Epidural Analgesia Inhibits the Renin and Aldosterone Response to Surgery

Renin activity and aldosterone concentration in plasma and excretion of sodium and potassium in urine were measured during a period of 24 hours in 12 patients undergoing hysterectomy under general anaesthesia or epidural analgesia. Analgesia extended from T4 to S5 and was effective throughout the study. The normal stress-induced increase in plasma renin activity and aldosterone was inhibited by epidural analgesia. Urinary excretion of potassium was significantly lower in the epidural group, but sodium and water retention showed no difference between groups. It is concluded that neurogenic stimuli from the surgical area are important release mechanisms of the renin-aldosterone response to surgery. The results suggest that post-operative sodium retention is caused by factors other than the mineralocorticoid system.     

A comparison of the endocrine effects of hypotension induced by nicardipine with those by sodium nitroprusside in dogs

Plasma catecholamines, plasma renin activity, plasma aldosterone and plasma cortisol during hypotension induced by sodium nitroprusside and nicardipine were studied in 27 mongrel dogs under 0.87% halothane in oxygen. They were randomly divided into three groups: sodium nitroprusside (group S: n = 8), nicardipine (group N: n = 8) and controls (group C: n = 9). Group C received no vasodilator therapy and served as a control. Mean arterial pressure was reduced and maintained at 60 mmHg for 60 minutes in hypotensive groups. No changes were noted in plasma catecholamines and plasma cortisol in group C throughout the experiment, but plasma renin activity and plasma aldosterone decreased progressively. During hypotension induced by sodium nitroprusside and nicardipine, plasma epinephrine was significantly higher than the control value. However, after the hypotensive drugs were discontinued, plasma epinephrine decreased slightly. During and after induced hypotension, plasma renin activity of group N and group S were significantly higher than the control values. The highest levels of plasma renin activity 36.7 ng.ml-1.hr-1 in group N and 23.2 ng.ml-1.hr-1 in group S were observed. Plasma aldosterone concentration was significantly higher than the control value in group N. The maximum increase occurred 30 minutes after discontinuation of the nicardipine and the highest concentration of plasma aldosterone was three times control value. In contrast, in group S, plasma aldosterone was unchanged from the control value. Plasma cortisol concentration of group N was significantly increased than the control value. However, in group S, plasma cortisol concentration showed a slight but not significant increase.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sodium and potassium status, plasma renin and aldosterone profiles in normotensive and hypertensive Johannesburg blacks

Many studies have suggested that there is an association between the sodium status, plasma renin and aldosterone profile and essential hypertension. We measured serum, urine and red blood cell (RBC) sodium and potassium, plasma renin and aldosterone levels in normotensive Whites, normotensive Blacks, mildly hypertensive Blacks, severely hypertensive Blacks and Blacks with malignant hypertension. There were no important differences between the groups studied as regarded the serum sodium, serum potassium and urinary sodium excretion values. However, the urinary potassium excretion was significantly lower in normotensive and hypertensive Blacks than in Whites. RBC sodium concentrations showed no significant differences in the mean values across the range of degrees of hypertension in Blacks, although they tended to be higher in the more severely hypertensive groups. Blacks with mild-to-moderate hypertension as well as the severely hypertensive group had significantly lower plasma renin levels than the normotensive group; only in the malignant hypertensives with advanced renal failure did the plasma renin and aldosterone levels rise.     

Inhibition of aldosterone response to surgery by saline administration

The renin-angiotensin system, ACTH and hyperkalaemia are known to induce increased plasma levels of aldosterone. In order to assess the relative significance of these mechanisms during surgical stress, aldosterone, cortisol and electrolytes in plasma were measured in 12 otherwise healthy women during and after cholecystectomy. The patients received either isotonic sodium chloride or 5 per cent glucose in water during the experimental period of 22 h. The results showed that the pronounced increase of aldosterone and the concomitant decrease of sodium in plasma found in patients given glucose in water could almost be inhibited by the administration of saline. Cortisol and potassium concentrations were identical in the two groups of subjects. It is concluded that the aldosterone response to surgery is mainly mediated via the renin-angiotensin system. This response is probably due to a reduced sodium content or volume of extracellular fluid, since it could almost be inhibited by administration of sodium chloride. The rationale of saline restriction during and after surgery is questioned.     

