Students varied widely in use of coping mechanisms. Over time, students shifted to using emotional strategies more frequently while decreasing their use of active strategies. Coping strategies were unrelated to preclinical academic performance (R = .09, adjusted R = .04, ns) but were related to clinical performance (R = .23, adjusted R = .18, p < .0001), with active coping associated with higher performance and emotional methods associated with lower performance. Insights: Students decreased use of active coping strategies and increased use of emotional coping strategies over time, but emotional strategies were associated with poorer clinical academic performance. These shifts in coping methods may be detrimental to student performance and learning. Improving students' ability to cope should be an educational priority.

Compared with the adult, the neonatal renal natriuretic response to acute volume expansion (VE) is attenuated. To test the hypothesis that antinatriuresis is mediated by endogenous angiotensin I (ANG II), Sprague-Dawley rats were given losartan, an ANG II type 1 (AT1)-receptor inhibitor (40 mg.kg-1.day-1) from birth to 14-17 days. Control littermates received saline vehicle. Anesthetized rats underwent acute saline VE for measurement of mean arterial blood pressure (MAP), plasma aldosterone concentration (Paldo), plasma atrial natriuretic peptide (PANP), glomerular filtration rate (GFR), sodium excretion (UNaV), potassium excretion (UKV), and urine guanosine 3',5'-cyclic monophosphate excretion (UcGMPV). Losartan increased basal urine flow fivefold, UNaV 10-fold, and UKV twofold. Acute VE induced marked diuresis, natriuresis, and kaliuresis in the losartan but not in the saline group. This occurred without change in Paldo and PANP and despite lower MAP, GFR, and UcGMPV. In addition, losartan did not affect release of cGMP from isolated glomeruli stimulated by ANP or sodium nitroprusside. We conclude that the limited renal response to acute VE in the neonate results from stimulation of tubular Na reabsorption by ANG II acting on the AT1 receptor.

Positive sodium balance is necessary for normal somatic growth of the neonate, and the neonatal renal response to volume expansion (VE) is attenuated compared with the adult. To test the hypothesis that dietary sodium modulates the developmental response to VE, preweaned rats were artificially reared with either a normal (25 meq/l)- or high-sodium (145 meq/l) diet for 7-8 days and were compared with adult rats receiving normal or high sodium. Serum sodium concentration remained normal in adults on high sodium, whereas neonates became hypernatremic. Glomerular filtration rate (GFR), urinary flow (V), and urinary sodium (UNaV) were measured before and after acute saline VE (1% body wt). While remaining constant in preweaned rats, GFR increased > 50% in adult rats after VE (P < 0.05). High sodium intake augmented V and UNaV after VE but was not sustained in neonates as in adults. Plasma atrial natriuretic peptide (ANP) and guanosine 3',5'-cyclic monophosphate excretion (UcGMPV) were measured, and baseline UcGMPV was lower in preweaned rats receiving normal sodium but increased to levels similar to adult levels after VE. Postexpansion plasma ANP was higher in preweaned rats than in adult rats and was not affected by dietary sodium regardless of age. We conclude that the attenuated postexpansion natriuresis in the neonate is due in part to an adaptive response to limited sodium intake. However, neonatal compensation to increased sodium intake is incomplete and independent of plasma ANP.

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The neonate conserves sodium avidly, and sodium intake is normally limited to that present in maternal milk. To evaluate the role of atrial natriuretic peptide (ANP) in this adaptation, preweaned rat pups were artificially reared and fed a formula with either normal sodium (25 mEq/L) or high sodium (145 mEq/L) for 7-8 d. To determine whether increased dietary sodium decreases ANP clearance receptor activity, animals were anesthetized, and the plasma ANP concentration (ANPp), urine flow (V), urinary sodium (UNa V), and cGMP excretion (UcGMP V) were measured before and after infusion of ANF(4-23), an ANP clearance receptor inhibitor (C-ANF), at 50 micrograms/kg/ min. Infusion of C-ANF increased ANPp 10-fold in both normal and high sodium groups, but V, UNa V, and UcGMP V increased only in animals receiving the high sodium diet (p < 0.05). Incubation of isolated glomeruli with 0.1 microM ANP increased extracellular cGMP more in high sodium than normal sodium groups (p < 0.05). We conclude that ANP clearance receptors in the neonate are highly activated regardless of sodium intake. Increased dietary sodium increases the renal diuretic and natriuretic response to circulating ANP through enhanced generation of cGMP.