Edge effects enhance selfing and seed harvesting efforts in the insect-pollinated Neotropical tree Copaifera langsdorffii (Fabaceae).

Edge effects may affect the mating system of tropical tree species and reduce the genetic diversity and variance effective size of collected seeds at the boundaries of forest fragments because of a reduction in the density of reproductive trees, neighbour size and changes in the behaviour of pollinators. Here, edge effects on the genetic diversity, mating system and pollen pool of the insect-pollinated Neotropical tree Copaifera langsdorffii were investigated using eight microsatellite loci. Open-pollinated seeds were collected from 17 seed trees within continuous savannah woodland (SW) and were compared with seeds from 11 seed trees at the edge of the savannah remnant. Seeds collected from the SW had significantly higher heterozygosity levels (Ho=0.780; He=0.831) than seeds from the edge (Ho=0.702; He=0.800). The multilocus outcrossing rate was significantly higher in the SW (tm=0.859) than in the edge (tm=0.759). Pollen pool differentiation was significant, however, it did not differ between the SW (=0.105) and the edge (=0.135). The variance effective size within the progenies was significantly higher in the SW (Ne=2.65) than at the edge (Ne=2.30). The number of seed trees to retain the reference variance effective size of 500 was 189 at the SW and 217 at the edge. Therefore, it is preferable that seed harvesting for conservation and environmental restoration strategies be conducted in the SW, where genetic diversity and variance effective size within progenies are higher.

Subcutaneous phaeohyphomycosis caused by Amesia atrobrunnea in Kuwait.

The recently described genus Amesia encompasses four species but only Amesia atrobrunnea (=Chaetomium atrobrunneum) is known to be pathogenic to humans. Here, we describe a case of subcutaneous phaeohyphomycosis in Kuwait in an apparently immunocompetent patient diagnosed by direct microscopy of the infected tissue and culture. The identity of A. atrobrunnea was established by typical morphological characteristics and by sequencing of internally transcribed spacer (ITS) region and D1/D2 domains of rDNA. To the best of our knowledge, this is the first report documenting etiologic role of this species in causing a locally invasive subcutaneous infection.

Left ventricular diastolic function in hypertension: relation to left ventricular mass and systolic function.

Initial studies of diastolic cardiac function in hypertension demonstrated that slowing of the maximal rate of left ventricular filling occurred before alterations in either ejection fraction or cardiac output. The present study was undertaken to determine: 1) the relation between hypertension, increased left ventricular mass and impaired left ventricular filling, and 2) the correlation between abnormalities in left ventricular diastolic function and its systolic performance. Eleven normal subjects (Group 1), 5 hypertensive patients without evidence of left ventricular hypertrophy (Group 2) and 18 hypertensive patients with increased left ventricular mass by echocardiography (Group 3) were studied by M-mode echocardiography, radionuclide (technetium-99m human serum albumin) first pass technique and gated blood pool scintigraphy. Indexes of systolic function (ejection fraction, maximal rate of ejection and percent left ventricular shortening) were essentially similar in hypertensive and normotensive subjects. No correlation was found between systolic blood pressure and left ventricular mass (r = 0.20, not significant). Maximal rate of left ventricular filling (P dV/dt) and fast filling fraction decreased progressively from Group 1 to Group 3 (2.36 +/- 0.4 [mean +/- standard deviation], 2.17 +/- 0.3 and 1.97 +/- 0.4 s-1, respectively, for P dV/dt and 46 +/- 7, 48 +/- 9 and 38 +/- 11%, respectively, for fast filling fraction); the difference from values in normal subjects reached statistical significance in hypertensive patients with left ventricular hypertrophy. Left ventricular maximal filling rate correlated inversely with left ventricular mass and left ventricular end-systolic diameter (r = -0.74), but positively with left ventricular fractional shortening and ejection fraction (r = 0.70).(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular function in coronary artery disease. Evaluation of slope of end-systolic pressure-volume line (Emax) and ratio of peak systolic pressure to end-systolic volume (P/Ves).

