Environmental photostability of SF6-etched silicon nanocrystals.

We report on the long-term environmental stability of the photoluminescent (PL) properties of silicon nanocrystals (SiNCs). We prepared sulfur hexafluoride (SF(6)) etched SiNCs in a two-stage plasma reactor and investigated their PL stability against UV irradiation in air. Unlike SiNCs with hydrogen-passivated surfaces, the SF(6)-etched SiNCs exhibit no photobleaching upon extended UV irradiation despite surface oxidation. Furthermore, the PL quantum yield also remains stable upon heating the SF(6)-etched SiNCs up to 160 °C. The observed thermal and UV stability of SF(6)-etched SiNCs combined with their PL quantum yields of up to ~50% make them attractive candidates for UV downshifting to enhance the efficiency of solar cells. Electron paramagnetic spin resonance indicates that the SF(6)-etched SiNCs have a lowered density of defect states, both as-formed and after room temperature oxidation in air.

Circadian rhythm of plasma aldosterone concentration in patients with primary aldosteronism.

Plasma aldosterone, cortisol, and renin activity were measured in nine recumbent patients with hyperaldosteronism, including seven with adenomas, one with idiopathic hyperplasia, and one with glucocorticoid suppressible hyperplasia. All had peak values of plasma aldosterone concentration from 3 a.m. to noon and lowest values at 6 p.m. or midnight. This rhythm was similar to the circadian pattern of plasma cortisol in the same patients. When these data were normalized to eliminate the wide variation in ranges of plasma aldosterone and cortisol between individuals, there was an excellent correlation (r = + 0.87, P < 0.005) between the two hormones. In contrast, plasma aldosterone concentrations did not correlate with plasma renin activity before or after normalization of data. Short term suppression of ACTH by administration of dexamethasone eliminated the circadian variation of plasma aldosterone in both patients with hyperplasia and in four of five patients with adenomas, while it markedly altered the rhythm in the fifth. Similar doses of dexamethasone were administered to four normal subjects and did not flatten the circadian rhythm of plasma aldosterone. These data suggest that patients with primary aldosteronism have a circadian rhythm of plasma aldosterone mediated by changes in ACTH.

Single-voided urine metanephrine assays in screening for pheochromocytoma.

To facilitate the screening for pheochromocytoma, we have validated the use of single-voided, spot urine specimens for the determination of total metanephrines. Metanephrine excretion was found to be quite constant throughout the day and night in ten patients with essential hypertension and seven patients with pheochromocytoma. The levels in single-voided specimens were closely correlated to those in 24-hour specimens in 100 hypertensive subjects. The mean +/- 2 SD metanephrine excretion in single-voided urine specimens from 500 hypertensive subjects was 0.351 +/- 0.356 mug/mg of creatinine.

The effect of posture and saline loading on plasma renin activity and aldosterone concentration in pregnant, non-pregnant and estrogen-treated women.

The effect of contraceptive ingestion and pregnancy on components of the renin-angiotensin-aldosterone system was compared in 17 non-pregnant women, 8 non-pregnant women taking oral contraceptives, and 11 pregnant women. Plasma renin substrate concentrations and the dynamic responses of plasma renin activity and aldosterone concentrations to upright posture and iv saline infusion were evaluated. Renin substrate was significantly higher in those women taking oral contraceptives and among the pregnant subjects than the other non-pregnant group. No significant differences in plasma renin activity or aldosterone concentrations were seen before or after postural stimulation among the 2 non-pregnant groups. After saline loading renin was higher and aldosterone lower in the contraceptive-treated group. In contrast, the pregnant group had significantly higher values at every point. The response to posture and saline among the pregnant subjects was similar in direction and magnitude to those of the non-pregnant groups. The urinary excretion of sodium before and after saline infusion was significantly lower in the pregnant group than in the non-pregnant groups. These observations suggest that estrogen-induced increases in renin substrate do not alone account for the increases in the renin-angiotensin-aldosterone system observed during pregnancy, but rather such increases appear to represent a physiological response to increased sodium need during pregnancy.

PIP: The effect of posture and saline loading on plasma renin activity (PRA) and aldosterone concentration in 11 pregnant, 17 nonpregnant, and 8 estrogen-treated women was investigated. Following saline loading, renin was higher and aldosterone lower in the contraceptive-treated group, while the pregnant group has markedly higher values at every point. The response to posture and saline was similar in direction and magnitude in all groups. The urinary excretion of sodium before and after saline infusion was singificantly lower (p less than .005) in the pregnant group than in the nonpregnant groups. The contraceptive group had a significantly higher (p less than .001) mean plasma renin substrate (PRS) than the nonpregnant group. The pregnant group had an even higher PRS when compared to those taking contraceptives (p less than .05). No marked differences in PRA or aldosterone concentrations were seen before or aft postural stimulation among the 2 nonpregnant groups. These results suggest that estrogen-induced increases in renin substrate do not alone account for the increase in the renin-angiotensin-aldosterone system observed during pregnancy, but rather such increases appear to represent a physiological response to increased sodium need during pregnancy.