Effects of atrial natriuretic peptide at a low dose on water and electrolyte metabolism during general anesthesia

STUDY OBJECTIVE: To assess the hemodynamic, renal, and endocrine effects of small continuous doses of atrial natriuretic peptide (ANP) in patients anesthetized with sevoflurane for gastrectomy. DESIGN: Prospective randomized study. SETTING: Operating room and wards of a university hospital. PATIENTS: 20 ASA physical status I and II patients scheduled for gastrectomy. INTERVENTION: Atrial natriuretic peptide (0.05 microg/kg/min; ANP group, n = 10) or saline (control group, n = 10) was infused continuously for 2 hours beginning at the start of the operation. MEASUREMENTS: Plasma concentrations of ANP, brain natriuretic peptide, cortisol, angiotensin II, and aldosterone; plasma renin activity; serum and urinary sodium, potassium, and chloride; and urinar output. MAIN RESULTS: The ANP group showed much greater urine volume and sodium, potassium, and chloride excretion than the control group, although the ANP group had a lower arterial blood pressure. The infusion did not affect surgery-induced increases in hormones. No patients experienced excessive hypotension, bradycardia, or other perioperative complications. CONCLUSIONS: Continuous intravenous infusion of ANP at 0.05 microg/kg/min during gastrectomy was associated with greater water and electrolyte excretion unaccompanied by changes in potentially interacting hormones. Low-dose infusion may be particularly safe and useful for controlling water and electrolyte metabolism intraoperatively.     

Effects of intraoperative administration of atrial natriuretic peptide

BACKGROUND: Biological activity of endogenous atrial natriuretic peptide (ANP) may decrease during cardiopulmonary bypass. To evaluate the effects of intraoperative administration of exogenous ANP in patients undergoing cardiopulmonary bypass, we conducted a prospective randomized study. METHODS: Eighteen patients undergoing mitral valve surgery were randomized to receive either ANP treatment (ANP group; n = 9) or no ANP treatment (control group; n = 9). Atrial natriuretic peptide was given immediately after initiation of cardiopulmonary bypass for 6 hours (0.05 microg x kg(-1) x min(-1)). Plasma ANP, brain natriuretic peptide and cyclic guanosine monophosphate (cGMP) levels, hemodynamic variables and renal function were assessed perioperatively. RESULTS: Administration of ANP increased plasma cyclic guanosine monophosphate levels, urine output and fractional sodium excretion, and decreased preload, afterload and plasma brain natriuretic peptide levels significantly (p < 0.05). Plasma cyclic guanosine monophosphate levels correlated with plasma ANP levels (r = 0.95, p = 0.0001), correlated with fractional sodium excretion (r = 0.53, p = 0.02), and correlated inversely with systemic vascular resistance (r = -0.54, p = 0.02). CONCLUSIONS: Intraoperative administration of ANP had potent effects on natriuresis and systemic vasodilation by elevating cyclic guanosine monophosphate levels. The results suggest that the technique is useful for the management of hemodynamics and water-sodium retention after cardiopulmonary bypass.     

Relationship of Plasma Aldosterone Concentration to Electrolytes and Acid-base Balance in Blood after Open Cardiac Surgery

Plasma aldosterone concentration was measured in 11 cardiac patients after open cardiac surgery, by the radioimmunoassay method, and the relationship of it to electrolytes and acid-base balance of blood was analyzed. Plasma aldosterone concentration was markedly elevated in patients with low cardiac output, who required postoperative drip infusion of Isoproterenol, and in addition, both remarkable metabolic alkalosis and increase of potassium excretion in urine were confirmed in these patients. Plasma aldosterone concentration correlated significantly with potassium excretion in urine and was inversely related with potassium balance. However, plasma potassium concentration or arterial pH had no correlation to it. Approximately an inverse correlation was found between the logarithm of the sodium/potassium ratio in urine and plasma aldosterone concentration. These data indicate that aldosterone is an important factor which produces potassium depletion after open cardiac surgery.     

