Treatment of pregnant women with asymptomatic trichomoniasis does not prevent preterm delivery. Routine screening and treatment of asymptomatic pregnant women for this condition cannot be recommended.

Osmoregulation was studied in eight women during late pregnancy and again 8-10 wk postpartum. Base-line plasma osmolality (Posmol) was significantly lower during (280.9 +/- 2.1 mosmol/kg, SD) than after (289.4 +/- 2.1 mosmol/kg) pregnancy yet 24-h urinary volume and plasma arginine vasopressin (PAVP) measured in vasopressinase-inactivated blood was similar in both groups (pregnancy, 1.39 +/- 0.56 pg/ml; postpartum, 1.25 +/- 0.62 pg/ml). After 12 h of dehydration PAVP rose similarly and significantly both during (2.25 +/- 0.81 pg/ml) and after (2.89 +/- 1.19 pg/ml) gestation, and Uosmol was similar on both occasions (pregnancy, 779 +/- 121 mosmol/kg; postpartum, 784 +/- 102 mosmol/kg). When Posmol was increased by the slow infusion of 5% saline PAVP increased as soon as body tonicity did both during and after pregnancy. PAVP correlated significantly with Posmol in each subject (range of r, 0.75-0.99) and the mean regression lines [pregnancy, PAVP = 0.32 (Posmol; -279), r = 0.79; postpartum, PAVP = 0.38 (Posmol, -285), r = 0.86] demonstrated that the apparent osmotic threshold for AVP secretion was 6 mosmol/kg lower during than after gestation. Similarly the Posmol at which the subject experienced a conscious desire to drink was lower in pregnant (287 +/- 1.6 mosmol/kg) compared with postpartum subjects (298 +/- 2.0 mosmol/kg; P less than 0.001). These data demonstrate decreased osmotic thresholds for AVP release and thirst during human pregnancy and explain why gravidas can maintain their new lower Posmol within narrow limits.

The vascular pathophysiology of preeclampsia, a hypertensive disorder unique to human pregnancy, has been postulated to be due to endothelial dysfunction, primarily manifest as deficient nitric oxide (NO) synthesis. We evaluated contraction (KCl and arginine vasopressin [AVP]) and dilation (acetylcholine and bradykinin) in small resistance-size omental arteries obtained during surgery from women with preeclampsia, postulating that these vessels would exhibit augmented contraction and diminished endothelium-dependent relaxation, most likely due to decreased NO synthesis. For comparison, vessels were also obtained from normotensive gravidas, pregnant women with chronic hypertension, or with chronic hypertension and superimposed preeclampsia, as well as from premenopausal nonpregnant controls. Vessels of approximately 200 micron in internal diameter were studied in vitro using a Mulvany-Halpern myograph. Maximal contraction due to either KCl or AVP was significantly augmented in vessels from women with preeclampsia; these vessels all exhibited endothelium- and cyclooxygenase-dependent phasic oscillations while vessels from all other groups exhibited only tonic contractions. Acetylcholine and bradykinin both led to dose- and endothelium-dependent relaxation which was unaffected by inhibitors of NO synthesis. Responses to bradykinin were similar in vessels from normal pregnant and preeclamptic women while those to acetylcholine were absent in vessels from women with preeclampsia. These data suggest specific defects in resistance-artery endothelium from women with preeclampsia.

Effects of sex steroids on osmoregulation were studied in intact and ovariectomized Sprague-Dawley rats treated for 2 wk with subcutaneously implanted hormone pellets containing 0.5 mg 17 beta-estradiol (E2) alone (group 1) or combined with 50 mg progesterone (PG; group 2) and 5.0 mg E2 alone (group 3) combined with PG (group 4). An additional group (5) of animals was given 14 daily injections with 100 micrograms/100 g body weight of E2. Controls for each group received vehicle alone. There were no alterations in basal plasma osmolality (Posmol) or vasopressin (PAVP), except for group 3 in which a small (2.5 mosmol/kg) decrement in Posmol was observed. However, mean PNa was decreased (0.9-3.4 meq/l) in hormone-treated rats, and alterations in Pglucose and/or Purea could not explain the Na-osmolal discrepancy. Intraperitoneal hypertonic saline resulted in stepwise increases in both Posmol and PAVP. Regression analysis of PAVP on Posmol demonstrated similar osmotic thresholds for AVP release in estrogen and control rats, but the slope (sensitivity of the response) was significantly (P less than 0.005) greater in hormone-treated animals. In contrast, the PAVP response to isosmotic volume depletion was not altered by estrogen. The enhanced response to osmotic stimuli could not be explained by alterations in plasma volume or pituitary AVP content and differed from PAVP -Posmol relationships observed by us previously in gravid rats. In other experiments Posmol and PAVP were similar during all stages of the estrus cycle, while Posmol was approximately equal to 10 mosmol/kg lower in 21-day gravid rats. These data demonstrate that, although estradiol has little effect on basal osmoregulation or hemodynamically mediated AVP release, PAVP responses to osmotic stimuli are markedly enhanced. These osmoregulatory effects, however, differ from those observed during rodent gestation.

Metabolic clearance rates (MCR) of arginine vasopressin (AVP) were measured serially in five women starting before conception, during gestational weeks 7-8 (early), 22-24 (middle), and 36-38 (late pregnancy), and again 10-12 wk postpartum. Hormonal disposal rates were determined after water loading to suppress endogenous AVP release using a constant infusion method designed to achieve three different steadystate concentrations of plasma AVP (PAvp) on each test occasion. Dose schedules were altered in mid-and late pregnancy to obtain comparable AVP levels at each stage of the protocol. Prehydration decreased plasma osmolality sufficiently to suppress AVP release, as circulating AVP-neurophysin measured serially in three of the women was undetectable. ( 1-3). Another interesting osmoregulatory change is that the rise in circulating AVP levels provoked by increases in body tonicity (APAVP/APmO1), unaltered early in gestation, is markedly decreased in the third trimester (3). This latter event could represent a reduced secretory response to osmotic stimuli, but might also reflect an increase in hormonal metabolic clearance rates (MCR). Indeed, in a preliminary report we have noted that the MCR are increased fourfold during the third trimester compared with measurements postpartum (4). The present study extends this latter observation. MCR of AVP were measured serially in volunteers, starting before conception, continuing throughout pregnancy, and again 10-12 wk postpartum. This study was designed to determine hormonal disposal rates at three different steady-state plasma concentrations during each test. Furthermore, by manipulating exogenous AVP infusion rates we succeeded in duplicating these levels and were able to compare their influence both on the MCR and urine osmolality (Uosmoi) first before, three times during, and again after pregnancy. Results were also correlated with circulating levels of cystineaminopeptidase (EC 3.4.11.3; vasopressinase), an enzyme recently implicated in the etiology of transient vasopressin-resistant diabetes insipidus (DI) of pregnancy (5). Methods SubjectsSerial studies were performed on five normotensive healthy subjects once before conception, between gestational weeks 7 and 8, 22 and 24, 36 and 38 (designated as early, mid-, and late pregnancy), and again 10-12 wk postpartum, when none were breast feeding or ingesting oral contraceptives. In addition, two women with a single kidney, one subject carrying twins and another triplets, were studied but only in late pregnancy and postpartum. All C) The