Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

Abstract: Angiotensin II (AII) binds to specific receptors in the lactotroph and stimulates PRL secretion from isolated rat pituitary cells. Since estrogens exert major regulatory actions on PRL secretion, the effects of estradiol (E2) on pituitary AII receptors and PRL responses were studied in vivo and in cultured rat anterior pituitary cells. In female rats, treatment with E2-containing Silastic capsules for 4 days caused a significant increase in PRA from 1.3 to 3 ng/ml X min and a 38% decrease in the binding of [125I]AII to anterior pituitary membrane-rich fractions (P less than 0.01). In vitro studies showed that treatment of cultured anterior pituitary cells with 1 nM E2 for 4 days caused a 57 +/- 6% decrease in AII receptor concentration with no change in binding affinity. Reduction of AII receptors by E2 in 4-day cultures was dose dependent and was demonstrable with E2 concentrations that occur in plasma during the estrous cycle (0.01-1 nM). The decrease in AII receptors in cells incubated with 1 nM E2 was near maximum after 24 h of culture, and results were similar when receptor concentrations were calculated per unit protein or per cell. Despite the substantial decrease in AII receptors, E2 treatment did not specifically decrease the responsiveness of the pituitary cells to AII stimulation. Thus, PRL responses to AII (10 nM) or TRH (100 nM) were unchanged after 1 day of E2 treatment and were increased after 4 days of treatment. These findings demonstrate that E2 has a direct inhibitory action on expression of pituitary AII receptors that is not accompanied by a decrease in AII-stimulated PRL secretion. In the rat pituitary, estrogen modulation of postreceptor events is the predominant determinant of lactotroph responsiveness during stimulation of PRL release by AII.
Effects of 17 beta-estradiol on angiotensin II receptors and prolactin release in cultured pituitary cells.

Abstract: To test the hypothesis that occlusive apneas result from sleep-induced periodic breathing in association with some degree of upper airway compromise, periodic breathing was induced during non-rapid-eye-movement (NREM) sleep by administering hypoxic gas mixtures with and without applied external inspiratory resistance (9 cmH2O X l-1 X s) in five normal male volunteers. In addition to standard polysomnography for sleep staging and respiratory pattern monitoring, esophageal pressure, tidal volume (VT), and airflow were measured via an esophageal catheter and pneumotachograph, respectively, with the latter attached to a tight-fitting face mask, allowing calculation of total pulmonary system resistance (Rp). During stage I/II NREM sleep minimal period breathing was evident in two of the subjects; however, in four subjects during hypoxia and/or relief from hypoxia, with and without added resistance, pronounced periodic breathing developed with waxing and waning of VT, sometimes with apneic phases. Resistive loading without hypoxia did not cause periodicity. At the nadir of periodic changes in VT, Rp was usually at its highest and there was a significant linear relationship between Rp and 1/VT, indicating the development of obstructive hypopneas. In one subject without added resistance and in the same subject and in another during resistive loading, upper airway obstruction at the nadir of the periodic fluctuations in VT was observed. We conclude that periodic breathing resulting in periodic diminution of upper airway muscle activity is associated with increased upper airway resistance that predisposes upper airways to collapse.
Induction of periodic breathing during sleep causes upper airway obstruction in humans.

Abstract: To examine the gastric emptying characteristics of selected test drinks varying in carbohydrate composition and concentration, twenty-five runners ingested 400 ml of a solution in one or more of a series of trials followed by either 15 min seated rest or 15 min running (50 to 70% VO2 max). The solutions tested at rest included water, 5.0% maltodextrin, 3.0% maltodextrin + 2% glucose (MG5.0), and 4.5% maltodextrin + 2.6% fructose (MF7.1). Solutions tested during running included water, MG5.0, MF7.1, 5.5% maltodextrin + 2% glucose, and 5.5% maltodextrin + 2% fructose. At rest and during running, water emptied significantly (P less than 0.5) faster than all other drinks. In the running trials, the volume of gastric residue of 5.5% maltodextrin + 2% fructose (221.7 +/- 11.0 ml) was significantly greater than water (103.4 +/- 19.0 ml), MG5.0 (153.3 +/- 16.8 ml), and MF7.1 (167.3 +/- 14.8), suggesting an inhibitory role of glucose on gastric emptying. Running resulted in a significantly lower volume of gastric residue of water, MG5.0, and MF7.1 (103.4 +/- 19.0, 153.3 +/- 16.8, and 167.3 +/- 14.8 ml, respectively) as compared to the corresponding drinks at rest (209.3 +/- 12.6, 287.7 +/- 16.0, and 271.0 +/- 17.8 ml, respectively). These results suggest a possible advantage for including maltodextrin and fructose as carbohydrate sources in athletic drinks. Furthermore, the rate of gastric emptying is enhanced while running, possibly due to increased mechanical movement of fluid within the stomach.
Effects of exercise and carbohydrate composition on gastric emptying.