Distal nephron sodium-potassium exchange in children with nephrotic syndrome

While recent literature data suggest that a primary impairment in sodium excretion is the basic abnormality in the pathogenesis of edema formation in the nephrotic syndrome, there is ample evidence that functional hypovolemia contributes to stimulation of renal sodium and fluid retention. Vasoactive hormones such as renin and aldosterone are involved in this process. Discrimination between both mechanisms would be possible by assessment of aldosterone bioactivity and will have therapeutical consequences by indicating the need for administration of i.v. albumin or diuretics. In this paper, several indices of aldosterone bioactivity were assessed in 85 patients with minimal lesion nephrotic syndrome (118 measurements were performed in patients while in remission and 210 following relapses), and in 41 nephrotic patients with different types of nephropathy and were related to plasma renin and aldosterone levels. A better correlation was found between log aldosterone and U(K+)/U(Na+) + U(K+) ratio than with other parameters measuring renal potassium handling such as transtubular potassium gradient, fractional excretion of potassium and urine K+/urine Na+ or urine K+ creatinine ratios. In patients with renal sodium retention (FE(Na)% less than 0.5), an U(K+)/U(Na+) + U(K+) ratio higher than 0.60 identifies patients with increased aldosterone levels and indicates functional hypovolemia. This index may therefore be used to assess which patients will benefit from i.v. albumin administration.     

Sodium, renin, aldosterone, catecholamines, and blood pressure in diabetes mellitus

Interrelations among plasma renin activity (PRA), aldosterone and cortisole levels, 0lood volume, exchangeable sodium, urinary catecholamines, and blood pressure were studied in 35 normal subjects and 60 age-matched non-azotemic patients with diabetes mellitus (60% with hypertension, 15% with orthostatic hypotension). Basal PRA, plasma aldosterone, cortisol, blood volume, plasma potassium, and urinary electrolytes were comparable in diabetic and normal subjects. Diabetic patients, however, had a 10% increase in body sodium (P less than 0.01), and 8% of them showed normal postural PRA responses and subnormal aldosterone responses; 22% had subnormal PRA and normal aldosterone responses, and 17% had subnormal responses of PRA and aldosterone. Non-PRA-related aldosterone responses could not be explained by ACTH or electrolytes. Orthostatic decreases in blood pressure correlated (P less than 0.01) with both catecholamine excretion and basal PRA. This suggests that in diabetes mellitus, body sodium is increased. Basal PRA and plasma aldosterone are usually normal, but their postural responses are frequently impaired. Absent aldosterone responses, despite normal PRA responsiveness, may reflect an adrenal abnormality or an ineffective form of renin. Marked postural aldosterone stimulation, unrelated to PRA, ACTH, or electrolytes, points to a potent unknown factor in aldosterone control. Low levels of free peripheral catecholamines and PRA may be complementary factors contributing to postural hypotension.     

Clinical study of perioperative changes in plasma potassium

Forty adult patients undergoing non-cardiac major surgery were divided into 2 groups. Group A (n = 20) was anesthetized by balanced intravenous procaine anesthesia and group B (n = 20) by epidural block. Blood volume, urine output, potassium in plasma as well as urine, pH, glucose, aldosterone, cortisol and insulin were measured from 24 hours before operation to 48 hours after operation. Evident perioperative trend of hypokalemia in patients with normal renal function was most likely due to the following factors: potassium loss prior to operation, improper pre- or post-operative replacement of fluids, perioperative stress, increasing of blood insulin and urine potassium excretion. Our results run against to the general concept that it may not be necessary to supply potassium with 72 hours after operation.     

Plasma renin activity and plasma aldosterone during anaesthesia and operative stress and beta-adrenergic blockade (author's transl)]

In 21 patients undergoing ear operations associated with minimal bleeding plasma renin activity and plasma aldosterone concentration were studied before and during surgical procedure, and in the postoperative state. Studies were performed in two groups, one without (n=9) and one with beta-adrenergic blockade by Practolol (n=12). Plasma renin activity increased significantly during halothane anaesthesia alone whereas the surgical manipulations did not further influence mean values significantly. Thus, it seems to be established that anaesthesia per se influences renin secretion. On the other hand Practolol does not show an inhibiting effect. The plasma renin increase following anaesthesia is due to the hemodynamic including renal hemodynamic, changes as well as to activation of the sympatho-adrenal system. Changes in plasma aldosterone are variable. For the greater part of patients with beta-adrenergic blockade an increase during the operative procedure was found. However, in some patients especially in the control group, plasma aldosterone was unchanged or decreased in spite of increasing renin values. Significantly lower plasma potassium concentration in these cases seems to indicate the important contributing role of potassium for the short-term regulation of aldosterone secretion. Plasma sodium concentration remained unchanged for the periods studied.     

