Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “intercept”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,405 records · Page 78Linked to original sources

Derivation of a new formula for calculating urinary electrolyte-free water clearance based on the Edelman equation.

In evaluating the renal mechanisms responsible for the generation of the dysnatremias, an analysis of free water clearance (FWC) and electrolyte-free water clearance (EFWC) is often utilized to characterize the rate of urinary free water excretion in these disorders. Previous analyses of FWC and EFWC have failed to consider the relationship among plasma water Na(+) concentration ([Na(+)](pw)), total exchangeable Na(+) (Na(e)), total exchangeable K(+) (K(e)), and total body water (TBW); (Edelman IS, Leibman J, O'Meara MP, and Birkenfeld LW. J Clin Invest 37: 1236-1256, 1958). In their derivations, the classic FWC and EFWC formulas fail to consider the quantitative and physiological significance of the slope and y-intercept in this equation. Consequently, previous EFWC formulas incorrectly assume that urine is isonatric when [Na(+) + K(+)](urine) = [Na(+)](p) or [Na(+) + K(+)](urine) = [Na(+)](p) + [K(+)](p) (where [Na(+)](p) and [K(+)](p) represent plasma Na(+) and K(+) concentrations, respectively). Moreover, previous formulas cannot be utilized in the setting of hyperglycemia. In this article, we have derived a new formula termed modified electrolyte-free water clearance (MEFWC) for determining the electrolyte-free water clearance, taking into consideration the empirical relationship between the [Na(+)](pw) and Na(e), K(e), and TBW: MEFWC = V [1 - 1.03[Na(+) + K(+)](urine)/([Na(+)](p) + 23.8)]. MEFWC, unlike previous formulas, is derived based on the requirement of the Edelman equation that urine is isonatric only when [Na(+) + K(+)](urine) = (Na(e) + K(e))/TBW = 0.97[Na(+)](p) + 23.1. Furthermore, since we have shown that the y-intercept in the Edelman equation varies directly with the plasma glucose concentration, in patients with hyperglycemia, MEFWC = V [1 - 1.03[Na(+) + K(+)](urine)/{[Na(+)](p) + 23.8 + (1.6/100)([glucose](p) - 120)}]. The MEFWC formula will be especially useful in assessing the renal contribution to the generation of the dysnatremias.

Animals↗

Diffusive transport of solute in the rat medullary microcirculation.

Outer medullary descending vasa recta (OMDVR) permeability to sodium (PNa) is much lower than to urea (Purea). Based on these findings, we hypothesized that sodium and urea diffuse across the OMDFR wall by separate routes. To further test this, we simultaneously perfused OMDVR with 22Na and 36Cl, [14C]urea, [3H]raffinose, or tritiated water. The permeability of OMDVR to 22Na and [3H]raffinose was found to increase markedly and reversibly with perfusion rate. PNa was highly correlated with the permeability to Cl (PCl) and to [3H]raffinose (Praf) (R = 0.90 and 0.95, respectively) but not with Purea (R = 0.23). Praf was also correlated with inulin permeability (PIn) (R = 0.93). The intercepts for the regressions of PNa with PCl and Praf and for Praf with PIn were zero. In contrast, OMDVR with low PNa retained very high diffusional water permeability (PD) and Purea, a finding consistent with separate routes for permeation of those tracers. We previously established that thiourea is a competitive inhibitor of OMDVR urea transport. In the presence of 100 mM thiourea, OMDVR PNa and Purea were correlated (R = 0.71) but retained an intercept much > 0. We conclude that Na, Cl, raffinose, and inulin are likely to traverse the OMDVR wall through a common pathway, whereas specific mechanisms exist to regulate the permeation by urea and water.

Animals↗

A simple, nonradioactive method for evaluating single-nephron filtration rate using FITC-inulin.

