Biomedical subjects

C A Parkinson

Publications and source records attributed to C A Parkinson.

10 recordsLinked to original sources

PubMed1998

Improving nursing education classroom environments.

This study describes the first use of a classroom environment questionnaire with a class in nursing education. An instructor of nursing students monitored classes using such a questionnaire. The questionnaire used was the College and University Classroom Environment Inventory and it was used to obtain practical and useful information about the learning environment in two different classes. Collaborative changes were made in the classes to improve the classroom environment and consequently the learning situation. Any instructor of nursing students could use this same process with this instrument.

Adult↗

PubMed1986

Aldosterone excretion rates in children and adults during sleep.

The present study undertook to examine aldosterone excretion during sleep as an integrated measurement of aldosterone production. A 24-hour urine collection was divided into awake and sleep fractions. Urinary aldosterone and electrolyte excretion were measured in 26 healthy children (mean age, 8.9 +/- 1.9 [SD] years) and 28 adults (mean age, 29.9 +/- 9.5 years). Aldosterone excretion in children was 5.6 +/- 3.9 (SD) micrograms/g creatinine during the awake period, which was significantly different from the 3.9 +/- 4.1 micrograms/g creatinine value recorded during sleep (p less than 0.002). In adults, awake aldosterone excretion was significantly greater than that during sleep; 4.9 +/- 2.7 versus 3.2 +/- 1.6 micrograms/g creatinine (p less than 0.001). Sleep aldosterone excretion values were highly correlated with the corresponding 24-hour aldosterone excretion values (r = 0.85, p less than 0.001) in children and in adults (r = 0.64, p less than 0.001). Sleep aldosterone excretion was correlated with 24-hour potassium excretion (p less than 0.02) only in children. Sleep aldosterone excretion correlated with neither sleep nor 24-hour sodium excretion in children or adults. Sleep electrolyte excretion rates were highly correlated with 24-hour excretion rates in both children and adults. Dexamethasone, 1 mg, administered the night before to suppress the normally high morning levels of endogenous adrenocorticotropic hormone, had no discernible effect on sleep aldosterone excretion. These results indicate that measurement of aldosterone excretion in an easily collected sleep urine sample provides a reliable index of aldosterone production in children and adults.

Adrenocorticotropic Hormone↗

PubMed1985

Decreases in renin and aldosterone secretion in alloxan diabetes: an effect of insulin deficiency.

The effect in the rat of alloxan diabetes (with and without insulin treatment) on renin and aldosterone secretion was examined. Rats with diabetes for 7 weeks were found to have lower PRA than nondiabetic controls. The decrease in PRA appeared to result from insulin deficiency since PRA was normal in diabetic rats given insulin. In a second set of animals, which were killed after 3 weeks, in vitro measurements of aldosterone production by perifused adrenal capsular tissue were carried out. Production of aldosterone was greatest by adrenal capsular tissue from insulin-treated diabetic rats where both basal and potassium-stimulated aldosterone production were higher than diabetic rats not given insulin. Although the reduced aldosterone production associated with untreated diabetes may have been a result of reduced in vivo exposure of adrenal tissue to angiotensin II, a chronic adrenotrophic influence of insulin could not be ruled out. In summary, insulin appears to be necessary for normal renin and aldosterone secretion in the diabetic rat.

Aldosterone↗

PubMed1984

The effect of captopril treatment on potassium-induced stimulation of aldosterone production in vitro.

Potassium and angiotensin (AII) show interdependence as stimuli of aldosterone production. However, potassium stimulates in vitro in the absence of AII. In the present study we examined for a contribution by AII to the in vitro stimulatory potential of potassium, an AII effect mediated on the adrenal before killing of the animal. Captopril, an angiotensin converting-enzyme inhibitor, was administered orally and by sc injection for 3 days so as to decrease levels of AII. Aldosterone secretory responses by adrenal capsules to graded increments in potassium were measured subsequently using a perifusion system. It was found that captopril pretreatment significantly reduced the magnitude of aldosterone secretory response to increments in potassium of 0.5 to 6.0 mM, from a baseline potassium concentration of 3.5 mM. Responses to the lowest increment in potassium, 0.5 and 1.0 mM, were virtually abolished by captopril treatment. The results suggest that AII sensitizes the adrenal glomerulosa such that very small changes in potassium concentration can affect aldosterone production.

Adrenal Glands↗

PubMed1981

Stimulation of aldosterone secretion by metoclopramide in humans: apparent independence of renal and pituitary mediation.

Metoclopramide (MP), a dopamine antagonist, stimulates secretion of aldosterone by a mechanism which has not been defined. We examined a potential role for either the kidney or the pituitary to mediate MPs effect on aldosterone secretion. Responses to MP administered i.v. were measured in six anephric and six hypopituitary patients as well as in six normal subjects. MP increased the plasma aldosterone concentration (PAC) in normal subjects in a fashion similar to what had previously been reported. MP produced no increase in plasma levels of renin activity (PRA), cortisol, potassium, or sodium. Three of six anephric patients (all of whom had undetectable PRA) responded to MP with increases in PAC; the magnitude of these responses correlated with the plasma potassium concentration. All six hypopituitary patients showed increases in PAC after MP administration. MP increased plasma prolactin levels in normal subjects and anephric patients; one hypopituitary patient had high basal plasma prolactin levels which increased with MP. In conclusion, neither the kidney nor the pituitary is involved in the mechanism for MP stimulated aldosterone production. These observations suggest that MP may act on the adrenal to evoke secretion of aldosterone.

