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Biomedical subjects

E B Pedersen

Publications and source records attributed to E B Pedersen.

At least 235 records · Page 13Linked to original sources
PubMed1988

Disturbed relationship between urinary prostaglandin E2 excretion, plasma arginine vasopressin and renal water excretion after oral water loading in early hepatic cirrhosis.

An oral water load of 20 ml kg-1 body weight was given to 11 patients with early hepatic cirrhosis and to 16 healthy control subjects. Urinary output (V), free water clearance (CH2O), urinary excretion of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha), and plasma concentration of arginine vasopressin (AVP) were determined before and during the first 4 h after loading. During basal conditions, PGE2 excretion was the same in patients (75 pg min-1, median, range 15-569) and controls (78 pg min-1, range 22-262), but during the first hour after water loading, PGE2 increased to a significantly higher level in cirrhotic patients (423 pg min-1, median) than in control subjects (162 pg min-1) (P less than 0.05). No difference in PGF2 alpha excretion was found between the two groups. Urinary output and CH2O were significantly lower after water loading in patients than in controls. Arginine vasopressin before water loading did not differ between patients and control subjects, but after loading it was unchanged in the patients, whereas a significant reduction (1.9 to 1.4 pmol l-1, P less than 0.01) was found in the control subjects. In controls, but not in patients, PGE2 was significantly positively correlated to V and CH2O, and negatively correlated to AVP after water loading. Thus, renal PGE2 excretion is increased and CH2O is decreased after water loading in patients with early hepatic cirrhosis, and a disturbed relationship seems to exist between PGE2 on the one hand, and AVP and renal water excretion, on the other, in these patients after water loading.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Acute and long-term renal effects of angiotensin converting enzyme inhibition in normotensive, normoalbuminuric insulin-dependent diabetic patients.

Glomerular filtration rate (GFR) (thalamate clearance), renal plasma flow (RPF) (hippuran clearance), and urinary albumin excretion rate (AER) were measured in 10 normoalbuminuric, normotensive insulin-dependent diabetic patients and 8 normal subjects before and during acute angiotensin converting enzyme (ACE) inhibition by means of enalapril (10 mg IV). The effect of placebo versus enalapril (30 mg day-1) was also studied for 3-month treatment periods in the insulin-dependent diabetic patients. Acute ACE-inhibition caused a decline in filtration fraction (FF) from 0.259 +/- 0.011 (+/- SE) to 0.237 +/- 0.013 (2p less than 0.01) in the diabetic patients, and from 0.210 +/- 0.010 to 0.188 +/- 0.006 (2p less than 0.02) in the normal subjects. Mean arterial blood pressure was lowered from 90 +/- 1 to 84 +/- 2 mmHg (2p less than 0.01) and from 91 +/- 1 to 86 +/- 2 mmHg (2p less than 0.05). No significant change in blood glucose, AER or fractional albumin excretion (theta Alb) was seen in either group. After 3 months of enalapril treatment FF was decreased from 0.253 +/- 0.011 to 0.235 +/- 0.011 (2p less than 0.05), AER from 5.6 x/ divided by 1.7 to 4.3 x/divided by 1.6 micrograms min-1 (2p less than 0.01) and theta Alb from 1.22 +/- 0.22 x 10(-6) to 0.92 +/- 0.12 x 10(-6) (2p less than 0.02). The decline in total renal resistance was not significant (0.175 +/- 0.013 to 0.165 +/- 0.012 mmHg ml-1 min-1) and significant changes in GFR, RPF, mean arterial pressure or HbA1c were not observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Albuminuria↗
PubMed1988

Increased atrial natriuretic peptide in the nephrotic syndrome. Relationship to the renal function and the renin-angiotensin-aldosterone system.

Atrial natriuretic peptide (ANP), angiotensin II (Ang II), and aldosterone (Aldo) in plasma and creatinine clearance (Ccr) were determined during basal conditions in 17 patients with the nephrotic syndrome and 20 control subjects. In addition, six of the patients were studied after seven remissions of the syndrome. In the nephrotic syndrome ANP was higher than in the control group (9.7 (median) versus 7.2 pmol/l, p less than 0.01), Ccr was lower (55 versus 99 ml/min, p less than 0.01). Angiotensin II and Aldo were the same in patients and control subjects. After remission of the syndrome ANP was reduced (11.2 to 5.4 pmol/l, n = 7, p less than 0.02) and Ccr increased (52 to 84 ml/min, n = 7, p less than 0.02), whereas Ang II and Aldo were unchanged. A significant, negative correlation was found between ANP and Ccr in the subgroup of patients in whom the syndrome remitted (Q = -0.547, n = 14, p less than 0.05). Atrial natriuretic peptide was not correlated to either Ang II or Aldo in either of the groups. It is concluded that patients with the nephrotic syndrome have elevated ANP, and it is suggested that a high ANP may be a compensatory phenomenon induced by a decreased renal ability to eliminate sodium and water.