Left ventricular function was assessed by measurement of systolic pressure-volume variables and ejection fraction in seven normal subjects (group I), five patients with coronary artery disease and normal symmetric left ventricular wall motion (group II) and eight patients with remote myocardial infarction and segmental akinesia (group III). Left ventricular volumes were obtained from right anterior oblique ventriculograms and pressures from catheter-tip micromanometer (14 patients) or fluid-filled catheters (6 patients) at two different systolic loads. P/Ves was calculated as the ratio of peak systolic pressure (P) to end-systolic volume (Ves) at rest, Emax as the slope of the end-systolic pressure volume line constructed at two systolic loads, and Vo as the volume axis intercept of this line. Emax was significantly (p less than 0.01) lower in patients with segmental akinesia (group III) (5.0 +/- 0.5) than in normal subjects (group I) (10.4 +/- 0.8) or patients with coronary artery disease and normal wall motion (group II) (9.9 +/- 0.8). In contrast, there was no significant difference in P/Ves among the three groups (6 +/- 1.0 in group I, 5 +/- 0.8 in group II, 3.7 +/- 0.5 in group III). Similarly, Ves and Vo failed to separate the three groups. Although ejection fraction was significantly (p less than 0.05) lower in group III (0.56 +/- 0.03) than in groups I and II (0.67 +/- 0.03 in both groups), there was considerable overlap of individual values in the three groups. In eight patients, measurements were repeated during isometric exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Nitrendipine, a calcium-entry blocker. Renal and humoral effects in human arterial hypertension.

Thirteen patients with hypertension and normal renal function received nitrendipine, a calcium entry blocker. Nitrendipine did not modify renal blood flow (RBF) or glomerular filtration rate (GFR), decreased mean arterial pressure (MAP) and total peripheral resistance, and did not significantly change cardiac output. Individual RBF changes did not correlate with MAP or cardiac output modifications. Mean arterial pressure changes were inversely correlated with basal renin levels and directly associated with age. Plasma catecholamines and plasma renin activity increased, but plasma aldosterone and plasma volume did not change significantly. However, the greater decrements of MAP tended to be associated with the greater increases in plasma volume. Data show that long-term calcium entry blockade by nitrendipine does not modify RBF or GFR despite the decreased renal perfusion pressure. Further, nitrendipine may be more effective in older patients and the presence of low renin.

Electrocardiogram in evaluation of resistance to antihypertensive therapy.

The effect of blood pressure control on the evolution of electrocardiographic evidence of left ventricular hypertrophy was investigated 50 patients with hypertension who were followed up for an average period of nine years. Blood pressure response to treatment was determined both from casual office readings and from weekly averages of twice daily home readings. Changes in the ECG, judged from both alteration in QRS voltage and in ST-T segment, were related to the degree of arterial pressure control. Usually, both home and office arterial pressure responded similarly to antihypertensive therapy, but when there was a difference, electrocardiographic changes correlated best with home prssure averages. Reduction in maximum precordial QRS voltage (Sv1+Rv5-6) correlated best with changes in home systolic pressure (r = .460; P less than .001), but correlation with diastolic pressure variation either at home or in the office did not attain statistical significance (P greater than .10). The present data stress the importance of home pressure measurements in the management of some patients with hypertension and provide evidence that casual office readings may sometimes misjudge the effectiveness of antihypertensive therapy.

Coronary blood flow measurements with left atrial injection of microspheres in conscious rats.

Since left atrial (LA) injection of microspheres has been shown to give more precise coronary blood flow (CBF) determinations, and also since studies in a conscious state have obvious advantages, we have developed a technique of chronic LA catheterisation for these purposes in rats. Through a thoracotomy in the third left intercostal space, the LA appendage was cannulated and a catheter (PE-10 tubing) advanced into the left atrium. The catheter itself was passed through the chest and exteriorised at the back of the neck. Following recovery over 24 to 48 h, flow studies with microspheres could be performed for 3 to 8 days. One-hundred and twenty procedures performed over a 4 month period were analysed. Left atrial catheterisation could be performed in approximately 45 min with no bleeding in 79% of cases and only minimal or moderate bleeding in the rest (13% and 4%, respectively); respiratory complications were rare (less than 1%). The rats recovered rapidly, and all catheters remained patent for the duration of the preparation. Infections developed in 5% and the total mortality rate was 7%; a complete haemodynamic study could be obtained in 130/120 rats (86%). Small renal infarcts were found in 25% of the rats, but neither the infarcts nor the intraoperative blood loss had any significant effect on haemodynamic indices and flow measurements performed 3 to 8 days after atrial catheterisation. Coronary blood flow values in 33 normal rats were within the range of values reported in the literature. These results demonstrate that chronic LA catheterisation is possible in rats with no major difficulties and will allow the precise determination of coronary blood flow with microspheres in conscious animals.

