Helping undergraduates repair faulty mental models in the student laboratory.

Over half of the undergraduate students entering physiology hold a misconception concerning how breathing pattern changes when minute ventilation increases. Repair of this misconception was used as a measure to compare the impact of three student laboratory protocols on learning by 696 undergraduate students at 5 institutions. Students were tested for the presence of the misconception before and after performing a laboratory activity in which they measured the effect of exercise on tidal volume and breathing frequency. The first protocol followed a traditional written "observe and record" ("cookbook") format. In the second treatment group, a written protocol asked students to complete a prediction table before running the experiment ("predictor" protocol). Students in the third treatment group were given the written "predictor" protocol but were also required to verbalize their predictions before running the experiment ("instructor intervention" protocol). In each of the three groups, the number of students whose performance improved on the posttest was greater than the number of students who performed less well on the posttest (P < 0.001). Thus the laboratory protocols helped students correct the misconception. However, the remediation rate for students in the "instructor intervention" group was more than twice that observed for the other treatment groups (P < 0.001). The results indicate that laboratory instruction is more effective when students verbalize predictions from their mental models than when they only "discover" the outcome of the experiment.

How accurate are our assumptions about our students' background knowledge?

Teachers establish prerequisites that students must meet before they are permitted to enter their courses. It is expected that having these prerequisites will provide students with the knowledge and skills they will need to successfully learn the course content. Also, the material that the students are expected to have previously learned need not be included in a course. We wanted to determine how accurate instructors' understanding of their students background knowledge actually was. To do this, we wrote a set of multiple-choice questions that could be used to test students' knowledge of concepts deemed to be essential for learning respiratory physiology. Instructors then selected 10 of these questions to be used as a prerequisite knowledge test. The instructors also predicted the performance they expected from the students on each of the questions they had selected. The resulting tests were administered in the first week of each of seven courses. The results of this study demonstrate that instructors are poor judges of what beginning students know. Instructors tended to both underestimate and overestimate students' knowledge by large margins on individual questions. Although on the average they tended to underestimate students' factual knowledge, they overestimated the students' abilities to apply this knowledge. Hence, the validity of decisions that instructors make, predicated on the basis of their students having the prerequisite knowledge that they expect, is open to question.

Pregnancy restores the renal vasodilator response to glycine in Dahl salt-sensitive rats.

To determine if pregnancy alters the impaired renal vasodilator responses in hypertensive Dahl salt-sensitive (Dahl S) rats, we measured glomerular filtration rate and effective renal plasma flow and calculated renal vascular resistance before, during, and after renal vasodilation with glycine (0.17 mmol/kg per minute IV). Conscious, midterm (day 11 to 14) pregnant and age-matched virgin Dahl S and Dahl salt-resistant (Dahl R) rats were fed an 8% NaCl diet for 4 weeks (n = 6 per group). Mean arterial pressure was elevated (P < .05) in Dahl S compared with Dahl R rats, with no significant difference between pregnant and virgin animals in either group. Pregnancy resulted in significant increases in plasma volume, baseline glomerular filtration rate, and renal plasma flow and a significant decrease in renal vascular resistance. The glycine-induced increase in filtration rate in virgin Dahl S rats (27 +/- 4%) was less (P < or = .01) than pregnant Dahl S (60 +/- 4%) and either group of Dahl R (virgin, 43 +/- 3%; pregnant, 45 +/- 5%) rats. Similarly, the 21 +/- 4% increase in renal plasma flow in virgin Dahl S rats was less (P < or = .01) than the pregnant Dahl S (45 +/- 4%) and either pregnant (45 +/- 5%) or virgin (45 +/- 5%) Dahl R rats. Glycine decreased renal vascular resistance only 12 +/- 2% in the virgin Dahl S compared with 31 +/- 3% in the pregnant Dahl S rats and 30 +/- 4% and 28 +/- 3% in pregnant and virgin Dahl R rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Nicotine impairs reflex renal nerve and respiratory activity in deoxycorticosterone acetate-salt rats.

