This study showed a decreased gastric emptying rate after blockage of the oxytocin receptors, whereas a pharmacological dosage of oxytocin did not affect the emptying rate. We have earlier described how oxytocin is released in response to a fatty meal in healthy women (1.0 ± 0.17 basally compared to 1.3 ± 0.26 pmol/l postprandially, p = 0.02)  and in patients with diabetes mellitus of both sexes (208.1 ± 148.7 basally compared to 250.6 ± 166.9 pg/ml postprandially, p = 0.02) [Ohlsson et al, unpublished observation], why it can be assumed that oxytocin release is induced also after intake of the present meal. By inhibition of the binding of endogenous oxytocin to the oxytocin receptors, the gastric emptying was delayed. As the antral area was reduced at 15 min after atosiban, one may speculate if retention of food in the proximal ventricle may be partly responsible for the delayed emptying rate, or a rapid initial emptying has occurred. The transport of food from the proximal to the distal part of the ventricle may be as important as the transport from the antrum to the duodenum.
The neurophyseal hormones vasopressin and oxytocin are cyclic nonapetides whose actions are mediated by stimulation of specific G protein-coupled receptors currently classified into V1 – vascular, V2 – renal and V3 – pituitary vasopressin receptors and oxytocin receptors. Vasopressin is the ligand having the highest affinity for the human V-receptors, while oxytocin is the ligand with the highest affinity for the oxytocin receptor. However, there is cross-reactivity of the ligands to the receptors .
Atosiban is an analogue of oxytocin and has been rationally designed to compete with endogenous oxytocin at myometrial and decidual oxytocin receptors. Clinical studies have revealed that atosiban is an effective and safe tocolytic agent . However, atosiban has an equal, if not a greater, affinity for vasopressin receptors compared with oxytocin receptors due to their close chemical homology [7, 8]. Furthermore, an additional intracellular process may be attributed as atosiban has been shown to dose-dependently inhibit oxytocin-induced second messengers [13, 14]. This intracellular inhibition was stronger against oxytocin than against vasopressin . No pure oxytocin receptor antagonist is available for clinical use, and may be very difficult to develop.
Thus, we cannot know that the inhibitory effect of atosiban on the gastric emptying is mediated exclusively through oxytocin receptors. The effects observed due to inhibition of endogenous oxytocin to oxyocin/vasopressin receptors by atosiban may theoretically be due to inhibition of endogenous vasopressin as well. However, the effect of vasopressin on the GI tract is only rudimentary examined, and we do not know if vasopressin is released in response to a meal. The expression of vasopressin receptors in the human GI tract has never been studied to our knowledge, although studies have shown the expression of vasopressin in gastric and duodenal cells in the rat . Vasopressin has been shown to influence gastric motility in women . One study  has shown that vasopressin increases the colonic peristalsis in a way similar to oxytocin . The precise mechanism for the action of atosiban in the GI tract has thus to be further evaluated. It remains to settle to what extent oxytocin, and to what extent vasopressin is involved in the regulation of GI motility. In the obstetrics, where atosiban has been developed as a tocolytic drug, this is not a problem as an increased expression of oxytocin receptors but not vasopressin receptors is found in the uterus during labour .
Earlier studies in man have shown that oxytocin improves gastric emptying [3, 4]. However, oxytocin in our present study failed to improve the emptying rate. This may depend on the dosage of the peptide. The reason for choosing this dosage was that this was the highest dosage recommended by the drug company. Further, this dosage has in an earlier dose-response study been shown to stimulate colonic peristalsis . It is a well-known phenomenon that stimulation of a receptor in increasing dosages may show a bell-shaped response [20, 21], explaining divergent effects of the same dosage depending on the receptor affinity and/or amount at different sites of the GI tract. Oxytocin may be of importance for the gastric emptying during physiological conditions, although not our actual pharmacological dosage was. The test meal per se may have given a high enough endogenous oxytocin secretion. Stimulation by our modest pharmacological dosage of oxytocin during these circumstances may be of no further benefit. Furthermore, the oxytocin receptor mRNA found  may be involved in regulation of slow waves, mixing movements and liquid emptying, effects not possible to be detected by this method. The actual method measured the gastric volume at two different time points, and thereby could the gastric emptying rate be calculated, but the gastric emptying process is not studied in detail.
Petring  used dosages of 0.33 U oxytocin/min in altogether 30 min, which should be compared to our dosage of 40 mU oxytocin/min. The dosages used by Hashmonai et al  to treat gastric atony were in the range of 20–80 mU/min, but lasted for three days. Although oxytocin has an effect on dysmotility in these dosages on an empty stomach, it is not clear that it might have any effects with the same dosages in healthy volunteers after a meal.
In contrast to the above findings in human, the motility in the rat stomach was inhibited by oxytocin [21, 22]. We haven't been able to identify any oxytocin receptors in the rat GI tract (Ohlsson et al, unpublished observation). This might explain why the effects evoked by oxytocin on gastric and intestinal motility in rat are mediated by release of cholcystokinin (CCK) (which inhibits gastric emptying) and CCK receptors, and differ from oxytocin effects evoked in human [21, 22].
This study has some limitations. Only one dosage of oxytocin was examined. This was a pilote trial, and it is difficult to examine the same subjects more than three times. Before planning next study, the optimal dosage of oxytocin for gastric motility must be titrated. So far, the interest for vasopressin has been modest, but after the present results also vasopressin will be further evaluated. However, before examining the effect of vasopressin on human GI tract, we have to examine if the receptors are present, and if there is a postprandial vasopressin response.