Plasma aldosterone response to ACTH in primary aldosteronism and in patients with low renin hypertension.

ACTH alpha 1-24 was infused at incremental rates of 12.5-200 mIU/30 min in dexamethasone-suppressed hypertensive patients on a regular sodium diet. The plasma aldosterone response to this stimulus in 8 patients with hyperaldosteronism due to an adrenal aldenoma and 11 with adrenal hyperplasia was significantly greater at all infusion rates (P less than 0.05) when compared with the response in 6 normal subjects on a similar diet. This responsiveness to ACTH in the patients with primary hyperaldosteronism was similar to that of the normal subjects on a low sodium diet. Twelve patients with low renin and 6 patients with normal renin essential hypertension were similarly studied. There was no significant difference in the median aldosterone response between these 2 groups and the normal subjects on a normal diet, but the response was significantly lower compared with that in patients with primary hyperaldosteronism. These data show that patients with hyperaldosteronism from an adrenal adenoma or hyperplasia have a consistent and exaggerated response to ACTH. The hyper-responsiveness is not apparently shared by the majority of patients with low renin essential hypertension and does not support the concept that this group is an intermediate form of primary aldosteronism. Individual patients within this group, however, may have such a response and might be identified by this type of testing.

Restoration of renin-aldosterone dynamics to normal following surgery in primary aldosteronism.

Little is known regarding the response of the renin-angiotensin-aldosterone system to dynamic maneuvers after surgical removal of an aldosterone-producing adenoma or whether normal renin-aldosterone relationships are restored following surgery. We utilized maneuvers designed to assess the adequacy of aldosterone suppression and renin stimulation to rapid changes in sodium and fluid volume status to examine these relationships in 21 patients before and after surgery for primary aldosteronism. All patients failed to suppress plasma aldosterone normally after intravenous saline infusion and failed to stimulate renin activity into the normal range following diuretic-induced sodium and volume depletion. No relationship between renin and aldosterone was discerned. The studies were repeated 6 mo. to 4 yrs. after unilateral adrenalectomy in all 21 patients. In every case the normal suppression of aldosterone and stimulation of renin was observed. Moreover a significant (p less than 0.001) relationship between renin and aldosterone was demonstrable. Thus in this population of patients with surgically responsive primary aldosteronism, no abnormality of aldosterone production persisted.

Diagnosis of secondary forms of hypertension. A comprehensive protocol.

An efficient protocol for the evaluation of hypertensive cases included renal arteriography, suppression and stimulation of the renin-aldosterone system, and, when indicated, renal venous renin measurements. It permitted identification of 38 patients with renal artery stenosis, 28 with primary aldosteronism, and 51 with high renin, 92 with normal renin, and 27 with low renin essential hypertension.

The effect of dexamethasone on the control of plasma aldosterone concentration in normal recumbent man.

In order to evaluate the control of the circadian rhythm of plasma aldosterone concentration in man, plasma aldosterone, cortisol, sodium and potassium concentrations, and plasma renin activity (PRA) were measured in samples obtained at 20-minute intervals from 0200 to 0800 in sodium repleted (180 mEq. per day of diet) and sodium depleted (22 mEq. per day of diet) normal subjects. During sodium replete studies, plasma aldosterone and cortisol concentrations were significantly correlated (p greater than 0.01) in all 4 subjects. Plasma aldosterone also correlated with PRA (p greather than 0.01) in 2 subjects and with potassium (p greater than 0.01) in one. Episodic increases in plasma aldosterone concentration were observed despite suppression of ACTH by dexamethasone treatment. Plasma aldosterone concentrations were significantly correlated with PRA (p greater than 0.05 and p greater than 0.01) in only 2 of 4 subjects under these conditions. Following sodium restriction, plasma aldosterone concentrations were not significantly correlated with plasma cortisol and only infrequently with either PRA or potassium. When dexamethasone was administered during the low sodium diet, correlations with PRA (p greater than 0.001) were seen in 2 of 3 subjects and with potassium (p greater than 0.01) in 1 of 3 subjects. There was no significant correlation between plasma aldosterone and sodium concentration during any of the studies. These results are compatible with the concept that the relative importance of PRA, ACTH, and potassium in inducing changes in aldosterone production during the early morning hours is partially dependent upon dietary sodium, but also varies between individuals studied during similar sodium diets. The episodic alterations of plasma aldosterone concentration continued after ACTH was suppressed by dexamethasone pretreatment. These changes, in the absence of a consistent significant correlation with PRA and sodium and potassium concentrations, further suggest that another factor(s) may be important in controlling aldosterone production in recumbent normal subjects.

The intravenous furosemide test: a simple way to evaluate renin responsiveness.