The determination of inulin concentration in nanoliter fluid samples is fundamental to micropuncture investigations of renal function, and this is generally accomplished through the use of radioisotopes. We report here a simple and reliable alternative to the use of radioisotopes that employs FITC-labeled inulin. Samples containing FITC-inulin are stored between oil columns in constant-bore microcapillary tubes, which are then used as cuvettes to determine fluorescence on a microscope fluorometer. Standard curves were generated and found to be linear, with correlation coefficients (R) exceeding 0.99 in every case. Although the fluorescence of FITC-inulin was found to be pH dependent, the pH and fluorescence of each 20- to 40-nl sample could be normalized by the addition of 1 nl of 0.5 M HEPES at pH 7.5. In mice prepared for standard micropuncture, simultaneous measurements of tubular fluid-to-plasma ratios (TF/P) using FITC-inulin and [125I]iothalamate were highly correlated (slope = 0.95, y-intercept = 0.01, R = 0.942), as were whole kidney measurements of glomerular filtration rate (GFR) (slope = 1.25, y-intercept = -53.5 microliter/min, R = 0.99). Micropuncture determinations of late-proximal samples from mice before and after treatment with acetazolamide showed expected changes: TF/P of FITC-inulin decreased from 1.89 +/- 0.07 to 1.48 +/- 0.10; single-nephron GFR (SNGFR) decreased from 9.64 +/- 1.1 to 6.65 +/- 1. 0 nl/min; and fractional fluid reabsorption decreased from 45.3 +/- 1.9 to 26.8 +/- 5.2%. Measurements of TF/P of FITC-inulin, volume, and SNGFR using this technique were stable for at least 2 wk when samples were stored in the dark at 4 degreesC. These data demonstrate that this simple method for determining inulin clearance represents a viable and accurate alternative to radioactive methods. This approach has the added benefits of being relatively inexpensive and leaving the micropuncture sample intact.

Absorption↗

Effects of specific muscle training on VO2 on-response and early blood lactate.

The relationship between half time of the O2 uptake on-response (t1/2 VO2on, seconds) and early blood lactate accumulation (delta Lab, mmol.1(-1) at the onset of submaximal arm and/or leg exercise was the object of a cross-sectional study of sedentary subjects (S,n = 3), and kayakers (K, n = 8), and of a longitudinal study on 11 untrained subjects of specific arm vs. leg training. In supine arm cranking (W = 125 watts) S had an average t1/2 VO2on of 82 s and a delta Aab of 9.2 mmol.1(-1) compared to 47 +/- 7 s and 4 +/- 1.4 mmol.1(-1), respectively, for K. In longitudinal trainees shorter t1/2 VO2on was accompanied by lower Lab for the trained limbs. Specific limb conditioning in swimmers and runners resulted in shorter t1/2 VO2on. A linear relationship was observed between delta Lab and t1/2 VO2on having an intercept on the time axis at congruent to 20 s and a slope proportional to muscle mass. Trained muscles were grouped closest to the intercept indicating local acceleration of the rate of O2 transfer approaching the t1/2 VO2on for isolated perfused muscle at the onset of work. Since t1/2 VO2on, we conclude that factors distal to the capillary are specifically involved in the local training response.

Adenosine Triphosphate↗

Rebreathing techniques for pulmonary capillary blood flow and tissue volume.

The variability of three methods of calculating pulmonary capillary blood flow (Qc) and pulmonary tissue plus capillary blood volume (Vt) during rebreathing was assessed in normal humans by using as markers acetylene, ethyl iodide, and dimethyl ether. The methods of analysis were as follows. Method I, the timing of the disappearance curves of the soluble gases was corrected by assuming that the C18O-disappearance curve intercepted at unity at time O. Method II, it was assumed that the acetylene Qc calculated by method I was correct; ethyl iodide and dimethyl ether Vt were solved by an equation using the disappearance slopes of these gases and the acetylene Qc value, thereby avoiding dependence on extrapolated intercept values. Method III, Vt was calculated by solving for a unique value of Qc between pairs of disappearance slopes of acetylene and dimethyl ether, acetylene and ethyl iodide, and ethyl iodide and dimethyl ether. Among the three methods, method I gave the most reproducible values for Vt as determined with acetylene or dimethyl ether. Using method I, both acetylene and dimethyl ether were equally acceptable gases for measurement of Vt; acetylene was a better marker for Qc measurements.

