Evaluation of a test using saralasin to differentiate primary aldosteronism due to an aldosterone-producing adenoma from idiopathic hyperaldosteronism

We evaluated a new method utilizing saralasin to differentiate primary aldosteronism due to an aldosterone-producing adenoma from idiopathic hyperaldosteronism. The test is based on the marked difference in sensitivity to angiotensin II of aldosterone-producing adenomas and hyperplastic adrenal glands and the partial angiotensin II agonist property of saralasin in low-renin states. Saralasin was infused into 14 patients with primary aldosteronism and the plasma aldosterone responses determined. Plasma aldosterone concentration increased in all eight patients with idiopathic hyperaldosteronism, whereas there was no increase in plasma aldosterone in six patients who had a solitary adenoma. We concluded that saralasin may be a clinically useful, noninvasive tool to distinguish patients with an aldosterone-producing adenoma from those who have idiopathic hyperaldosteronism.     

RESPONSE OF PLASMA ALDOSTERONE TO FLUDROCORTISONE IN PRIMARY HYPERALDOSTERONISM AND OTHER FORMS OF HYPERTENSION

The response of plasma aldosterone to fludrocortisone administration (400 mug 12-hourly for 3 days) was studied in twenty-two patients with primary hyperaldosteronism. No difference was observed in the response between those patients with an adrenal adenoma and those with bilateral adrenocortical hyperplasia, there being no significant change in plasma aldosterone levels across the test period. No separation between the groups was seen when basal plasma renin concentration was related to the aldosterone level following fludrocortisone. It is concluded that the test is of little value in the pre-operative differentiation of these conditions. Twenty-three patients with no demonstrable cause for their hypertension and four with elevated levels of plasma deoxycorticosterone were similarly studied for comparison. These groups demonstrated a normal fall in plasma aldosterone levels following fludrocortisone.     

Rectal hyperpolarization following intestinal bypass for obesity

The electrical potential difference across the rectal mucosa in six shunt-operated women was compared with that obtained in 26 normal females. The potential difference was considerably increased in all the patients, whereas the plasma concentrations and the transmural fluxes of sodium, chloride, and potassium were within normal ranges. Based on measurements of plasma renin and plasma aldosterone concentrations in three of the patients, the possibility of secondary hyperaldosteronism could be ruled out.     

Malignant aldosterone-producing adrenal tumour: reoccurrence with glucocorticoid excess without hyperaldosteronism

We describe a case of hypokalaemic hypertension due to hyperaldosteronism caused by a unilateral adrenocortical tumour with unfavourable histopathology suggestive of malignancy. After removal, the aldosterone excess disappeared. The patient's clinical course was uneventful, until she presented with extensive metastases of adrenal carcinoma four years later. Biochemical abnormalities were now consistent with glucocorticoid excess without hyperaldosteronism. She died four months later. Although malignant aldosterone-producing adrenal tumours are very rare, the present case underscores that clinicians should be aware that primary hyperaldosteronism can occur in the context of adrenocortical carcinoma.     

Body-sodium and blood volume in a patient with licorice-induced hypertension

A 68-year-old man a nine-year history of licorice ingestion had moderate hypertension and low plasma potassium. Exchangeable sodium and blood volume were increased to 128 and 111%, respectively of the expected values; plasma renin and aldosterone levels were suppressed. Plasma norepinephrine concentration was distinctly elevated but the pressor response to infused norepinephrine was normal. After licorice withdrawal, blood pressure, plasma potassium and blood volume reverted to normal levels within three weeks, exchangeable sodium and plasma renin within four months. Exchangeable sodium in our patient with licorice-induced hypertension was increased to a comparable extent as in primary hyperaldosteronism. Moreover, blood pressure in relation to body sodium or plasma potassium did not differ between the exogenous or the endogenous types of mineralocorticoid excess. This observation does not support the possibility that in primary hyperaldosteronism excess aldosterone secretion per se could play an important pressor role independently from sodium retention.     