Adrenocorticotropic Hormone↗

PubMed1981

The effect of sodium on aldosterone metabolic clearance.

The effect of sodium intake on the aldosterone metabolic clearance rate (MCR) was examined in 5 normal subjects. Measurements were made under conditions where dietary sodium ranged from 10 to 1500 meq/day. There were no consistent changes in MCR over these extremes of sodium intake, and the plasma level of aldosterone correlated only with the aldosterone urinary excretion rate. In an additional group of 6 normal subjects, a single dose of 100 meq sodium administered orally had no effect on the aldosterone MCR. The findings indicate that aldosterone metabolism is unaffected by sodium intake.

Adult↗

PubMed1980

Increased aldosterone metabolic clearance in hypertensive patients treated with minoxidil: an effect of greater hepatic perfusion.

Since minoxidil was previously shown to raise plasma renin activity (PRA) but not the plasma aldosterone concentration (PAC), the effect of minoxidil on the rate of aldosterone metabolic clearance was studied. After the addition of minoxidil to the antihypertensive regimen of 7 hypertensive patients, the aldosterone metabolic clearance rate increased from 1,110 +/- 91 to 1,570 +/- 180 liters/day (p less than 0.01), an overall increase of 41%. Hepatic blood flow, estimated from the clearance from plasma of indocyanine green, was increased in a group of minoxidil-treated patients compared to a comparable group not treated with minoxidil (p less than 0.01). Thus, although minoxidil induces an increase in PRA, PAC does not change, since aldosterone metabolic clearance increases. Minoxidil increased hepatic blood flow, and it was probably by this mechanism that the drug accelerated the rate of aldosterone clearance.

Adult↗

PubMed1980

Effects of propranolol on aldosterone plasma concentration and aldosterone metabolic clearance in hypertensive patients.

Although propranolol administration produces a lowering of PRA, PAC does not decrease in a similar fashion. In the present study the effects of propranolol on the aldosterone MCR were examined. Eight patients with essential hypertension were studied while receiving treatment with a diuretic and again after propranolol (160 to 320 mg/day) was added to the therapeutic regimen. Propranolol therapy was associated with a 25% decrease in PRA (p less than 0.05) and changes in PACs that were variable but not significantly different from diuretic therapy alone. The aldosterone MCR decreased from 1420 +/- 120 to 1120 +/- 90 L/24 hr in response to propranolol (p less than 0.01). The average production rate of aldosterone (MCR X PAC) did not change after propranolol treatment despite a decrease in PRA. There were no changes in plasma concentrations of potassium or in ACTH secretion (as reflected by levels of cortisol) to explain a role for propranolol to sustain aldosterone secretion. Thus propranolol administered to hypertensive patients pretreated with a diuretic can affect circulating levels of aldosterone apart from changes in PRA. Propranolol therapy produces a moderate reduction in aldosterone MCR and appears to augment aldosterone production by a mechanism exclusive of known stimuli.

Adult↗

PubMed1979

Minoxidil increases aldosterone metabolic clearance in hypertensive patients.

It has been shown that despite an effect of minoxidil to increase PRA, plasma levels of aldosterone do not change. We observed similar findings in seven hypertensive patients undergoing treatment with minoxidil; PRA activity increased markedly, whereas the plasma aldosterone concentration showed no consistent change. The aldosterone MCRs in these patients increased by 41% in response to minoxidil, from 1110 +/- 91 to 1570 +/- 180 (SEM) liters/day; this appeared to explain why plasma aldosterone levels did not increase in parallel with renin activity. Hepatic blood flow (estimated from the clearance of indocyanine green) in a group of patients receiving minoxidil was greater than that in an otherwise comparable group (P less than 0.02). This increase in hepatic perfusion may, at least in part, have accounted for the increase in aldosterone MCR.

Adult↗

PubMed1978

A new approach to the difficult assessment of aldosterone secretion in anephric patients.

A new method for the assessment of endogenous formation of aldosterone in anephric patients is described. (1, 2-3H) aldosterone was administered i.v. to patients 1-2 days before hemodialysis, and then the specific activity (SA) of tetrahydroaldosterone glucosiduronate, the major aldosterone metabolite, was measured in the dialysate using a specific radioimmunoassay. The aldosterone secretion rate was determined from the extent of isotope dilution by endogenous metabolite. Aldosterone secretion rates measured in 10 patients were for the most part low. The secretion rate determined in blood from the aldosterone metabolic clearance rate and plasma aldosterone concentration closely approximate secretion rate values obtained by the isotope dilution method in 3 of 4 patients. In 2 patients in whom ACTH was administered chronically, radio-labeled aldosterone was administered at the start of the study and then the day to day aldosterone secretory response to ACTH was determined from the SA of tetrahydroaldosterone in blood. Aldosterone secretion continuously increased for as long as ACTH was administered.

Adolescent↗