Smoking exacerbates the increase in arterial pressure in hypertension. The effect of nicotine on the baroreceptor-mediated reflex responses of renal nerve activity (RNA), heart rate, and respiratory activity (minute diaphragmatic activity [MDA]) after bolus injections of phenylephrine was compared in deoxycorticosterone acetate (DOCA)-salt sensitive and normotensive rats. Osmotic minipumps that dispensed either nicotine (2.4 mg/kg/day) or saline were implanted in DOCA and normotensive rats for 18 days. Anesthetized DOCA-nicotine, DOCA-saline, control-nicotine, and control-saline rats had mean arterial pressures (MAP) of 117 +/- 3, 110 +/- 9, 90 +/- 3, and 89 +/- 5 mm Hg, respectively. Nicotine decreased the sensitivity (p less than 0.05) of baroreceptor reflex control of RNA (% delta RNA/delta MAP) in the DOCA-nicotine rats (-0.92 +/- 0.08) compared with the DOCA-saline (-1.44 +/- 0.16), control-nicotine (-1.45 +/- 0.08), or control-saline (-1.45 +/- 0.21) rats. The reflex decrease in respiratory activity (% delta MDA/delta MAP x 100) was impaired (p less than 0.01) in both control-nicotine (-24.5 +/- 3.3) and DOCA-nicotine (-18.2 +/- 4.6) rats compared with control-saline (-59.2 +/- 9.1) and DOCA-saline (-52.5 +/- 9.9) rats. The reflex decrease in heart rate (absolute delta HR/delta MAP) in both DOCA-nicotine (1.56 +/- 0.17) and control-nicotine (1.54 +/- 0.24) rats was augmented compared with DOCA-saline and control-saline rats (0.91 +/- 0.12 and 0.97 +/- 0.14).(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium, parathyroid hormone, and vitamin D in the "prehypertensive" Dahl salt-sensitive rat.

The purpose of this study was to determine if alterations of calcium and calcium regulating hormones precede the onset of NaCl-induced hypertension in the Dahl salt-sensitive (S) rat. After a 5-day balance study, serum ionized calcium, parathyroid hormone (PTH), and 1,25-dihydroxy vitamin D concentrations were measured in Dahl-S and salt-resistant (R) rats that had been maintained on a "normal" (1%) or high (7%) NaCl intake. Blood pressure was higher in Dahl-S than Dahl-R (P less than .01), but was not affected by 5 days of high NaCl. On both NaCl intakes, urine calcium excretion was increased, serum calcium was decreased, and serum PTH and 1,25 dihydroxy vitamin D were increased in Dahl-S compared to Dahl-R (P less than .01). On the high NaCl intake, fecal calcium was greater in Dahl-S than in Dahl-R, and net 5-day calcium balance was less positive in Dahl-S (P less than .05). Thus, alterations of calcium, PTH, and vitamin D precede NaCl-induced hypertension in Dahl-S. These alterations may contribute to the development of hypertension in this animal model.

Parasympathetic impairment of baroreflex control of heart rate in Dahl S rats.

To test the hypothesis that impaired baroreflex control of heart rate in Dahl salt-sensitive (S) rats is due to an impairment of the parasympathetic limb of the bradycardic response, baroreflex sensitivity was evaluated in conscious, chronically instrumented Dahl S and salt-resistant (R) animals. Sensitivity was impaired in Dahl S rats when bolus doses of phenylephrine were administered (0.863 +/- 0.042 vs. 1.43 +/- 0.055 ms/mmHg), but it was not different than in R rats when tested with sodium nitroprusside. When the sensitivities before and after blocking the parasympathetic nervous system with atropine were compared, it was revealed that 82% of the reflex bradycardia resulting from bolus doses of phenylephrine was due to the parasympathetic nervous system, whereas the majority (73%) of the bradycardia induced by 5-min infusions of phenylephrine was due to withdrawal of sympathetic tone. Neither baroreflex sensitivity to infusions of phenylephrine (73% sympathetic) or to infusions after atropine (100% sympathetic) were significantly different between S and R rats. Therefore, the impairment of the heart rate reflex in Dahl S rats is due to an impairment of the parasympathetic limb of the response. In addition, a high-salt diet before the development of hypertension did not alter baroreflex sensitivity in either Dahl S or R rats.