The role of aldosterone antagonists in the management of resistant hypertension

Resistant hypertension is an increasingly common problem faced by primary care physicians and specialists and will undoubtedly become even more common as the adult population ages and gains weight. In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), at least 8% of subjects were resistant to treatment based on the need for three or more antihypertensive agents. Characteristics of patients with resistant hypertension include being older, black, obese, and diabetic, and having chronic kidney disease as well as untreated sleep apnea. Hyperaldosteronism is common in patients with resistant hypertension, with a prevalence of approximately 20%. This, however, is likely an underestimation of the role aldosterone excess plays in causing drug resistance. In subjects with resistant hypertension, suppressed renin levels are common, exceeding 75% in our studies, suggesting aldosterone excess effects beyond cases of true primary hyperaldosteronism. Recent studies indicate that aldosterone antagonists provide significant blood pressure reduction when added to antihypertensive regimens of patients with resistant hypertension. Interestingly, the blood pressure reduction with use of spironolactone is not limited to patients with hyperaldosteronism, consistent with the concept of aldosterone excess as a continuum from low-renin hypertension with normal aldosterone levels to true primary hyperaldosteronism.     

Rectal potential differences in irritable bowel syndrome and in inflammatory bowel diseases in man

We have studied rectal potential difference (pd) in 200 subjects: 30 healthy volunteers or control patients, 46 patients with irritable bowel syndrome (IBS) and painless diarrhoea (group I), 60 IBS patients without diarrhoea (group II) and 64 patients with inflammatory bowel disease (IBD) with (group III, n = 41) or without (group IV, n = 23) rectal involvement. Pd measurement used a rectal perfused probe and a subcutaneous needle both connected, via agar-KCl bridges, to calomel electrodes and a millivoltmeter. Statistical analysis used Student's t-test for paired and unpaired data and Mann-Whitney U-test as appropriate. Mean rectal pd values were, respectively -43.5 +/- 8.7 mV in control group, -32.9 +/- 10.2 mV in IBS-group I patients (P less than 0.001), -41.3 +/- 12 mV in IBS-group II patients (NS), -21.4 +/- 14.1 mV in IBD patients with rectal involvement (P less than 0.001), and -45.1 +/- 14.3 mV in IBD-group IV patients (NS). A histological examination was performed in 36 IBS patients; mean rectal pd was significantly decreased in patients showing abnormal patterns (n = 27, pd = -31.8 +/- 9 mV) compared to patients with normal mucosa (n = 9, pd = -41.1 +/- 6.5 mV; P less than 0.01). These results show that: (1) potential difference is significantly decreased in patients with ulcerative and rectal involvement; (2) in patients with Crohn's disease, normal rectal pd values do not assess the appearance of colonic mucosa above; (3) patients with IBS and diarrhoea also present a significant diminution in mean rectal pd. Although the mechanisms involved remain unclear, rectal pd measurement appears to be an objective test for intestinal mucosae weakness in functional or inflammatory diseases of the large intestine and rectum.     

Low-renin ("primary") hyperaldosteronism. Differential diagnosis and distinction of sub-groups within the syndrome.

Hypokalemia in a hypertensive patient is commonly diuretic-induced. However, if hypokalemia persists after stopping diuretic therapy, possible mineralocorticoid excess, including primary hyperaldosteronism, must be considered. Hypertension with secondary hyperaldosteronism may occur with malignant-phase hypertension and with renal or renovascular disease. However, secondary hyperaldosteronism is associated with raised circulating levels of renin and angiotensin II, while in primary hyperaldosteronism plasma concentrations of renin and angiotensin II are inappropriately low.Hypertension and hypokalemia may also be associated with an excess of a mineralocorticoid other than aldosterone. Syndromes associated with an apparently isolated excess of 11-deoxycorticosterone, of 18-hydroxy-11-deoxycorticosterone and of corticosterone have been described. Plasma renin may be suppressed as in primary hyperaldosteronism, but aldosterone values are normal or low. Hypertension, hypokalemia, and renin suppression may also occur in Cushing's syndrome, associated with abnormalities of corticosteroid synthesis and during ingestion of licorice-containing drugs. Again, aldosterone values are normal or low.Once the diagnosis of primary hyperaldosteronism has been confirmed, the rare cases of glucocorticoid-remediable hyperaldosteronism and hyperaldosteronism associated with adrenal or ovarian carcinoma must be excluded. There-after, it is necessary to distinguish between the two commonest forms, a unilateral adrenocortical adenoma and bilateral hyperplasia of the zona glomerulosa. The statistical technique of quadric analysis used prospectively has correctly predicted adrenal pathology in 23 of 24 patients. Other methods for differentiating the two groups include comparisons of aldosterone response to sodium loading, comparison of postural and diurnal changes in plasma aldosterone, adrenal venography, and examination of the adrenal glands by ultrasound and by scintillation scanning.     