Adult↗
PubMed1988

Increased atrial natriuretic peptide in an early stage of chronic glomerulonephritis.

Atrial natriuretic peptide (ANP), angiotensin II (AII), aldosterone (Aldo), arginine vasopressin (AVP) in plasma, urinary excretion of prostaglandin E2 (PGE2) and urinary sodium excretion rate (UNaV) were determined in 11 normotensive patients with chronic glomerulonephritis and a normal glomerular filtration rate (GFR) and in 14 healthy control subjects before, during and after intravenous infusion of a 2.5% sodium chloride solution. During basal conditions ANP was increased in patients compared with controls (9.8 pmol/l (median) versus 7.2 pmol/l, p less than 0.01). After sodium infusion ANP was unchanged in the patients but significantly increased in the controls. AII, Aldo, AVP in plasma and urinary PGE2 excretion were the same in patients and controls. The urinary sodium excretion rate was significantly increased in patients compared with controls during sodium infusion (p less than 0.05). No correlations were found between ANP and UNaV, AII or Aldo in either patients or controls. The relationship between serum osmolality (Sosm) and AVP was normal in the patients. It can be concluded that in normotensive patients with chronic glomerulonephritis and normal GFR, ANP is increased during basal conditions and the response to acute volume expansion may be blunted. The renin-angiotensin system, the osmoregulatory system and urinary PGE2 excretion are normal and respond in a normal way to volume expansion. It is suggested that the increased level of ANP can be viewed as a compensatory phenomenon to an abnormal sodium or volume homeostasis in the early stages of chronic glomerulonephritis.

Adolescent↗
PubMed1988

Increased plasma levels of atrial natriuretic peptide in patients with chronic renal failure: effect of noradrenaline infusion.

Basal plasma atrial natriuretic peptide (ANP) and blood pressure were measured in 11 patients with chronic renal failure before requirement of dialysis, 13 patients on chronic dialysis, and 28 control subjects (Study 1). Changes in ANP during noradrenaline infusion were determined in eight patients with chronic renal failure before dialysis, 12 patients on chronic dialysis, and 17 control subjects (Study 2). ANP was also measured in 14 healthy control subjects during angiotensin II infusion (Study 3). Study 1 showed a significantly greater ANP in patients before the stage of dialysis (median 23 pg/ml) and in dialysis patients (34 pg/ml) than in control subjects (19 pg/ml) P less than 0.01 for both. In Study 2, noradrenaline induced an increase in ANP in the non-dialysed patients (P less than 0.05) and in the control subjects (P less than 0.01), but not in the dialysis patients. According to Study 3, ANP was unchanged during angiotensin II infusion. Blood pressure was increased in all groups during noradrenaline and angiotensin II infusions. It can be concluded that ANP Is increased both in patients with chronic renal failure before requirement of dialysis and in patients on maintenance dialysis. It is suggested that noradrenaline stimulates ANP release.

Adolescent↗
PubMed1988

Reduced angiotensin II induced vascular reactivity in chronic renal failure.

Eight patients with chronic renal failure before the stage of dialysis (Group 1), 11 patients on regular dialysis treatment (Group 2) and 14 healthy control subjects (Group 3) were studied before, during and after angiotensin II (AII)-infusion. Blood pressure (BP), heart rate (HR), plasma levels of AII, aldosterone (Aldo), arginine vasopressin (AVP), noradrenaline (NA) and adrenaline (A), and serum concentrations of parathyroid hormone (PTH), calcium and magnesium were determined. AII induced vascular reactivity was reduced both in Group 1 and 2 compared with Group 3. Basal AII was the same in the three groups, and only in dialysis patients was AII induced vascular reactivity negatively correlated to basal AII. Aldo and NA were higher in Group 2 than in Group 3, and AVP was higher in both groups of patients compared with controls. HR declined during AII induced elevation of BP in the control subjects but not in the patients. Neither PTH, serum calcium nor serum magnesium was correlated to BP or vascular reactivity. It can be concluded that AII induced vascular reactivity is reduced both in patients with renal failure before dialysis and in patients on regular dialysis treatment. Basal blood levels of Aldo and NA are increased in dialysis patients and AVP is increased in both groups of patients, but neither these abnormalities nor blood levels of PTH, calcium or magnesium seem to be the background upon which the abnormal vascular reactivity develops.

