DEVELOPMENTAL-CHANGES IN GASTRIC FUNDUS SMOOTH-MUSCLE CONTRACTILITY AND INVOLVEMENT OF EXTRACELLULAR CALCIUM IN FETAL AND ADULT GUINEA-PIGS

Citation
Da. Paul et al., DEVELOPMENTAL-CHANGES IN GASTRIC FUNDUS SMOOTH-MUSCLE CONTRACTILITY AND INVOLVEMENT OF EXTRACELLULAR CALCIUM IN FETAL AND ADULT GUINEA-PIGS, Pediatric research, 36(5), 1994, pp. 642-646
Citations number
16
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00313998
Volume
36
Issue
5
Year of publication
1994
Pages
642 - 646
Database
ISI
SICI code
0031-3998(1994)36:5<642:DIGFSC>2.0.ZU;2-L
Abstract
Delayed gastric emptying is a common problem in preterm infants. The f actors underlying this gastroparesis remain unsettled but may involve immaturity of smooth muscle contraction. The present study was designe d to test this hypothesis. Muscle strips from the gastric fundus of fe tal and adult guinea pigs were studied in vitro for their contractile response to receptor activation (acetylcholine and bethanechol) and me mbrane depolarization (potassium chloride). The dose-response curves w ere analyzed for differences in active force development (kg/cm(2)). T he role of extracellular calcium (Ca2+) in the contractile responses w as determined by contracting the tissues in a zero-Ca2+ physiologic sa line solution and in the presence of nifedipine, a voltage-dependent C a2+ channel blocker. The results demonstrate the following: 1) tissues from adult animals developed significantly more active force when tes ted with acetylcholine, bethanechol, and potassium chloride; 2) tissue s from the fetal animals were relatively unresponsive to contraction w ith potassium chloride compared with the adult; and 3) both nifedipine and incubation in a zero-Ca2+ physiologic saline solution had a signi ficantly greater inhibitory effect on the contractions of adult than f etal muscle strips. Our data indicate that smooth muscle in the gastri c fundus develops increasing force with maturation. The increased cont ractility in the adult fundus appears to be due to an increased involv ement of extracellular calcium influx, in part through voltage-depende nt Ca2+ channels.