Insulin and hypertension--the mechanisms of high blood pressure during chronic insulin infusion

The purpose of this study was to assess the effects of chronic insulin infusion on blood pressure and urinary sodium excretion in Wistar rats. Fifteen Male Wistar rats weighing about 220 g were used. The rats were housed in metabolic cage and measured urine volume. Osmotic minipumps filled with insulin (0.57 U/day, Insulin group, n = 9) or saline (0.014 cc/day, Control group, n = 6) were implanted subcutaneously under ether anaesthesia, and blood pressure, urine volume, urinary sodium excretion (UNaV), plasma renin activity (PRA), plasma norepinephrine concentration (PNE) were measured for 4 weeks. In insulin group, there were no significant changes on plasma glucose levels, but systolic blood pressure rose significantly from 119 mmHg to 140 mmHg after 4 weeks. In this group, urine volume, UNaV, and PRA were significantly lower than those of control group and PNE was tended higher but not significant (P less than 0.1). Exogenous NE was given intravenously to assess the endogenous NE activity. Blood pressure elevation caused by exogenous NE in insulin group was suppressed significantly than that of control group. On the basis of these findings, we conclude that insulin can cause high blood pressure due to sodium retention and activation of endogenous NE.     

风湿性心脏瓣膜病围术期电解质变化的研究

目的对心肌细胞内、外钾、镁离子进行研究,旨在掌握电解质与心肌保护的关系及其变化规律,调整电解质的平衡,减少心肌损伤和心律失常。方法选择２７例风湿性心脏病（ｒｈｅｕｍａｔｉｃｈｅａｒｔｄｉｓｅａｓｅ,ＲＨＤ）患者和８例先天性心脏病（ｃｏｎｇｅｎｉｔａｌｈｅａｒｔｄｉｓｅａｓｅ,ＣＨＤ）患者分为ＲＨＤ组和ＣＨＤ组,在围术期测定血液、心肌细胞内和尿中钾、镁离子的含量以及血浆醛固酮水平。结果ＲＨＤ组心肌钾、镁含量术前低于ＣＨＤ组,尿排钾、镁的高峰在术后２４小时内。醛固酮水平ＲＨＤ组中二尖瓣病变患者术前就高于正常,术后２４小时达高峰。结论维持围术期钾、镁离子的平衡,可明显减少心律失常和心肌损伤的发生;现行的术前补钾量和时间不足,在加强补钾的同时,应配合补充镁;术后２４小时内,也应补充钾和镁制剂     

Hyponatremia and natriuresis following subarachnoid hemorrhage in a monkey model

A monkey model of subarachnoid hemorrhage (SAH) was used to study both the incidence of hyponatremia and natriuresis and the associated changes in antidiuretic hormone (ADH) secretion and salt and water balance. Following SAH, seven of nine monkeys became natriuretic and hyponatremic. The natriuretic period lasted an average of 4.4 +/- 0.4 days. The mean nadir of serum sodium content was 125.7 +/- 1.6 mEq/liter, and occurred on the average on the 5th day following SAH. The sodium balance after SAH was negative as compared to the preoperative positive sodium balance (p less than 0.001). The plasma vasopressin level was usually elevated for a day following surgery, but there was no significant difference in the levels during the preoperative period and during the period of natriuresis following SAH. The daily urine output and aldosterone levels were not significantly different, and the plasma volume was slightly, but not significantly, decreased after SAH. Four of the animals that had a hyponatremic and natriuretic response following SAH showed a normal regulation of vasopressin in response to both a water challenge and hypertonic saline challenge. The three monkeys that underwent sham procedures did not become hyponatremic and natriuretic postoperatively. The sham-operated monkeys did not show significant differences in their plasma vasopressin levels, urine volume, plasma volume, and aldosterone levels following surgery. These observations are more consistent with primary natriuresis as the cause of hyponatremia rather than the syndrome of inappropriate secretion of ADH. The cause of the renal loss of sodium is not known, but the possibility of a brain natriuretic factor or an alteration in the neural control of the kidney should be considered.     

Hypothesis: a simple algorithm to distinguish between hypoaldosteronism and renal aldosterone resistance in patients with persistent hyperkalemia