Adolescent↗
PubMed1987

Atrial natriuretic peptide during pacing in controls and patients with coronary arterial disease.

At rest, during cardiac catheterization, aortic plasma levels of immunoreactive atrial natriuretic peptide did not differ between 10 controls with atypical chest pains and normal coronary arteries and 9 patients with stable angina pectoris and coronary arterial disease (55.2 +/- 19.8 vs. 64.8 +/- 19.8 pg/ml, NS). Nor did atrial natriuretic peptide values differ between the two groups during or after atrial pacing (150 beats/minute), which induced electrocardiographic and metabolic signs of acute myocardial ischaemia in the patients with coronary arterial disease but in none of the controls. Pacing, when carried out for more than 300 seconds, induced an increase of plasma atrial natriuretic peptide that correlated with duration of pacing (r = 0.80, P less than 0.001), and similarly in controls and patients with coronary arterial disease. In a second part of the study, which included 2 controls and 2 patients with coronary arterial disease, post-pacing coronary sinus concentrations of atrial natriuretic peptide were 10-20 times higher than peripheral levels (415- greater than 890 pg/ml). The concentration of atrial natriuretic peptide rose as blood from the caval veins (34 +/- 7 pg/ml) entered the right atrium (56 +/- 24 pg/ml), but thereafter was unchanged in the pulmonary artery (51 +/- 3 pg/ml) and the aorta (46 +/- 9 pg/ml). In conclusion, the results gave no evidence for ischaemic heart disease without congestive cardiac failure to be associated with altered levels of atrial natriuretic peptide. It was confirmed that atrial pacing stimulates the secretion of atrial natriuretic peptide which is produced by the heart and released via the coronary sinus into the circulation.

Atrial Natriuretic Factor↗
PubMed1987

Relationship between urinary prostaglandin E2 and F2 alpha excretion and plasma arginine vasopressin during renal concentrating and diluting tests in renal transplant recipients.

Urinary excretion of prostaglandin E2 (PGE2 and F2 alpha (PGF2 alpha) and plasma concentration of arginine vasopressin (AVP) were determined during urinary concentrating and diluting tests in renal transplant recipients and control subjects. During the concentrating test PGE2 and PGF2 alpha remained unchanged in the renal transplant recipients, whereas both PGE2 and PGF2 alpha were significantly reduced in the control subjects. During the diluting test PGE2 and PGF2 alpha increased in both groups but, contrary to PGF2 alpha, PGE2 was significantly higher in all periods in the transplant recipients compared to the controls. However, the prostaglandin excretion rates per kidney were significantly higher in the renal transplant recipients than control subjects, for all periods during both the concentrating and the diluting test. Arginine vasopressin was significantly higher in renal transplant recipients than control subjects during basal conditions, increased to a significantly higher level in the transplant recipients after thirst, but was reduced to the same levels in the two groups during the diluting test. It is concluded that the increased excretion of prostaglandins in renal transplant recipients may be a compensatory phenomenon representing an adaptation to a reduced renal mass in order to maintain adequate renal water excretion. Although a direct relationship between the prostaglandin excretions of PGE2 and PGF2 alpha and AVP does not seem to exist, it is possible that the higher prostaglandin excretion in the renal transplant recipients may be a counterbalancing mechanism to the higher AVP level, which most likely is secondary to a decreased responsiveness to vasopressin of the renal collecting ducts in the transplanted kidney.

Adult↗
PubMed1987

Exaggerated natriuretic response to isotonic volume expansion in hypertensive renal transplant recipients: evaluation of proximal and distal tubular reabsorption by simultaneous determination of renal plasma clearance of lithium and 51Cr-EDTA.