New approach to local thermodilution: use of pig tail catheters to avoid basic difficulties.

The use of pit tail catheters and the placing of the thermistor distal to the lumen for the cold injectate have allowed the development of a new catheter for local thermodilution with many advantages. Apart from its small size and possibility of percutaneous introduction, the spatial orientation of the thermistor to the rest of the catheter and to the port of injection ensures: (a) its absolute thermal insulation; (b) avoidance of contact with vessel walls: and (c) constant spatial relationship between the lumen for injection and the thermistor as regards the dynamics of flow and temperature change.

Cardiac hypertrophy and antihypertensive therapy.

Biochemical (myocardial DNA, RNA, and hydroxyproline) and humoral (plasma [PRA] and kidney [KRA] renin activity) factors were determined in spontaneously hypertensive rats (SHR) and normotensive Wistar controls (NR) before and following treatment with minoxidil or propranolol. Minoxidil (150 mg.litre-1 drinking water) effectively controlled blood pressure (17.3 kPa vs 24.9 kPa [130 mmHg vs 187 mmHg], P less than 0.001) despite marked and sustained increases in both PRA and KRA ventricular weight which were not reduced and myocardial DNA, RNA, and hyperdroxyproline which were increased by minoxidil (P less than 0.01). In contrast propranolol did not reduce blood pressure in SHR but ventricular weight was reduced somewhat (3.1 +/- 0.4 mg.g-1 vs 3.4 +/- 0.09 mg.g-1, P less than 0.05); in both SHR and NR, KRA, and PRA were lowered by pranolol. Methyldopa which controlled blood pressure and lowered PRA led to a reversal of hypertrophy. Thus, although blood pressure control is obviously important for reversing cardiac hypertrophy, it may not be the sole factor for the development and reversal of cardiac hypertrophy.

Biochemical changes associated with development and reversal of cardiac hypertrophy in spontaneously hypertensive rats.

This study is the first report describing the sequence of biochemical alterations of myocardium during the progression of naturally occurring hypertrophy in spontaneously hypertensive rats (SHRs) and then with its reversal by alpha-methyldopa therapy. Changes in DNA, RNA, hydroxyproline, as well as incorporation of 14C lysine into cardiac myosin, were compared with the pattern found in suitably matched controls. A significant increase in RNA, hydroxyproline, and 14C incorporation was observed in SHRs. Antihypertensive treatment caused reversal of hypertrophy and normalization of all biochemical parameters except hydroxyproline, the concentration of which increased significantly as myocardial weight decreased. These compositional changes may help explain the conflicting result of the haemodynamic effects of cardiac hypertrophy.

Effects of antihypertensive drugs on heart and resistance vessels.

STUDY OBJECTIVE - The aim of the study was to examine the effects of antihypertensive drugs on heart and resistance vessels to see whether regression of peripheral vascular hypertrophy accompanies reduction in cardiac mass. DESIGN - Matched groups of spontaneously hypertensive and control rats were treated for 12 weeks with captopril (average dose 65 mg.kg-1.d-1) or hydrochlorothiazide (73 mg.kg-1.d-1) and compared to untreated groups. Perfusion pressure, which has been validated as an index of hypertrophy of resistance vessels, was determined in hind limbs of pithed rats at constant blood flow and maximum vasodilatation. SUBJECTS - Experimental animals were 14 week old male spontaneously hypertensive (SHR) rats (n = 41) and strictly age matched Wistar Kyoto rats (n = 12). SHR rats were assigned at random to three groups: (a) captopril treated (n = 15), (b) hydrochlorothiazide treated (n = 15), (c) control (n = 11). MEASUREMENTS and RESULTS - Mean perfusion pressure was 29.5(SEM 0.4) mm Hg in untreated Wistar Kyoto rats and 37.4(0.5) mm Hg in untreated SHR rats. In comparison with untreated SHR rats, treatment with captopril lowered blood pressure, perfusion pressure [35.2(0.3) v 37.4(0.5) mm Hg, p less than 0.01)], and left ventricular to body weight ratio [2.28(0.03) v 2.63(0.05) mg.g-1, p less than 0.01)]. Treatment with hydrochlorothiazide also lowered blood pressure but had no significant effect on left ventricular weight to body weight ratio [2.54(0.04)]. However, perfusion pressure was reduced to 35.3(0.5) mm Hg, p less than 0.01. CONCLUSIONS - For equal regression of vascular hypertrophy, captopril and hydrochlorothiazide had different effects on regression of left ventricular hypertrophy. Thus left ventricular and vascular structural changes may respond differently to the same drug in the same animal.