Calcium and calcium regulating hormones in the "prehypertensive" Dahl salt sensitive rat (calcium and salt sensitive hypertension).

The purpose of this study was to determine if alterations of calcium and calcium regulating hormones precede the onset of NaCl induced hypertension in the Dahl salt sensitive (S) rat. After a 5 day balance study, serum ionized calcium, PTH, and 1,25 dihydroxy vitamin D concentrations were measured in Dahl-S and salt resistant (R) rats that had been maintained on a "normal" (1%) or high (7%) NaCl intake. Blood pressure was higher in Dahl-S than R (P less than .01), but was not affected by 5 days of high NaCl. On both NaCl intakes, urine calcium excretion was increased, serum calcium was decreased, and serum PTH and 1,25 dihydroxy vitamin D were increased in Dahl-S compared to Dahl-R (P less than .01). On the high NaCl intake, fecal calcium was greater in Dahl-S than in Dahl-R, and net 5 day calcium balance was less positive in Dahl-S (P less than .05). In contrast to NaCl, a high dietary intake of sodium with anions other than chloride (NaAA) fails to produce hypertension in the Dahl-S rat. NaAA loading resulted in decreased urine calcium excretion (P less than .01), and after 5 days of the high NaAA diet, serum calcium and PTH did not differ in Dahl-S and Dahl-R. Thus, alterations of calcium, PTH, and vitamin D precede NaCl-induced hypertension in Dahl-S. These alterations may contribute to the development of hypertension in this animal model.

Effect of salt deprivation on blood pressure in rats.

In most cases blood pressure (BP) is directly related to NaCl intake. In some studies, BP is increased by low salt intake. The effect of Na and Cl deprivation or selective Na deprivation on BP in the normotensive Sprague-Dawley rat was investigated. In study 1, rats were uninephrectomized and fed low NaCl, normal NaCl, or low Na-normal Cl for 3 wk. BP was higher (P less than 0.05) in rats fed low NaCl and low Na-normal Cl than normal NaCl. Plasma renin activity was stimulated by low NaCl intake but was not different between the other two groups. After captopril treatment, BP was lower in the low NaCl group (73.1 +/- 3.6 mmHg) than in the normal-NaCl (99.2 +/- 6.7 mmHg) or low Na-normal Cl (92.0 +/- 6.7 mmHg) groups. In study 2, intact rats (n = 8 per group) were fed low (less than 0.01%), normal (1%), or high NaCl (4%) for 1 wk. BP and heart rate were higher in the low-NaCl group (P less than 0.05) than in the other two groups. Plasma volumes were not different among the groups. In study 3, two groups of eight rats were given either low NaCl or 2% NaCl for 2 wk. BP (131.4 +/- 3.6 mmHg) and heart rate (402 +/- 11 beats/min) were higher in the low-NaCl group than in the 2% NaCl group (121.1 +/- 3.2 mmHg and 369 +/- 9 beats/min, respectively). In the normotensive Sprague-Dawley rat, low NaCl intake elevated BP when compared with normal or high NaCl intake. Part of the increase in the uninephrectomized, Cl-supplemented group is not dependent on the renin-angiotensin system.

Induction, prevention and mechanisms of contrast media-induced acute renal failure.

This study describes the development of an experimental model of reversible acute renal failure following infusion of contrast media radiographic dye. Experiments were also performed to investigate possible methods of prevention as well as examine single nephron mechanisms involved in the pathogenesis of the renal failure. Acute renal failure was consistently produced by indomethacin treatment (18 mg/kg) and an intravenous infusion of contrast media (7 ml/kg) into New Zealand rabbits that had been on a low sodium diet for one week. Glomerular filtration rate (GFR), measured by daily creatinine clearance in unanesthetized animals, was significantly decreased (P less than 0.001) 24, 48, and 72 hours following infusion of the contrast dye. Two weeks after induction of acute renal failure, GFR had returned to control. GFR was unchanged during the same time period when the sodium deprived rabbits were given either indomethacin or contrast media alone. Chronic administration of DOCA (1 mg/kg s.c.) and saline drinking water which increased sodium and solute excretions and decreased plasma renin activity also prevented the decrease in GFR. However, acute infusion of either saline or mannitol, which transiently increased sodium and solute excretions and decreased plasma renin activity, did not protect against the development of acute renal failure. Light microscopy revealed no glomerular or tubular changes and no visible obstruction. Micropuncture experiments were performed on three additional groups of anesthetized rabbits: control, acute renal failure, and recovery. Recovery rabbits were allowed a two week period after renal failure before they were micropunctured.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of dietary chloride on salt-sensitive and renin-dependent hypertension.

