Gastric somatostatin (SRIF) regulates gastric acidity by inhibiting gastric acid and gastrin secretion. SRIF secretion is increased by gastric acidity and also directly by regulators of gastric acid secretion such as gastrin. This direct effect has not been described in the developing animal, nor have the roles of intermediaries such as histamine and gastric acidity been defined. The present study aimed to establish the regulatory role of gastrin and histamine during development on SRIF secretion and also to determine whether the effects of gastrin and histamine are independent of gastric pH. Pentagastrin and histamine were infused on separate occasions into fetal sheep, newborn lambs, and 28-day-old lambs. To determine the roles of endogenous histamine and gastric pH, ranitidine (a histamine-2 receptor antagonist) and omeprazole (a H+/K+ ATPase inhibitor) were coinfused with the agonists. Plasma SRIF and gastrin concentrations were measured by RIA. Pentagastrin stimulated SRIF secretion in the fetus after 131 days of gestation (term is 147 days), whereas stimulation by histamine was effective only after birth. The SRIF stimulatory effect of pentagastrin in 28-day-old lambs was abolished by ranitidine, which also reduced this effect in the adult sheep. This inhibitory effect of ranitidine was shown to be a result of blockade of stimulatory H2 receptors, because in the adult blockade of acid secretion with omeprazole failed to attenuate the response of histamine. These results indicate that in the fetus, gastrin receptors, but not histamine receptors, are functionally involved in the stimulation of SRIF secretion. After birth, both gastrin and histamine stimulate SRIF, but the effect of gastrin is mediated at least in part by the release of endogenous histamine. These responses occur independently of changes in gastric acidity, supporting the concept of a direct negative feedback between SRIF and gastrin.
Immunoreactive-endothelin (ir-ET) has previously been detected in human fetal effluents from in vitro perfused placentae. To date however, because of a lack of radio-immunoassay specificity, the ET isoforms in fetal effluents had not been determined, nor had placental maternal effluents been examined for ETs. The aim of this study was to identify the isoforms of ET released into the maternal and fetal circulations of the human in vitro bilaterally perfused placenta. Both circulations of placentae, obtained after normal vaginal delivery, were perfused with a modified Krebs solution and maternal and fetal effluents from the start of the second hour of perfusion were collected, extracted on Scp-pak C18 cartridges, concentrated by vacuum evaporation and separated by reverse-phase HPLC separation. HPLC fractions were measured by ET-RIA and compared to known synthetic standards. Maternal and fetal effluents contained ET-1 (natural and oxidised ET-1), ET-2 and ET-3 (n = 5). Maternal and fetal release of ET-1 was 2.2 +/- 0.7 and 1.4 +/- 0.1 fmol/min/g wet weight of tissue respectively, ET-2 was 0.4 +/- 0.2 and 0.5 +/- 0.2 and fmol/min/g respectively, and ET-3 was 0.5 +/- 0.2 and 0.7 +/- 0.4 fmol/min/g respectively. There were no significant differences between the release of either ET-1, ET-2 or ET-3 in the maternal or fetal circulations. In conclusion, this study indicated that ET-1, ET-2 and ET-3 were all released into both the maternal and fetal effluents from the in vitro perfused human placenta.
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