Ronald G. Salome ◽  
Rama K. Mallampalli

We examined whether administration of very low-density lipoproteins (VLDL) to pregnant rats increases surfactant phosphatidylcholine (PtdCho) content in fetal pre-type II alveolar epithelial cells. VLDL-triglycerides are hydrolyzed to fatty acids by lipoprotein lipase (LPL), an enzyme activated by heparin. Fatty acids released by LPL can incorporate into the PtdCho molecule or activate the key biosynthetic enzyme cytidylyltransferase (CCT). Dams were given BSA, heparin, VLDL, or VLDL with heparin intravenously. Radiolabeled VLDL given to the pregnant rat crossed the placenta and was distributed systemically in the fetus and incorporated into disaturated PtdCho (DSPtdCho) in pre-type II cells. Maternal administration of VLDL with heparin increased DSPtdCho content in cells by 45% compared with control ( P < 0.05). VLDL produced a dose-dependent, saturable, and selective increase in CCT activity. VLDL did not significantly alter immunoreactive CCT content but increased palmitic, stearic, and oleic acids in pre-type II cells. Furthermore, hypertriglyceridemic apolipoprotein E knockout mice contained significantly greater levels of DSPtdCho content in alveolar lavage and CCT activity compared with either LDL receptor knockout mice or wild-type controls that have normal serum triglycerides. Thus the nutritional or genetic modulation of serum VLDL-triglycerides provides specific fatty acids that stimulate PtdCho synthesis and CCT activity thereby increasing surfactant content.


1980 ◽  
Vol 187 (3) ◽  
pp. 851-856 ◽  
Author(s):  
G Vallette ◽  
C Benassayag ◽  
L Savu ◽  
J Delorme ◽  
E A Nunez ◽  
...  

The novel endogenous serum ligands of rat alpha 1-foetoprotein previously demonstrated in different mammalian sera were identified by g.l.c.–mass-spectrometric methods as a mixture of non-esterified long-chain and predominantly unsaturated fatty acids. Detailed comparative analyses of these ligands extracted from foetal- and pregnant-rat sera, rat amniotic fluid and foetal human sera are presented. We also show that an important fraction of these ligands remains associated with the rat alpha 1-foetoprotein after purification; analyses are given for the composition of this lipid moiety of the foetoprotein. The physiological relevance of these results is discussed.


1992 ◽  
Vol 70 (4) ◽  
pp. 491-500 ◽  
Author(s):  
Nicholas Sperelakis ◽  
Yoshihito Inoue ◽  
Yusuke Ohya

Smooth muscle cells normally do not possess fast Na+ channels, but inward current is carried through two types of Ca2+ channels: slow (L type) Ca2+ channels and fast (T type) Ca2+ channels. Whole-cell voltage clamp was done on single smooth muscle cells isolated from the longitudinal layer of the 18-day pregnant rat uterus. Depolarizing pulses, applied from a holding potential of −90 mV, evoked two types of inward current, fast and slow. The fast inward current decayed within 30 ms, depended on [Na]o, and was inhibited by tetrodotoxin (TTX) (K0.5 = 27 nM). The slow inward current decayed slowly, was dependent on [Ca]o (or Ba2+), and was inhibited by nifedipine. These results suggest that the fast inward current is a fast Na+ channel current and that the slow inward current is a Ca2+ slow channel current. A fast-inactivating Ca2+ channel current was not evident. We conclude that the ion channels that generate inward currents in pregnant rat uterine cells are TTX-sensitive fast Na+ channels and dihydropyridine-sensitive slow Ca2+ channels. The number of fast Na+ channels increased during gestation. The averaged current density increased from 0 on day 5, to 0.19 on day 9, to 0.56 on day 14, to 0.90 on day 18, and to 0.86 pA/pF on day 21. This almost linear increase occurs because of an increase in the fraction of cells that possess fast Na+ channels. The Ca2+ channel current density was also higher during the latter half of gestation. These results indicate that the fast Na+ channels and Ca2+ slow channels in myometrium become more numerous as term approaches, and we suggest that the fast Na+ current may be involved in spread of excitation. Isoproterenol (β-agonist) did not affect either ICa(s) or INa(f), whereas Mg2+ (K0.5 = 12 mM) and nifedipine (K0.5 = 3.3 nM) depressed ICa(s). Oxytocin had no effect on INa(f) and actually depressed ICa(s) to a small extent. Therefore, the tocolytic action of β-agonists cannot be explained by an inhibition of ICa(s), whereas that of Mg2+ can be so explained. The stimulating action of oxytocin on uterine contractions cannot be explained by a stimulation of ICa(s).Key words: sodium current, fast sodium current, calcium currents, myometrial smooth muscle cells, pregnant uterine muscle.


Sign in / Sign up

Export Citation Format

Share Document