Adult↗

In vivo evaluation of transcutaneous CO2 partial pressure monitoring.

Correlation between transcutaneous and arterial CO2 partial pressure (Ptcco2, and Paco2) under normal and hemorrhagic shock conditions was evaluated in rabbits. Under normal conditions the Paco2-to-Ptcco2 least-squares regression line had a slope of 1.03 an intercept of 4.57 Torr, and a root mean variance of +/- 3.79 Torr. Under hemorrhagic shock conditions the slope remained similar, but the intercept increased, producing a significant difference between arterial and transcutaneous values. The correlation line shifts to the left so that, for a given Paco2, the Ptcco2 value increases. The transcutaneous response time (90%) under conditions produced by breathing 10% CO2 lagged 2.8 +/- 1.4 min behind that of the breathing 10% CO2 lagged 2.8 +/- 1.4 min behind that of the Paco2. The difference between transcutaneous and arterial CO2 observed during hemorrhagic shock and the lag in transcutaneous response time can be altered by topical application of dimethyl sulfoxide, by altering both flow and permeability. These results indicate that good Ptcco2-to-Paco2 correlation exists under normal conditions and that hemorrhagic shock will produce tissue CO2 accumulation and therefore higher than arterial Ptcco2 values.

Animals↗

Relationship between CO and transit times for dye and thermal indicators in central circulation.

We investigated two factors that may influence the estimation of lung water by the thermal-dye double-indicator-dilution method: 1) changes in cardiac output (CO), and 2) thermal equilibration with cardiac tissue. In theory, the difference between mean transit times of thermal and dye indicators (delta MTT) is proportional to the extravascular volume of distribution of the thermal indicator (VODev) and inversely related to CO. The delta MTT also includes a time element DT due to the difference in response times of the measuring instruments such that delta MTT = VODev/CO + DT. In nine anesthetized dogs we recorded 286 aortic thermal and dye curves following left atrial (LA) and right atrial (RA) injections as CO was increased from 2.35 to 6.65 ml X s-1 X kg-1 by isoproterenol infusion, and a regression of delta MTT on CO-1 was performed. DT was measured in vitro for comparison with the y-intercept. In six of nine dogs the slope of the regression for LA injections was not different from zero, indicating that there is no measurable volume of distribution for thermal indicator in cardiac tissue. For RA injections the relationship between delta MTT and CO-1 was linear in all experiments, with an average correlation coefficient of 0.97 +/- 0.01 (SE), indicating that the VODev was constant over a threefold increase in CO. Although the in vitro measurement of DT agreed closely with the average of the y-intercepts of the regressions, small between-subject differences in DT can lead to apparent flow-related changes in extravascular thermal volume computed in the conventional fashion using the in vitro estimate of DT.

Animals↗

Estimation of response curves in closed-loop physiological control.

Several recent reports have addressed the problem of estimating the response slope from repeated measurements of paired data when both stimulus and response variables are subject to biological variability. These earlier approaches suffer from several drawbacks: useful information about the relationships between the error components in a closed-loop system is not fully utilized; the response intercept cannot be directly estimated; and the normalization procedure required in some methods may fail under certain circumstances. This paper proposes a new, general method of simultaneously estimating the response slope and intercept from corrupted stimulus-response data when the errors in both variables are specifically related by the system structure. A direct extension of the least-squares approach, this method [directed least squares (DLS)] reduces to ordinary least-squares methods when either of the measured variables is error free and to the reduced-major-axis (RMA) method of Kermack and Haldane (Biometrics 37: 30-41, 1950) when the magnitudes of the normalized errors are equal. The DLS estimators are scale invariant, statistically unbiased and always assume the minimum variance. With simple modifications, the method is also applicable to paired data. If, however, the relation between error components is uncertain, then the RMA method is optimal, i.e., having the least possible asymptotic bias and variance. These results are illustrated by using various types of closed-loop respiratory response data.