Electrical potential difference, sodium absorption and potassium secretion by the human rectum during carbenoxolone therapy.

The transmucosal electrical potential difference (pd) and the sodium and potassium net fluxes were measured in the rectum of subjects taking carbenoxolone. There was a rise in transmucosal pd persisting throughout treatment in all subjects which was accompanied by an increase in sodium absorption and potassium secretion. Comparison of the pd changes produced by carbenoxolone with those due to the mineralocorticoid 9-alpha-fluorocortisol showed that carbenoxolone had about 1/1000th the potency on a weight basis and the two drugs appeared to be additive in their effects. Topical instillation of carbenoxolone into the rectum produced an elevation of pd which persisted for three days. Amiloride and bendrofluazide did not interfere with these actions of carbenoxolone but spironolactone abolished them. One patient who developed fluid retention and hypokalaemia had a rectal pd similar to that of the other patients who had no side effects.     

Periodic hypokalaemic paralysis, adrenal adenoma, and normal colonic transport of sodium and potassium

A 47-year-old woman was cured of hypokalaemia and recurrent paralysis by the excision of an adrenal adenoma. Hypertension was initially ameliorated but was not cured. Suppression of plasma renin activity was abolished when the adenoma was excised. Repeated measurement of plasma corticosteroids before operation showed a slight increase in aldosterone and normal plasma concentrations of deoxycorticosterone, corticosterone, and cortisol. No evidence of excess mineralocorticoid was obtained from measurement of the electrolyte composition of colonic fluid or of rectal potential difference, although both these variables responded normally to salt depletion and exogenous aldosterone. The diagnostic importance of the paradoxically normal colonic measurements is emphasized and the possibility is considered that the adenoma may have secreted an unidentified hormone.     

Primary hyperaldosteronism--12 clinical cases]

STUDY OBJECTIVES: To show clinical, biochemical, and morphological data of 12 patients with primary hyperaldosteronism: eight with an aldosterone-producing adenoma and four with adrenal hyperplasia. To compare clinical and biochemical parameters of the patients with adenoma and hyperplasia. For those with adenoma, to verify clinical and biochemical modifications after adrenalectomy. PATIENTS AND METHODS: In the 12 patients with hyperaldosteronism, retrospective analysis of clinical (age, sex, blood pressure), biochemical (plasmatic and urinary potassium, plasmatic aldosterone, plasma renin activity, and plasmatic aldosterone/renin activity ratio), and morphological (computed tomography, magnetic resonance, and norcholesterol scintigraphy) data was performed. RESULTS: 1--In the 12 patients with hyperaldosteronism (seven female), the age was 51.0 +/- 10.2 years (mean +/- standard deviation), the systolic pressure 200.9 +/- 34.5 mm Hg and the diastolic pressure 120.0 +/- 12.3 mm Hg. Hypertension was diagnosed 12.0 +/- 10.1 years before. As biochemical evidence, we found kalaemia of 3.06 +/- 0.28 and urinary potassium of 63.4 +/- 16.5 mEq/l, renin activity 0.98 +/- 1.02 ng/ml/h, plasmatic aldosterone of 49.4 +/- 36.0 ng/dl, aldosterone/renin activity > 30 in 83% of the cases. As morphological evidence, computed tomography allowed diagnosis in nine patients, suggested it in two, being doubtful in one. Performed on four patients, resonance confirmed the tomography in three and was not contributive in one. The scintigraphy performed in four patients visualized two adenomas, was negative in one adenoma and in one hyperplasia. 2--In the eight patients with adenoma (six female), the youngest age and the highest diastolic pressure compared with patients with hyperplasia were statistically significant (p < 0.01 and 0.05). In the adenomas, the biochemical changes were more pronounced, but not statistically significant. The plasmatic aldosterone/renin activity ratio was also higher in the adenoma cases. 3--After the adrenalectomy, blood pressure became normal in five patients and was more easily therapeutically controlled in three. The average systolic and diastolic pressures decreased and the biochemical parameters became normal in all patients. The pre/post surgical modification of these parameters had statistical significance (systolic pressure decrease, p < 0.01; diastolic pressure decrease, p < 0.01; kalaemia increase, p < 0.001; renin activity increase, p < 0.01; aldosterone decrease, p < 0.02). The plasmatic aldosterone/renine activity ratio normalized in all patients. CONCLUSIONS: In diagnosing primary hyperaldosteronism, biochemical (kalaemia, urinary potassium, plasmatic aldosterone, renin activity, aldosterone plasmatic/renin activity) and tomography studies were important. On comparing the patients with hyperplasia with those with adenoma, we found that the latter are younger and exhibit higher diastolic pressure, both findings with statistical significance. After adenoma surgery, blood pressure became normal in five patients and improved in three, these findings, and the improvement of the kalaemia, plasmatic aldosterone, and renin activity parameters were statistically significant.     