Aim: Many patients with hyperkalemia have a readily identifiable cause, which leads to appropriate management. In others, particularly those with a reduced glomerular filtration rate, differentiating between (relative) hypoaldosteronism (HA) and renal aldosterone resistance (RAR) can be problematic. The aim of this study was to see if a plasma aldosterone to potassium algorithm could be defined which would help identify patients with hyperkalemia owing to suboptimal levels of aldosterone, thereby validating treatment with 9-alpha-fluhydrocortisone, instead of cation exchange resins, if more conservative treatment fails. Methods: A literature search for, and analysis of, studies providing details of plasma aldosterone and plasma potassium in normals (made hyperkalemic)and patients with a plasma potassium >5.3 mmol/L, and a contemporaneous plasma aldosterone. Results: One study was found in which normals were made significantly hyperkalemic (to 6.3 mmol/L). These subjects, while on a high sodium, low potassium (western) diet (n = 5), provided an arbitrary definition of a simple aldosterone to potassium algorithm for diagnosis (factored aldosterone (FAldo) = plasma aldosterone/(plasma K – 4.2)). The limit for FAldo is set at 280(pmol/L) or 10(ng/dL): results below the limit suggest HA; above the limit, RAR. This algorithm was then tested against, and, when plasma potassium was greater than 5.3, found to be consistent with, reported patients with confirmed HA (n = 33) and pseudohypoaldosteronism (n = 23). The ratios in reported patients with renal failure (n = 43) were consistent with either HA (n = 30) or RAR(n = 13). Hypothesis: In hyperkalemic patients a plasma aldosterone to potassium algorithm may help distinguish HA from RAR, thereby guiding therapy.     

Increased sodium requirement following early postnatal surgical correction of congenital uropathies in infants

Serum electrolyte equilibrium and plasma aldosterone concentrations were monitored in 19 infants who had severe obstructive uropathy or grade 5 vesico-ureteral reflux and were undergoing surgical correction in the first 2 months of life. Before surgery high plasma aldosterone levels were observed in 8 patients, but serum sodium and potassium concentrations were normal. Plasma concentrations of aldosterone were elevated in all patients during the week following surgery and 7 patients developed severe hyponatraemia, hyperkalaemia and weight loss despite very high plasma aldosterone concentrations. As a consequence 5 infants were infused with sodium chloride (4 mEq/kg per day) before and for 36h after surgery; this prevented metabolic imbalance. We conclude that infants undergoing surgical correction of uropathies may require a high sodium intake to maintain electrolyte balance and adequate growth.     

Aldosterone in congestive heart failure: analysis of determinants and role in sodium retention.

In patients with congestive heart failure (CHF), the role of aldosterone in the abnormal sodium (Na+) retention and the determinants of plasma aldosterone (PA) including plasma atrial natriuretic factor (hANF), plasma renin activity (PRA), and plasma potassium (K+) have not been fully elucidated. We therefore studied the effect of the specific aldosterone antagonist, spironolactone, on urinary Na+ and K+ excretion and plasma hormone responses in 6 Na(+)-retaining CHF patients. After withdrawal of diuretics 4 days prior to the study, the CHF patients were placed on a Na+ intake of 100 mmol/day for 9 days. Spironolactone, 200 mg p.o. bid, was administered for the last 4 days of the 9-day study period. PRA and norepinephrine increased with spironolactone treatment (both p less than 0.05). Plasma hANF before spironolactone was significantly elevated and decreased during spironolactone therapy (p less than 0.05). Urinary Na+ excretion significantly increased during spironolactone administration and the positive Na+ balance was reversed in the CHF patients. Moreover, the urine Na+:K+ concentration ratio significantly increased during spironolactone administration. Analysis of the relationship between PA, plasma K+, PRA, and plasma hANF indicated that PRA is the primary determinant of PA in patients with CHF. Thus, the present results indicate that the renin-angiotensin-aldosterone system is an important mediator of Na+ retention in CHF, as evidenced by the reversal of the positive Na+ balance with a specific aldosterone antagonist. This natriuretic effect can be demonstrated in the presence of potential antinatriuretic influences including stimulation of the renin-angiotensin and sympathetic nervous systems and a decrease in plasma hANF.     