Animals↗

Distribution of pulmonary vascular resistance in experimental fibrosis.

To elucidate mechanisms of pulmonary hypertension in interstitial fibrosis, we compared the left lower lobes (LLL) of six dogs in which fibrosis was induced by radiation and bleomycin with the normal right lower lobes (RLL) for 1) slope and intercept of the vascular pressure-flow (P-Q) curves, 2) segmental resistances with arterial and venous occlusion under base-line conditions, after serotonin and vasodilators, and 3) light-microscopic morphology and morphometry. We found that 1) the total volume and vascular compliance of the fibrotic LLL were five and four times less, respectively, than controls, 2) the slope and intercept of the P-Q curves in the LLL were 154.0 +/- 65.8 (SE) mmHg.l-1.min-1 and 8.2 +/- 1.5 mmHg, respectively, compared with 18.3 +/- 2.3 and 3.2 +/- 0.9 for the RLL, 3) the resistance of the arterial, middle, and venous segments in the LLL were higher than in the RLL, but middle segment resistance rose disproportionately, and 4) constriction of the arterial segment with serotonin was similar in LLL and RLL, and vasodilators were ineffective. Histologically, fibrosis involved 36% of the lung, and the capillary bed was severely obliterated. Arteries showed an increased percentage of medial and intimal thickening and peripheral muscularization; venous abnormalities were less marked. We conclude that pulmonary fibrosis increases vascular resistance mainly in the middle segment, largely by loss of tissue and obliteration of the microvasculature.

Animals↗

Nature of pulmonary hypertension in canine oleic acid pulmonary edema.

It has recently been suggested that pulmonary hypertension secondary to oleic acid lung injury mainly results from an increase in the critical closing pressure of the pulmonary vessels [Boiteau et al., Am. J. Physiol. 251 (Heart Circ. Physiol. 20): H1163-H1170, 1986]. To further test this hypothesis, we studied 1) the pulmonary arterial pressure- (Ppa) flow (Q) relationship with left atrial pressure (Pla) kept constant (n = 7) and 2) the Ppa-Pla relationship with Q kept constant (n = 9) in intact anesthetized and ventilated dogs before and after lung injury induced by oleic acid (0.09 ml/kg iv). Q was manipulated by use of a femoral arteriovenous bypass and a balloon catheter inserted in the inferior vena cava. Pla was manipulated with a balloon catheter placed by thoracotomy in the left atrium. Ppa-Q plots were rectilinear before as well as after oleic acid. Before oleic acid, the extrapolated pressure intercept of the Ppa-Q plots approximated Pla. Oleic acid administration resulted in a parallel shift of the Ppa-Q plots to higher pressure; i.e., the pressure intercept increased, whereas the slope was not modified. Increasing Pla at constant Q before oleic acid led to a proportional augmentation of Ppa. After oleic acid, however, changes in Pla over the same range affected Ppa only at the highest levels of Pla. These results suggest that oleic acid lung injury increases the critical closing pressure that exceeds Pla, becomes the effective outflow pressure of the pulmonary circulation, and is responsible for the pulmonary hypertension.

Animals↗

Effects of PEEP on pulmonary hemodynamics in intact dogs with oleic acid pulmonary edema.