Cardiac factors in response to antihypertensive treatment.

The cardiac status of hypertensive patients will influence not only the indications for and choice of antihypertensive agents but can also alter the effectiveness of antihypertensive therapy. The heart may interfere with adequate blood pressure control either because of marked increases in cardiac output or as result of decompensation activating various pressor mechanisms or through the generation of pressor reflexes. Reflex increases in cardiac output may blunt or even nullify the effect of reduction in peripheral resistance by vasodilators. Cardiac decompensation from incidental disease or secondary to some antihypertensive drugs can lead to hypertension rather than reduction in blood pressure. It is particularly liable to develop from excessive fluid retention, particularly when associated with reduction of cardioadrenergic support. Coronary insufficiency from either coexisting coronary disease or triggered by injudicious antihypertensive treatment can stimulate pressor reflexes leading to marked fluctuations in arterial pressure. Alterations in left ventricular relaxation and rapid filling have been reported with some antihypertensive drugs; these changes could conceivably influence blood pressure responses through their effect on reflexes from low pressure baroceptors.

Converting enzyme inhibition with an orally active compound in hypertensive man.

The short-term cardiovascular and endocrine effects of an orally active angiotensin converting enzyme inhibitor, SQ14,225, were evaluated in 17 subjects with drug-resistant hypertension (10 with essential and seven with renovascular hypertension). On normal dietary sodium, SQ14,225 (after 3 days at average dose of 664 mg/day) reduced mean arterial pressure (MAP) significantly (from 141 +/- 4 to 122 +/- 4 mm Hg, (SE), p less than 0.001). However, only eight of the patients achieved blood pressures within the normotensive range. Of eight patients with residual hypertension, seven exhibited further decreases in MAP (from 132 +/- 4 to 108 +/- 6 mm Hg (SE), p less than 0.001) when dietary sodium was reduced to 10 mEq/day. No rebound hypertension was noted when treatment was temporarily discontinued for 3 days in 11 patients. The reductions in blood pressure were not associated with either orthostatic hypotension or interference with baroreceptor reflexes. The values of supine plasma renin activity (PRA) were not always predictive of blood pressure responsiveness to the drug. With treatment, plasma aldosterone concentrations (PAC) decreased modestly (values from 40 +/- 9 to 22 +/- 3 ng/dl (SE), p less than 0.05). The plasma concentrations of cortisol, norepinephrine and serum potassium were left unchanged during the period of studies. The present study has not defined the exact mechanism by which SQ14,225 lowered blood pressure. Nevertheless, it indicates that this agent may be a practical therapeutic adjunct in the treatment of certain subsets of the human hypertensive population. The lack of serious interference with cardioscular and humoral homeostasis adds to its attractiveness as a therapeutic agent.

Reversal of cardiac hypertrophy in humans.

Reversal of left ventricular (LV) hypertrophy has definitely been proved to follow effective blood pressure control in hypertensive patients. This reduction in cardiac mass does not depend solely on blood pressure levels as measured in routine follow-up; it varies markedly with the type of drug used and even among patients treated with the same antihypertensive agent. The factors influencing the degree of regression of hypertrophy include stability of blood pressure control (entailing diurnal variations and response to stress), neurohumoral disturbances or fluid retention induced by the antihypertensive drug, and the presence of associated cardiac disease, as well as individual variations such as genetic background and possibly age. LV performance at rest was not depressed by the reduction in cardiac mass but remained normal in relation to changes in LV end-systolic stress.

beta-Receptors and contractile reserve in left ventricular hypertrophy.