Morbid Obesity,Hypertensive Disease and the Renin-Angiotensin-Aldosterone Axis

Background: Resistance to insulin and secondary hyperinsulinemia seem to be the putative link between morbid obesity (MO) and hypertensive disease (HD). Adipose tissue can secrete leptin and angiotensinogen, among other substances. Leptin activates the sympathetic nervous system, leading to HD. Angiotensinogen is a substrate for renin, therefore taking part in the renin-angiotensin-aldosterone axis and the regulation of blood pressure. In MO, both hypertrophy and hyperplasia of the adipocytes lead to an increase in the secretion of both substances, leading to loss of the equilibrium between the levels of both hormones. The aim of the present study was to evaluate these abnormalities and their potential reversibility following bariatric surgery. Methods: Data from 100 patients with MO was retrospectively evaluated. Anthropometric data, the plasma renin activity (PRA), plasma levels of aldosterone, ACE, potassium and sodium were collected both prior to surgery and 6, 12, 24 and 36 months after surgery. Results: The waist-hip ratio (WHR) before surgery allowed classification of our patients in two groups: central obesity (WHR ≥0.90 in men and ≥0.85 in women); peripheral obesity (WHR <0.90 in men and <0.85 in women). In patients with central obesity, high levels of PRA, aldosterone and ACE with sodium retention and potassium loss and high insulin levels, were found. These changes were not found in patients with peripheral obesity. After gastric bypass, these abnormalities tended to disappear, mainly in the first 6 months. Conclusions: The reduction of BMI and WHR after gastric bypass confirmed this operation to be effective against MO. The high basal levels of insulin and the high rate of HD and diabetes in patients with central obesity seem to indicate that they suffer a metabolic syndrome with significant hormonal imbalances and sodium retention. Patients with peripheral obesity only showed a peripheral resistance against insulin, probably with a shorter duration of the hormonal action, but they did not show hormonal abnormalities or sodium retention. After gastric bypass these abnormal hormone levels tended to normalize.     

Effect of prolonged pneumoperitoneum on intraoperative urine output during laparoscopic gastric bypass

BACKGROUND: Intraoperative oliguria is common during laparoscopic operations. The objective of this study was to evaluate the effects of prolonged pneumoperitoneum during laparoscopic gastric bypass (GBP) on intraoperative urine output and renal function. METHODS: 104 patients with a body mass index between 40 and 60 kg/m2 were randomly assigned to laparoscopic (n = 54) or open (n = 50) GBP. Intraoperative urine output was recorded at 30-min intervals. Blood urea nitrogen and creatinine levels were measured at baseline and on postoperative days 1, 2, and 3. Levels of antidiuretic hormone, aldosterone, and plasma renin activity were also measured in a subset of laparoscopic (n = 22) and open (n = 24) GBP patients at baseline, 2 hours after surgical incision, and in the recovery room. RESULTS: The laparoscopic and open groups were similar in age, gender, and body mass index. There was no significant difference in amount of intraoperative fluid administered between groups (5.4 +/- 1.6 L, laparoscopic versus 5.8 +/- 1.7 L, open), but operative time was longer in the laparoscopic group (232 min versus 200 min, p < 0.01). Urinary output during laparoscopic GBP was 64% lower than during open GBP at 1 hour after surgical incision (19 mL versus 55 mL, p < 0.01) and continued to remain lower than that of the open group by 31-50% throughout the operation. Postoperative blood urea nitrogen and creatinine levels remained within the normal range in both groups. Serum levels of antidiuretic hormone, aldosterone, and plasma renin activity peaked at 2 hours after surgical incision with no significant difference between the two groups. CONCLUSION: Prolonged pneumoperitoneum during laparoscopic gastric bypass significantly reduced intraoperative urine output but did not adversely alter postoperative renal function.     

Effects of the aldosterone receptor antagonist potassium canrenoate on renal blood flow and urinary output during prolonged increased intraabdominal pressure (IAP) in pigs

Background Increased intraabdominal pressure can be found after major abdominal trauma and necrotizing pancreatitis and is used during laparoscopic surgery. The purpose of this study was to investigate the effect of the aldosterone receptor antagonist (potassium canrenoate) on renal hemodynamics and urinary output in pigs during increased intraabdominal pressure (IAP).Methods The IAP was kept at 30 mmHg for 3 h by instillation of Ringers solution into the peritoneal cavity. Eight animals were treated with potassium canrenoate and eight animals served as controls. Renal blood flow, hormones in femoral artery blood, and the urinary output were measured.Results The administration of potassium canrenoate was followed by increased aldosterone concentrations in arterial blood, increased blood concentration of potassium, and increased concentration of sodium in the urine, indicating satisfactory inhibition of aldosterone. Potassium canrenoate did not cause changes in cardiac output and arterial pressure. It did not affect the renal vascular resistance that increased at an IAP of 30 mmHg, or the renal blood flow that remained constant during the experiments. The group treated with potassium canrenoate had higher mean urinary output than the controls, but the difference was not significant.Conclusion Increased IAP in pigs is associated with markedly reduced urinary output and increased serum concentrations of aldosterone. Although the urinary output did not increase significantly, the increased sodium concentration in the urine of canrenoate-treated animals suggests that the high blood level of aldosterone contributes to the oliguria under increased IAP.