The effects of positive end-expiratory pressure (PEEP) on the pulmonary circulation were studied in 14 intact anesthetized dogs with oleic acid (OA) lung injury. Transmural (tm) mean pulmonary arterial pressure (Ppa)/cardiac index (Q) plots with transmural left atrial pressure (Pla) kept constant were constructed in seven dogs, and Ppa(tm)/PEEP plots with Q and Pla(tm) kept constant were constructed in seven other dogs. Q was manipulated by using a femoral arteriovenous bypass and a balloon catheter inserted in the inferior vena cava. Pla was manipulated using a balloon catheter placed by thoracotomy in the left atrium. Ppa(tm)/Q plots were essentially linear. Before OA, the linearly extrapolated pressure intercept of the Ppa(tm)/Q relationship approximated Pla(tm). OA (0.09 ml/kg into the right atrium) produced a parallel shift of the Ppa(tm)/Q relationship to higher pressures; i.e., the extrapolated pressure intercept increased while the slope was not modified. After OA, 4 Torr PEEP (5.4 cmH2O) had no effect on the Ppa(tm)/Q relationship and 10 Torr PEEP (13.6 cmH2O) produced a slight, not significant, upward shift of this relationship. Changing PEEP from 0 to 12 Torr (16.3 cmH2O) at constant Q before OA led to an almost linear increase of Ppa(tm) from 14 +/- 1 to 19 +/- 1 mmHg. After OA, Ppa(tm) increased at 0 Torr PEEP but changing PEEP from 0 to 12 Torr did not significantly affect Ppa(tm), which increased from 19 +/- 1 to 20 +/- 1 mmHg. These data suggest that moderate levels of PEEP minimally aggravate the pulmonary hypertension secondary to OA lung injury.

Animals↗

Effects of left atrial pressure on the pulmonary vascular response to hypoxic ventilation.

We investigated the effects of hypoxic ventilation on the pulmonary arterial pressure- (P) flow (Q) relationship in an intact canine preparation. Mean pulmonary P-Q coordinates were obtained during hypoxic ventilation and during ventilation with 100% O2 at normal and at increased left atrial pressure. Specifically, we tested the hypothesis that, over a wide range, changes in left atrial pressure would alter the effects of hypoxic ventilation on pulmonary P-Q characteristics. Seven dogs were studied. When left atrial pressure was normal (5 mmHg), the mean value of the extrapolated intercept (PI) of the linear P-Q relationship was 10.9 mmHg and the slope (incremental vascular resistance, IR) of the P-Q relationship was 2.2 mmHg.l-1.min. Hypoxic ventilation increased PI to 18 mmHg (P less than 0.01) but did not affect IR. Subsequently, during ventilation with 100% O2, when left atrial pressure was increased to 14 mmHg by inflation of left atrial balloon, PI increased to 18 mmHg. IR was 1.6 mmHg.l-1.min. Again, hypoxic ventilation caused an isolated change in PI. Hypoxia increased PI from 18 to 28 mmHg (P less than 0.01). As in the condition of normal left atrial pressure, hypoxic ventilation did not affect IR. We conclude that, in an anesthetized intact canine preparation, hypoxic ventilation causes an isolated increase in the extrapolated pressure intercept of the pulmonary P-Q relationship. Furthermore the effects of hypoxic ventilation on pulmonary P-Q characteristics are not affected by the resting left atrial pressure.

Animals↗

Peripheral pulmonary vascular resistance.

The pressure-flow relationship has been studied in a peripheral portion of the lung vasculature in anesthetized dogs with use of a double-lumen catheter wedged in a distal pulmonary artery. One lumen was used to infuse mixed venous blood in the wedged area and the other to measure the corresponding perfusion pressure. Flow ranged from 0 to 9.2 ml/min, and the mean volume of the wedged area (n = 59) was 0.75 +/- 0.05 (SE) ml. In the areas where the distal pulmonary artery was in the same direction as the catheter ("coaxial"), the mean pressure-flow curve showed a negligible gamma-intercept and no significant difference between ascending and descending flow. The slope of the initial part of the ascending limb (peripheral pulmonary vascular resistance) varied from site to site and did not show a significant correlation with the overall pulmonary vascular resistance; it was inversely correlated with the volume of the wedged area (r = -0.35, P < 0.05) and directly, as expected, correlated with the y-intercept (r = 0.78, P < 0.001) and hysteresis (r = 0.48, P < 0.001). The results of two consecutive pressure-flow runs in the same site showed similar results, with no difference exceeding the error of measurement. In contrast, the slope increased by 71% during hypoxia (fraction of inspired O2 was 0.10, n = 5). This procedure seems suitable to determine the effects of physiological or pharmacological interventions on the pulmonary vessels, without interference of the systemic circulation.