Re-evaluation of the captopril test for the diagnosis of primary hyperaldosteronism

OBJECTIVE: We aimed to re-evaluate the captopril test in the diagnosis of primary hyperaldosteronism. DESIGN: Serum aldosterone and plasma renin activity were measured supine prior to and 60, 90, 120 minutes after oral captopril, 25 mg. PATIENTS: We have performed this test in ten patients with primary hyperaldosteronism, two with hypertension and secondary hyperaldosteronism and in ten normokalaemic patients with essential hypertension. MEASUREMENTS: Validity was assessed by mathematical prediction methods. RESULTS: Using a ratio of aldosterone to plasma renin activity greater than or equal to 1400 pmol/l per microgram/ml/h as a predictor of primary hyperaldosteronism, the captopril test had a sensitivity of 100%, a specificity of 83% and a predictive value of 82% with a 60-minute post captopril evaluation being sufficient. Nevertheless, this test was only marginally superior to a careful analysis of the supine values where a similar ratio in the presence of a normal or suppressed plasma renin activity predicted primary hyperaldosteronism with a sensitivity also of 100% but a slightly lower specificity of 75% and predictive value of 77%. CONCLUSION: Application of the captopril test to patients identified as abnormal by screening confirms all cases of primary hyperaldosteronism but false positive or equivocal results, necessitating further investigation, may occur in some patients with essential hypertension.     

Genetic study of patients with dexamethasone-suppressible aldosteronism without the chimeric CYP11B1/CYP11B2 gene

Glucocorticoid-remediable aldosteronism is an inherited disorder caused by a chimeric gene duplication between the CYP11B1 (11beta-hydroxylase) and CYP11B2 (aldosterone synthase) genes. The disorder is characterized by hyperaldosteronism and high levels of 18-hydroxycortisol and 18-oxocortisol, which are under ACTH control. The diagnosis of glucocorticoid-remediable aldosteronism had been traditionally made using the dexamethasone suppression test; however, recent studies have shown that several patients with primary aldosteronism and a positive dexamethasone suppression test do not have the chimeric CYP11B1/CYP11B2 gene. The aim of this work was to evaluate whether other genetic alterations exist in CYP11B genes (gene conversion in the coding region of CYP11B1 or in the promoter of CYP11B2) that could explain a positive dexamethasone suppression test and to determine another genetic cause of glucocorticoid-remediable aldosteronism. We also evaluated the role of 18-hydroxycortisol as a specific biochemical marker of glucocorticoid-remediable aldosteronism. We studied eight patients with idiopathic hyperaldosteronism, a positive dexamethasone suppression test, and a negative genetic test for the chimeric gene. In all patients we amplified the CYP11B1 gene by PCR and sequenced exons 3-9 of CYP11B1 and a specific region (-138 to -284) of CYP11B2 promoter. We also measured the levels of 18-hydroxycortisol, and we compared the results with those found in four subjects with the chimeric gene. None of eight cases showed abnormalities in exons 3-9 of CYP11B1, disproving a gene conversion phenomenon. In all patients a fragment of 393 bp corresponding to a specific region of the promoter of CYP11B2 gene was amplified. The sequence of the fragment did not differ from that of the wild-type promoter of the CYP11B2 gene. The 18-hydroxycortisol levels in the eight idiopathic hyperaldosteronism patients and four controls with chimeric gene were 3.9 +/- 2.3 and 21.9 +/- 3.5 nmol/liter, respectively (P < 0.01). In summary, we did not find other genetic alterations or high levels of 18-hydroxycortisol that could explain a positive dexamethasone suppression test in idiopathic hyperaldosteronism. We suggest that the dexamethasone suppression test could lead to an incorrect diagnosis of glucocorticoid-remediable aldosteronism.     