In fourteen hypertensive and fourteen normotensive renal transplant recipients, and in a group of thirteen healthy controls, changes in natriuresis, glomerular filtration rate (GFR), and tubular reabsorption of sodium were determined in relation to intravenous infusion of 2 mmol isotonic sodium chloride per kg body weight. An exaggerated natriuresis was demonstrated in the hypertensive renal transplant recipients. This new finding indicates that the augmented natriuresis following plasma volume expansion, which is a characteristic finding in subjects with arterial hypertension, is not mediated by the renal nerves. Investigation of the tubular reabsorption rates of sodium by simultaneous determination of the renal clearance of 51Cr-EDTA and lithium showed that in the hypertensives the changes in tubular handling of sodium were different from those registered in the normotensive subjects. The increased sodium excretion in the hypertensive renal transplant recipients was caused by an increased output of sodium from the proximal tubules which was not fully compensated for by an increased distal reabsorption. Whether this increased delivery of sodium to the distal segments was caused by changes in GFR or in the proximal tubular reabsorption of sodium could not be clarified in the present study and warrants further investigations.

Absorption↗
PubMed1987

Recumbent cranial diabetes insipidus. Studies in a patient with adipsia, hypernatremia, poikilothermia and polyphagia.

A male, aged 16, with chronic hypernatremia, adipsia, polyphagia, and poikilothermia was studied regarding regulation and secretion of arginine vasopressin. During recumbency at night, low plasma arginine vasopressin levels and increased volumes of dilute urine were found; whereas plasma arginine vasopressin levels and urine osmolalities rose and urine volumes decreased during ambulation in the daytime. Neither a 25% reduction of mean arterial pressure nor hypertonic saline infusion increased plasma arginine vasopressin or urine osmolalities. Treatment with 1-desamino-D-arginine-vasopressin at 6 p.m. and a scheduled fluid intake according to actual body weight eradicated hypernatremia and hyperosmolality. These data demonstrate a complete loss of arginine vasopressin secretion to osmotic stimulation, a partial defect of arginine vasopressin secretion to non-osmotic stimulation, an abolished response to stimulation of high-pressure-baroreceptors, but an intact responsiveness to stimulation of low-pressure-baroreceptors.

Adolescent↗
PubMed1987

Effect of intravenous sodium loading on renal tubular handling of sodium and water in unilaterally nephrectomized humans.

Glomerular filtration rate (GFR), proximal absolute and fractional reabsorption of isotonic fluid (PAR and PFR) and distal absolute and fractional reabsorption of sodium (DARNa and DFRNa) were measured using the lithium clearance technique in nine unilaterally nephrectomized people (UNP) 1-11 years postnephrectomy and in 14 controls before, during and after an intravenous sodium load. Glomerular filtration rate per kidney was 53% higher in UNP and decreased slightly but significantly (p less than 0.01) in both groups during sodium loading. The PAR per kidney was significantly higher in UNP (p less than 0.01) but PFR was the same as in controls. Both groups responded to sodium loading with a significant decrease in both PAR and PFR. In UNP, DARNa per kidney was significantly higher than in controls (p less than 0.01) but DFRNa was the same in the two groups. Sodium loading resulted in a further increase in DARNa and a decrease in DFRNa in both groups. Both groups responded to sodium loading with a similar increase in fractional sodium excretion. It is concluded that unilateral nephrectomy is followed by an increase in GFR, PAR and DARNa but with maintenance of fractional reabsorption in both proximal and distal tubuli. In response to an intravenous sodium load, the remnant kidney is able to respond in a normal way with a further increase in DARNa. The adjustments necessary to maintain sodium balance after unilateral nephrectomy take place in both proximal and distal tubuli.

Adult↗
PubMed1987

Abnormal proximal tubular sodium handling in normotensive patients with chronic glomerulonephritis and normal glomerular filtration rate.

In 11 normotensive patients with biopsy verified chronic glomerulonephritis and 14 controls, glomerular filtration rate (GFR), proximal and distal tubular handling of sodium determined by the lithium clearance technique, and overall tubular sodium handling determined by absolute and fractional sodium excretion were measured before, during and after intravenous infusion of a 2.5% sodium chloride solution. Patients and controls were comparable by means of GFR in that no significant differences were found between the two groups either before, during or after sodium chloride infusion. During infusion both groups responded by a decrease in GFR (p less than 0.01 in both groups). Patients exhibited an increased natriuretic response during infusion both when measured as absolute and fractional sodium excretion (p less than 0.05 both). During the infusion the increase in absolute proximal output and decrease in fractional proximal and distal tubular sodium reabsorption were more pronounced in patients than in controls (p less than 0.05). It is concluded that patients with chronic glomerulonephritis at a very early stage of the disease where blood pressure and GFR are still normal respond with exaggerated natriuresis to hypertonic sodium chloride infusion. The exaggerated natriuresis is due to a decreased fractional proximal tubular sodium reabsorption in response to sodium loading.