Animals↗

Morphometry of methacholine-induced bronchoconstriction in the rat.

It has been suggested that parenchymal viscoelasticity accounts for a large proportion of resistive pressure losses induced by smooth muscle agonists. We used morphometric methods to evaluate the relative contributions of parenchyma and airways to mechanical changes during methacholine- (MCh) induced bronchoconstriction. We measured tracheal pressure and tidal volume in 17 open-chest mechanically ventilated Sprague-Dawley rats (frequency = 1.5 Hz, tidal volume = 2 ml, positive end-expiratory pressure = 5 cmH2O) after saline (n = 7, C), 16 mg/ml MCh (n = 5, L), and 256 mg/ml MCh (n = 5, H) aerosols. We calculated pulmonary resistance (RL) and elastance (EL) by fitting the equation PL = VRL + VEL + K, where PL is transpulmonary pressure, V is flow, and V is volume. V was obtained numerically from V. Lungs were rapidly frozen in liquid N2 30 s after aerosolization and processed with freeze substitution. Using midsagittal slices of left lung, we measured airway narrowing as the ratio of lumen area (aBM) subtended by the basement membrane perimeter (LBM) to predicted maximal lumen area (ABM = LBM2/4 pi). Air space size was estimated as mean linear intercept (Lm) and parenchymal distortion as standard deviation of linear intercepts (SDi). Lm was increased in L and H animals, reflecting hyperinflation; aBM/ABM in 0.17- to 0.43-mm-diam airways decreased progressively from C to L to H animals, reflecting bronchoconstriction. By use of stepwise multiple linear regression, the contribution of Lm to variance in mechanics was found to consistently exceed or equal that of aBM/ABM. SDi contributed little once Lm was taken into account.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosols↗

Lung tissue distortion in response to methacholine in rats: effect of lung volume.

We have previously shown that, after induced constriction, there is substantial distortion of the parenchymal tissues. In this study we investigated whether differences in parenchymal morphology occurred when the lung was constricted at different lung volumes. We measured tracheal pressure and calculated lung resistance in mechanically ventilated rats under control conditions and after aerosol administration of methacholine (256 mg/ml) at different positive end-expiratory pressures (PEEP = 7, 5, and 3 cmH2O). The lungs were frozen with liquid nitrogen at different PEEP levels and processed via freeze substitution. We measured airway constriction as the ratio of the airway lumen to the ideally relaxed area, alveolar size by measuring the mean linear intercept between alveolar walls, and tissue distortion as the standard deviation of the number of intercepts in the 40 fields sampled per lung. The increase in lung resistance was largest at PEEP = 3 cmH2O. Whereas airway constriction decreased and alveolar size increased at higher lung volume (PEEP = 7 cmH2O), tissue distortion did not change. These data suggest that parenchymal distortion after induced constriction was not attributable to airway narrowing and/or closure.

Aerosols↗

Comparison of techniques for measuring pulse-wave velocity in the rat.