We have previously reported that 1) selective dietary sodium loading (without chloride) does not produce hypertension in rats of the Dahl salt-sensitive strain (DS) and 2) selective chloride loading (without sodium) lowers plasma renin activity in the intact Sprague-Dawley rat maintained on a low NaCl diet. The present study examined the effect of selective dietary chloride loading on two models of hypertension: the DS and the renin-dependent one-kidney, one clip Sprague-Dawley rat. The DS were pair-fed (n = 7/group) a "normal" NaCl, a high NaCl (4%), or a "normal" sodium-high chloride diet for 11 weeks. From Week 7 until the end of the experiment, the high NaCl-fed animals had higher (p less than or equal to 0.05) blood pressures than animals fed either the normal NaCl or normal sodium-high chloride diet, which were not different from each other. Thus, in the DS, hypertension depends on high dietary intakes of both sodium and chloride. In one-kidney, one clip hypertensive rats, selective chloride loading failed to lower plasma renin activity (9 +/- 1 vs 7 +/- 1 ng angiotensin I/ml/hr) or to prevent hypertension (160 +/- 10 vs 166 +/- 9 mm Hg). Thus, selective dietary chloride loading (without sodium) does not alter blood pressure in either salt-sensitive or renin-dependent hypertension.

Importance of chloride for deoxycorticosterone acetate-salt hypertension in the rat.

Selective dietary sodium loading (without chloride) fails to produce hypertension in the Dahl salt-sensitive rat. This study attempted to evaluate the effect of selective sodium loading on blood pressure in another NaCl-dependent model of hypertension--deoxycorticosterone acetate (DOCA)-salt hypertension. Three groups of uninephrectomized rats were studied for 32 days on one of the following regimens: (1) high NaCl diet plus DOCA, (2) high dietary sodium intake without chloride plus DOCA, and (3) high NaCl diet without DOCA. Both indirect and direct arterial pressure were higher (p less than 0.01) in the DOCA-NaCl group than in the other two groups. In the two DOCA-treated groups, net sodium and potassium balance and total carcass sodium and potassium content did not differ. In the DOCA-NaCl group, higher blood pressures were associated with a more positive chloride balance and total carcass chloride content (p less than 0.01), an expanded extracellular fluid volume (p less than 0.05), and increased renal vascular resistance (p less than 0.01). Higher renal vascular resistance in DOCA-NaCl animals suggests that chloride contributes to NaCl-induced vasoconstriction.

Salt-sensitive hypertension: contribution of chloride.

The effect of the anion associated with sodium loading on the development of hypertension in the Dahl salt-sensitive rat was determined. For 5 weeks rats were fed a diet containing normal or high concentrations of sodium chloride or high concentrations of sodium provided as a mixture of sodium bicarbonate, phosphate, and amino acids. After 1 week on these diets and until the end of the study the rats receiving high concentrations of sodium chloride had higher systolic blood pressures than the rats in the other two groups. There were no statistically significant group differences in plasma volume, arterial pH, or plasma concentrations of Na+, K+, Cl-, Ca2+, or creatinine, or in renomedullary prostaglandin E2 production. Compared to the animals receiving normal concentrations of sodium chloride, those receiving high concentrations of sodium chloride or amino acids showed decreased plasma renin activity and plasma aldosterone concentrations. Thus, the anion ingested with sodium alters the development and severity of hypertension in the Dahl salt-sensitive rat.