To identify patients with low-renin hypertension, we measured plasma renin activity after the administration of 40 mg of furosemide intravenously and 30 minutes of upright posture in 127 normotensive subjects and 363 patients with essential hypertension. Plasma renin activity 30 minutes after intravenous furosemide was found to be closely correlated to the level found after either 2 or 4 h of standing or 3 days of a low-salt diet plus 2 h of upright posture. Renin responsiveness was significantly lower in hypertensive patients, blacks, and women, compared with normotensive subjects, whites, and men respectively. The level of plasma renin activity in most normal white subjects was greater than 1.0 ng/ml - h and in most normal blacks was greater than 0.5 ng/ml - h. It was below those levels in 23% of white hypertensive and 25.2% of black hypertensive patients respectively. The mean level of plasma renin activity fell with increasing age of hypertensive patients. This procedure is recommended as a safe, easy, and reliable test for assessing renin responsiveness and identifying the low-renin state.

Sequential changes in the renin--angiotensin--aldosterone systems and plasma progesterone concentration in normal and abnormal human pregnancy.

To investigate the role of components of the renin-angiotensin-aldosterone system and plasma progesterone concentrations in the pathophysiology of hypertension in pregnancy, sequential measurements were made throughout pregnancy in 45 normotensive subjects, 41 other pregnant patients in whom hypertension became manifest only during pregnancy and 26 patients with chronic hypertension antedating pregnancy. Among the normotensive subjects plasma renin activity and substrate, plasma aldosterone and progesterone concentrations were elevated as early as the sixth week of gestation. While consistent, progressive, further increases were noted in renin substrate, aldosterone and pregesterone concentrations during pregnancy, plasma renin activity did not continue to rise. In both hypertensive groups, plasma renin activity and aldosterone concentration were significantly suppressed during the last trimester despite levels of renin substrate and progesterone that were not significantly different than those observed in normotensive pregnancy. These observations confirm earlier studies reporting suppression near term of plasma renin activity in toxemia and indicate from these prospective observations that they are secondary effects. These studies, in addition, demonstrate parallel suppression of plasma aldosterone concentration in toxemia. The current report also indicates that this suppression is not due to a decrease in renin substrate concentration and that a hypothesized deficiency of plasma progesterone, which was not observed in the hypertensive subjects, does not play a permissive role in the development of hypertension.

The role of ACTH in the episodic release of aldosterone in patients with idiopathic adrenal hyperplasia, hypertension, and hyperaldosteronism.

The relationship of plasma aldosterone concentration to its identified stimuli was examined in three patients with hypertension, hyperaldosteronism, and idiopathic adrenal hyperplasia. Four patients with hyperaldosteronism due to adrenal adenomas served as controls. Plasma aldosterone, cortisol, sodium, and potassium concentrations and renin activity were measured in blood samples taken at 20 minute intervals from 2 A.M. to 8 A.M. during recumbency and sleep. The tests were performed on all patients following a regular sodium diet both before and after short-term treatment with dexamethasone. Two of the three subjects with adrenal hyperplasia were re-examined after 2 weeks of dexamethasone therapy. All four control patients with adenomas had episodic increases of plasma aldosterone which were significantly correlated with those of plasma cortisol (r = +0.48 to +0.90). This confirms the previously reported relationship between aldosterone and ACTH in such patients. Two patients with idiopathic adrenal hyperplasia had a similar secretion pattern and a highly significant correlation of the two hormones (r = +0.76 and +0.77); one did not (r = 0.13). Short-term dexamethasone pretreatment attenuated the episodic release pattern and partially suppressed the mean plasma concentrations of aldosterone in the four patients with an adenoma and in the two patients with idiopathic hyperplasia whose plasma aldosterone and cortisol concentrations were positively correlated. There was no such effect in the third patient. The first two patients with idiopathic hyperplasia were subsequently retested following 2 weeks of dexamethasone treatment to determine if the episodic secretion pattern of plasma aldosterone would correlated with other stimuli following this period of ACTH suppression. One showed little change from the pattern observed after short-term glucocorticoid treatment. The second had a similarly blunted aldosterone response until ACTH secretion led to a resumption of episodic changes in plasma aldosteerone concentrations. These data indicate that ACTH frequently is the dominant stimulus of the episodic secretion of aldosterone in patients with either adrenal adenomas or hyperplasia. When ACTH is suppressed, the hypersecretion of aldosterone is presumably sustained by an intrinsic adrenal abnormality or by an as yet unidentified stimulus.

Primary aldosteronism: diagnosis, localization, and treatment.

New diagnostic techniques have enhanced the detection of primary aldosteronism. However, the response of blood pressure after operation in unilateral and bilateral adrenal disease is different. We have compared four localizing techniques--adrenal venography, adrenal isotopic scanning, a modified adrenal venous sampling for steroid measurements, and the anomalous postural decrease in plasma aldosterone concentration--in 51 patients with primary aldosteronism, all of whom had undergone operative confirmation. Adrenalectomy resulted in normal blood pressure in 59%, improvement in 25%, and no change in 16%. Correct localization of the lesion was obtained in 47% by the adrenal isotopic scan, in 66% by adrenal venography, and in 91% by the modified adrenal venous hormone technique despite four false-positives. Of the 26 patients with an anomalous postural decrease in plasma aldosterone, 88% had a unilateral lesion.