Primary hyperaldosteronism without suppressed renin due to secondary hypertensive kidney damage

Primary hyperaldosteronism is characterized by high plasma and urinary aldosterone and suppressed PRA. Renin suppression is due to aldosterone-dependent sodium retention and mild extracellular volume expansion. We observed three patients with primary hyperaldosteronism, severe refractory hypertension, and normal to high normal PRA levels whose aldosterone/renin ratios were still elevated because of disproportionately high aldosterone levels. All available medical data on the patients as well as publications on the aldosterone/renin relationship in primary hyperaldosteronism were reviewed to explain the unusual findings. In one patient, histologically proven renal arteriolosclerosis was the probable cause of the escape of PRA from suppression by an aldosterone-producing adenoma. In the other two patients, hypertensive kidney damage due to primary hyperaldosteronism was the most likely explanation for the inappropriately high PRA, as in patient 1. All patients had high normal or slightly elevated serum creatinine levels and responded to 200 mg spironolactone/day with increased serum creatinine and hyperkalemia. Hyperkalemia was probably due to a decreased filtered load of sodium and a spironolactone-induced decrease in mineralocorticoid function. Two patients were cured of hyperaldosteronism by unilateral adrenalectomy but still need some antihypertensive therapy, whereas one patient has probable bilateral adrenal disease, with normal blood pressure on a low dose of spironolactone. In patients with severe hypertension due to primary hyperaldosteronism, PRA can escape suppression if hypertensive kidney damage supervenes. An increased aldosterone/PRA ratio is still useful in screening for primary hyperaldosteronism. These patients may respond to spironolactone therapy with a strong increase in serum creatinine and potassium. Early specific treatment of primary hyperaldosteronism is therefore indicated, and even a patient with advanced hypertension will profit from adrenalectomy or cautious spironolactone treatment.     

Cardiac consequences of primary hyperaldosteronism

The activation of the renin-angiotensin system is associated with vascular and cardiac hypertrophy. But there are few data on the renal and cardiac consequences of the hypersecretion of aldosterone. In the experimental setting, hyperaldosteronism leads to an excess of fibrous interstitial tissue and cardiac hypertrophy. In man, these consequences are those of hyperaldosteronism. The aim of this study was to assess the cardiac consequences of hyperaldosteronism in a series of 31 patients with a documented Conn adenoma, in comparison with a matched population of 31 patients with primary hypertension. For the same level of blood pressure, cardiac hypertrophy is more prominent in hyperaldosteronism and there is a positive correlation between the level of plasma aldosterone and left ventricular wall thickness. Left ventricular hypertrophy is of the concentric type. In addition, an increase in myocardial fibrosis (that can now be quantified by echocardiography) is observed, with a positive correlation between plasma aldosterone and reflected ultrasound which might correspond to increased myocardial collagen. These anatomic modifications of myocardial structure result in diastolic dysfunction. Overall, Conn adenoma is associated in accelerated disease, which is partly independent of the level of blood pressure.     

Primary hyperaldosteronism: A missed diagnosis in ‘essential hypertensives’?

Background: It has been recognised recently that primary hyperaldosteronism may be more common than previously thought, the frequency of diagnosis being improved by screening using a plasma aldosterone concentration to renin activity ratio. Aims: To determine the frequency of primary hyperaldosteronism, screening with both plasma aldosterone to renin concentration (PRC) and activity (PRA) ratios, in normokalaemic subjects previously diagnosed as having essential hypertension. Methods: Plasma potassium, aldosterone and PRCs and PRA and blood pressure (BP) were measured in 74 hypertensive subjects previously diagnosed by one physician as having essential hypertension. A normal range for plasma aldosterone/renin ratios was determined in 147 control subjects. Hypertensive subjects with elevated aldosterone/renin ratios were further assessed for primary hyperaldosteronism using saline loading and fludrocortisone suppression. Those in whom plasma aldosterone concentration exceeded 140 pmol/L after suppression tests underwent adrenal vein sampling for measurement of aldosterone and Cortisol concentrations as well as adrenal CT scanning to diagnose the cause of primary hyperaldosteronism. The main outcome measures were a diagnosis of aldosterone producing adenoma or bilateral adrenal hyperplasia based upon adrenal vein sampling. Results: Four subjects (5%) had an elevated plasma aldosterone to renin ratio using PRC and six (8%) using PRA. Two subjects (2.7%) in this selected population had primary hyperaldosteronism, both of whom had BP > 160/110 mmHg at the time of testing. Conclusions: The frequency of normokalaemic primary hyperaldosteronism appears to be greater than previously thought, though the true incidence in the general population of hypertensive subjects remains unknown. The sensitivity of diagnosis (but not specificity) may be improved by measurement of the plasma aldosterone/renin ratio and PRC is at least as adequate as PRA for this process.     