The inotropic responsiveness to adrenergic stimulation is diminished in hypertension associated with left ventricular hypertrophy (LVH). This was shown in hypertrophied hearts from renal hypertensive rats (RHR) (two-kidney, one clip hypertension, Goldblatt) 6 weeks after renal artery clipping when compared to age-matched normotensive sham-operated controls (NR). The isoproterenol-stimulated inotropic responses (delta peak dP/dt) of isolated hearts perfused at constant pressure were significantly lower in RHR than in NR (p less than 0.001 by analysis of variance and covariance, including repeated measures). This reduction in ventricular responsiveness of isolated hearts from RHR did not extend to other inotropic agents such as calcium ions and the cardiotonic cardiac glycoside scillaren. Assay of beta-adrenergic receptors by binding to (-) [3H] dihydroalprenolol showed that left ventricular beta-receptor numbers (fmol per mg membrane protein) were significantly reduced in RHR compared to NR (28.2 +/- 1.1 vs 36 +/- 2.6, p less than 0.01) with no significant change in affinity (Kd,nM) (1.9 +/- 0.27 vs 2.26 +/- 0.34,NS). The results of this study suggest that LVH in renovascular hypertension is associated with impairment in inotropic responsiveness to beta-receptor stimulation parallel with and, in part, related to, a reduction in ventricular beta-receptor concentrations. Such blunting of inotropic responsiveness to beta-adrenergic stimulation may be one of the mechanisms in the progression from LVH to heart failure in hypertensive disease.

Left ventricular hypertrophy in rats with renovascular hypertension. Alterations in cardiac function and adrenergic responses.

Performance of the hypertrophied left ventricle was studied by determination of the inotropic response to different stimuli in renal hypertensive rats (two-kidney, one clip Goldblatt, RHR, n = 13) and matched sham-operated controls (NR, n = 11). A model was developed to determine maximal pressure development (transient aortic ligation), maximal pumping ability (rapid transfusion, 2 ml/30 sec), and responses to beta stimulation (isoproterenol, 0.01 to 0.10 micron g/kg/min), using dP/dt/P40 as a load-independent index of contractility. With rapid blood transfusion, RHR developed a higher ventricular systolic pressure (211.5 +/- 10.1 mm Hg vs 194.0 +/- 9.3 (SE), p less than 0.001) but at the expense of higher end-diastolic pressure (LVEDP) (12.2 +/- 1.1 mm Hg vs 7.7 +/- 1.0, p less than 0.02). The maximal response of dP/dt/P40 to isoproterenol was diminished in RHR (29.5 +/- 3.2 sec-1 vs 49.6 +/- 5.2, p less than 0.01) whereas the maximal developed pressure (MDP) was greater in RHR than in NR (239.2 +/- 7.5 mm Hg vs 197.0 +/- 3.9, p les than 0.001). A positive correlation was found between MDP and ventricular weight (r = 0.846, p less than 0.001) in contrast with the negative correlation found between ventricular weight and maximal dP/dt/P40 response to isoproterenol (r = 0.677, p less than 0.001). Thus, cardiac hypertrophy in RHR allowed higher developed ventricular pressures but at the expense of higher LVEDP; at the same time, however, the ability to increase contractility in response to beta adrenergic stimulation was decreased. The contrast in results obtained using different tests of cardiac function indicates the need for a multifactorial approach. It also suggests a subtle transformation in this hypertrophy of the pattern of cardiac adaptation to the increased load.

Impaired cardiac contractile response to isoproterenol in the spontaneously hypertensive rat.

To test the ability of the hypertrophied ventricle to increase its contractility in response to sympathetic stimulation, we compared the chronotropic, inotropic, and relaxation responses to graded in fusions of isoproterenol in spontaneously hypertensive rats (SHR) with responses of matched Wistar-Kyoto (WKY) controls. A closed-chested, direct ventricle puncture was used for the study. The SHR required a higher threshold dose (0.04 vs 0.01 micrograms/kg/min) for a significant chronotropic response, and their maximal response of heart rate was smaller than in WKY (delta HR = +12.5 +/- 5.4 vs +22.8 +/- 10.7 beats/min, p less than 0.01). Contractility indices did not increase in the SHR after isoproterenol infusion: (delta dP/dt +2224.3 +/- 1304.7 mm Hg/sec; delta dP/dt/P = +5.1 +/- 9.3 sec-1, p greater than 0.05) in sharp contrast with the marked increases observed in WKY (delta dP/dt = +4682.1 +/- 435.0 mm Hg/sec, p less than 0.01; delta dP/dt/P +78.6 +/- 8.0 sec-1, p less than 0.001). Left ventricular relaxation rate was marked diminished by isoproterenol in SHR (delta neg dP/dt = -2598.6 +/- 855.0 mm Hg/sec) whereas it was not altered significantly in normotensive rats. Thus, cardiac contractile and chronotropic responses were markedly diminished in SHR, possibly as a result of diminished beta adrenoreceptor mediation; further, the impairment of the relaxation rate induced by isoproterenol in SHR might also interfere with contractile cardiac performance during stress.