We evaluated methods for measuring average and regional pulse-wave velocity along the full length of the aorta in 18-mo-old ether-anesthetized male spontaneously hypertensive rats. Catheter-tip manometers were placed in the ascending and descending thoracic aorta via the right carotid and left femoral arteries, respectively. As the distal catheter was withdrawn at 1-cm intervals, the relationship between the distal catheter insertion distance and distance between transducers was determined from the intercept of the insertion distance vs. transmission delay regression line. Methods that assessed the foot-to-foot time delay between pressures accurately predicted the separation between catheters (measured distance of 1.43 cm; intercept of 1.40 +/- 0.5 cm; P = not significant) were highly reproducible (coefficient of variation of 2.3% for repeated measurements) and showed minimal variability (range 509 +/- 30 to 600 +/- 29 cm/s) along the full length of the aorta. Methods that made use of the pressure-pressure transfer function were spatially (range of values along the aorta 367 +/- 17 to 722 +/- 39 cm/s) and temporally more variable, especially during vasoconstriction with methoxamine, due to the effects of reflected waves.

Animals↗

Red cell distortion and conceptual basis of diffusing capacity estimates: finite element analysis.

To understand the effects of dynamic shape distortion of red blood cells (RBCs) as it develops under high-flow conditions on the standard physiological and morphometric methods of estimating pulmonary diffusing capacity, we computed the uptake of CO across a two-dimensional geometric capillary model containing a variable number of equally spaced RBCs. RBCs are circular or parachute shaped, with the same perimeter length. Total CO diffusing capacity (DLCO) and membrane diffusing capacity (DMCO) were calculated by a finite element method. DLCO calculated at two levels of alveolar PO2 were used to estimate DMCO by the Roughton-Forster (RF) technique. The same capillary model was subjected to morphometric analysis by the random linear intercept method to obtain morphometric estimates of DMCO. Results show that shape distortion of RBCs significantly reduces capillary diffusive gas uptake. Shape distortion exaggerates the conceptual errors inherent in the RF technique (J. Appl. Physiol. 79: 1039-1047, 1995); errors are exaggerated at a high capillary hematocrit. Shape distortion also introduces additional error in morphometric estimates of DMCO caused by a biased sampling distribution of random linear intercepts; errors are exaggerated at a low capillary hematocrit.

Algorithms↗

Effects of oral contraceptives on body fluid regulation.

To test the hypothesis that estrogen reduces the operating point for osmoregulation of arginine vasopressin (AVP), thirst, and body water balance, we studied nine women (25 +/- 1 yr) during 150 min of dehydrating exercise followed by 180 min of ad libitum rehydration. Subjects were tested six different times, during the early-follicular (twice) and midluteal (twice) menstrual phases and after 4 wk of combined [estradiol-norethindrone (progestin), OC E + P] and 4 wk of norethindrone (progestin only, OC P) oral contraceptive administration, in a randomized crossover design. Basal plasma osmolality (P(osm)) was lower in the luteal phase (281 +/- 1 mosmol/kgH(2)O, combined means, P < 0.05), OC E + P (281 +/- 1 mosmol/kgH(2)O, P < 0.05), and OC P (282 +/- 1 mosmol/kgH(2)O, P < 0. 05) than in the follicular phase (286 +/- 1 mosmol/kgH(2)O, combined means). High plasma estradiol concentration lowered the P(osm) threshold for AVP release during the luteal phase and during OC E + P [x-intercepts, 282 +/- 2, 278 +/- 2, 276 +/- 2, and 280 +/- 2 mosmol/kgH(2)O, for follicular, luteal (combined means), OC E + P, and OC P, respectively; P < 0.05, luteal phase and OC E + P vs. follicular phase] during exercise dehydration, and 17beta-estradiol administration lowered the P(osm) threshold for thirst stimulation [x-intercepts, 280 +/- 2, 279 +/- 2, 276 +/- 2, and 280 +/- 2 mosmol/kgH(2)O for follicular, luteal, OC E + P, and OC P, respectively; P < 0.05, OC E + P vs. follicular phase], without affecting body fluid balance. When plasma 17beta-estradiol concentration was high, P(osm) was low throughout rest, exercise, and rehydration, but plasma arginine vasopressin concentration, thirst, and body fluid retention were unchanged, indicating a lowering of the osmotic operating point for body fluid regulation.

Adult↗