The use of aldosterone-renin ratio as a diagnostic test for primary hyperaldosteronism and its test characteristics under different conditions of blood sampling

Recent reviews recommended the use of the aldosterone/renin ratio (ARR) to screen for primary hyperaldosteronism. However, widely different cutoff levels have been proposed, and test characteristics of ARR under different conditions of sampling are not known. We conducted a retrospective review among 45 subjects with carefully validated diagnoses of primary hyperaldosteronism and 17 subjects with essential hypertension to study the utility of ARR. Sixty-two patients with 75 sets of plasma renin activity (PRA), aldosterone, and ARR values from a postural study and 48 sets of values from a saline suppression test were analyzed. Ninety-four percent of these subjects underwent investigations because of hypokalemic hypertension.ARR yielded larger areas under the curve in the receiver-operating-characteristics curve than PRA or aldosterone under all conditions of testing. Our results confirmed the superiority of ARR to either aldosterone or PRA alone as a diagnostic test for primary hyperaldosteronism.ARR cutoff levels were significantly affected by the condition of testing. Depending on posture and time of day, it varied from 13.1-35.0 ng/dl per ng/ml.h in our study population. When using ARR for screening primary hyperaldosteronism, posture and time of sampling should be standardized both within and between centers to minimize variability in cutoff levels.     

Aldosterone as a key mediator of the cardiometabolic syndrome in primary aldosteronism: an observational study

OBJECTIVE: Primary aldosteronism (PA) is characterized by the onset of both cardiac and gluco-metabolic alterations. The aim of this study was to evaluate the impact of aldosterone excess on the development of such complications, and the effects of surgical and pharmacological treatment on their long-term outcome. METHODS: We prospectively re-examined 61 patients: 25 with aldosterone-producing adenoma (APA), after surgery, and 36 patients with idiopathic hyperaldosteronism (IHA) on pharmacological treatment. The lipid, fasting and dynamic glucose profiles and the echocardiographic parameters were evaluated at diagnosis and at follow-up. RESULTS: After adrenalectomy all patients had normalization of aldosterone levels and were cured of hypokalaemia, and a resolution of hypertension was achieved in 12 of 25 patients. APA patients showed a significant reduction of both plasma glucose (P=0.017) and insulin levels (P=0.001) after 75 g oral glucose tolerance test. Stabilization of glucose metabolism complications was observed in IHA patients. Multiple regression analysis at diagnosis showed a positive correlation between homeostasis model assessment (HOMA) insulin resistance index and HOMA beta cell and serum aldosterone levels in both APA and IHA. Echocardiographic parameters were improved in both APA and IHA at follow-up and the difference was statistically significant for left ventricular mass index (P=0.017) and interventricular septum thickness (P=0.007) in APA patients. CONCLUSIONS: The removal of aldosterone excess in APA patients induces the regression of both cardiac and gluco-metabolic complications, indicating aldosterone as a main determinant of such alterations. In IHA patients the medical treatment seems to avoid the possible progression of the these alterations that appear to be stable.     

Biomechanical wall properties of the human rectum. A study with impedance planimetry.

Biomechanical properties of the rectal wall were studied in 17 healthy adult volunteers (nine men and eight women). With impedance planimetry it is possible to obtain simultaneous measurements of pressure and rectal cross sectional area (CSA) during balloon inflations. Rectal distensions were done with an intraluminal balloon using specified pressures up to 40 cmH2O above baseline rectal pressure. Balloon inflation elicited a phase of rapid increase in rectal CSA followed by a phase of slow increase until a steady state was reached. Steady state occurred within 67 to 140 seconds with the shortest period at the highest distension pressures. Steady state rectal CSA values had a non-linear relation to increasing distension pressure. Rectal CSA values in women showed a tendency of being slightly higher than male values at all pressure steps with a significant difference at 3 and 5 cm H2O. Biomechanical parameters were calculated from rectal CSA pressure relations. Circumferential wall tension increased in a linear way. Rectal compliance decreased in a non-linear way with no further decline between 30 and 40 cmH2O. The pressure elastic modulus increased steeply until a distension pressure of 35 cmH2O with no further increase to 40 cmH2O. This suggests that rectal tone is reduced as the muscle fails to resist further distension at 35 cmH2O and higher pressures. Impedance planimetry offers new possibilities for investigation of anorectal physiology through the study of segmental biomechanical wall properties of the human rectum.