Effect of converting enzyme inhibitor (SQ14,225) on myocardial hypertrophy in spontaneously hypertensive rats.

The potent converting enzyme inhibitor (CEI) SQ14,225, which is known to prevent the formation of angiotensin II (AII) has been used to evaluate the role of AII in the development and reversal of cardiac hypertrophy. The present study describes the effect of CEI on blood pressure (BP) and myocardial hypertrophy (prevention and reversal) in the spontaneously hypertensive rat (SHR). A group of 3-week- and 8-week-old male SHR was treated with CEI (30 mg/kg in drinking water) for 6 weeks. An additional group of SHR was also treated with a combination of CEI and a diuretic (hydrochlorothiazide, 500 mg/liter). Heart weight, BP, deoxyribonucleic acid (DNA), ribonucleic acid (RNA), hydroxyproline, myocardial catecholamines, and plasma renin activity (PRA) were determined. In the prevention study, we found a significant reduction in the ratio of heart weight to body weight along with the prevention of hypertension (200 vs 145 mm Hg, p less than 0.001). Similar reductions in BP and heart weights were obtained with the reversal group. A better BP control was noted in the CEI and hydrochlorothiazide group. The reduction of heart weight was associated with a reduction in RNA and hydroxyproline content. In all groups, we found a significant increase in PRA (p less than 0.001) and a slight increase in tissue catecholamine concentration. No change in kidney weight was found in any group. Data clearly showed that oral administration of CEI prevented and reversed cardiac hypertrophy in SHR. Reversal was associated with a decrease in myocardial collagen content. These data indicate that prevention of AII formation in combination with BP control can prevent and reverse cardiac hypertrophy in SHR. Of course, whether or not CEI acts only through the renin angiotension system is still speculative.

Cardiac pumping ability following reversal of hypertrophy and hypertension in spontaneously hypertensive rats.

Direct measurements of arterial pressure, stroke volume (SV), and cardiac output (CO) were obtained in ether-anesthetized rats with established spontaneous hypertension (SHR) treated with alpha-methyldopa and compared to both untreated hypertensive and normotensive Wistar-Kyoto (WKY) rats. Left ventricular pumping ability was determined by the maximum levels of SV and CO reached during rapid intravenous volume loading with blood. Treatment with methyldopa reduced the SHR arterial blood pressure (average 57 mm Hg) and reversed the cardiac hypertrophy toward normal. In comparison to untreated SHR, therapy increased heart rate and CO and decreased peripheral resistance. During volume-loading, the levels of SV and CO at matched left ventricular end-diastolic pressures were significantly higher in treated vs untreated SHR. To evaluate the role of blood pressure in the improved peak pumping ability observed in treated rats, a phenylephrine infusion was used to equalize pressures while repeating cardiac function studies. In normotensive WKY and untreated SHR, left ventricular pump function was not greatly affected. A pronounced depression in peak SV and peak CO was observed only in treated SHR. The data indicate that treatment with methyldopa is associated with improved ventricular function in part related to the reduction in arterial pressure.

Selective hypoaldosteronism despite prolonged pre- and postoperative hyperreninemia in primary aldosteronism.

In a prospective study of 7 patients with aldosterone-producing adenoma (APA), long-term (6-72 months) preoperative stimulation of plasma renin activity (PRA) by diuretic therapy (spironolactone plus hydrochlorothiazide) did not prevent selective aldosterone deficiency postoperatively. In all patients aldosterone excretion rate (AER) fell to subnormal values (from a mean of 97 to 2.6 mug/24 h) following removal of APA, although PRA remained elevated. Generalized adrenocortical insufficiency was excluded by the demonstration of normal baseline plasma cortisol and urinary 17-OHCS and the appropriate response to ACTH stimulation. In 6 of 7 patients studied 1-3 months postoperatively, short-term (4 days) sodium deprivation evoked normal increases in PRA, but AER response was blunted (except in 1). Restudy of 3 of 6 patients after 6-12 months revealed that aldosterone production had returned to normal. These results indicate that renin deficiency is not the principal cause of postoperative selective hypoaldosteronism in these patients. On the other hand, they appear to substantiate the possibility raised by in vitro and in vivo studies that spironolactone can directly inhibit aldosterone biosynthesis.