Adolescent↗
PubMed1987

Malignant arterial hypertension. Relationship between blood pressure control and renal function during long-term observation of patients with malignant nephrosclerosis.

Eleven patients with malignant arterial hypertension and malignant nephrosclerosis, verified by percutaneous renal biopsy, were examined during an observation period of 47 months (median). All patients received antihypertensive therapy. Patients were divided into three groups with regard to development of renal function during the observation period. In two patients (group I), the integrated average blood pressure (IA-BP) was 134/95 mmHg (median) and the calculated creatinine clearance (Ccr) increased from 19 to 56 ml/min (medians). In four patients (group II), IA-BP was 154/102 mmHg and Ccr remained stable-at approximately 60 ml/min. In five patients, (group III), IA-BP was 189/114 mmHg, owing to lack of patient compliance and absence from regular control, and Ccr was reduced from 26 ml/min to less than 5 ml/min. During the first 2 months of antihypertensive therapy, renal function was temporarily reduced in 7 of the 11 patients. It is concluded that effective blood pressure control in patients with malignant arterial hypertension and malignant nephrosclerosis can be accompanied by a considerable improvement, or at least a preservation of renal function.

Adult↗
PubMed1987

Effect of chronic hypokalaemia on renal concentrating ability and secretion of arginine vasopressin.

Two patients with a Bartter-like syndrome, who had been hypokalaemic for 129 and 55 months, and 13 normokalaemic control subjects were investigated during 24 h of water deprivation. The hypokalaemic patients had urine volumes, urine osmolalities, osmolar clearances and tubular capacities for water reabsorption within the normal range. During thirst, plasma-arginine vasopressin increased much more markedly in the patients (3.4 to 11.1 pmol/l and 3.0 to 17.7 pmol/l) than in the control subjects (2.1 pmol/l (median), range 1.0-3.1, to 3.7 pmol/l, range 1.7-6.4). Plasma angiotensin II increased during water deprivation in the patients (33 to 53 pmol/l and 147 to 208 pmol/l) but not in the control subjects (9 pmol/l (median), range 3-15, to 11 pmol/l, range 3-15). Plasma aldosterone was the same in patients and control subjects and did not change in response to thirst. It is suggested that renal concentrating ability can be preserved in patients with chronic potassium depletion by means of a compensatory increase in the secretion of antidiuretic hormone.

Adult↗
PubMed1986

Effect of captopril on renal haemodynamics and the renin-angiotensin-aldosterone and osmoregulatory systems in essential hypertension.

The effect of captopril on renal plasma flow (RPF), glomerular filtration rate (GFR), plasma concentrations of renin, angiotensin II (Ang II), aldosterone (Aldo) and arginine vasopressin (AVP), serum osmolality (Sosm), free water clearance (CLH2O), fractional urinary excretion of electrolytes and blood pressure (BP), was examined in 10 patients with moderate essential hypertension. Placebo plus furosemide was given for 6 weeks, followed by a 6-week period on captopril and furosemide. The renin-angiotensin-aldosterone system was partly blocked by captopril, resulting in a 18% fall in BP. GFR was reduced by 8% during captopril treatment, whereas RPF remained unchanged. Water loading-induced suppression of Ang II and AVP was inhibited by captopril therapy. Without affecting BP in the placebo period, water loading almost abolished the captopril-induced reduction in BP. It is concluded that non-acute captopril treatment of moderates essential hypertension reduces GFR slightly, possibly by producing dilatation of efferent arterioles. The antipressor effect of captopril is lessened during volume expansion, which may be secondary to reduced activity of the renin-angiotensin-aldosterone and osmoregulatory systems.

Adult↗
PubMed1986

Renal water excretion before and after remission of nephrotic syndrome: relationship between free water clearance and kidney function, arginine vasopressin, angiotensin II and aldosterone in plasma before and after oral water loading.

An oral water load of 20 ml/kg body wt. was given to eight patients with nephrotic syndrome before and after remission of the syndrome, and to 13 healthy control subjects. Urine volume (D), free water clearance (C water), plasma concentrations of arginine vasopressin (AVP), angiotensin II (ANG II) and aldosterone (Aldo), were determined before and three times during the first 4 h after loading. D and C water increased to a significantly lower level (P less than 0.01) after water loading in patients with nephrotic syndrome than in control subjects, but D and C water were normal after remission of the syndrome. The maximum increase in C water (delta C water max.) was 1.07 ml/min (median) before remission and 7.93 ml/min after, compared with 8.01 ml/min in the control group. Creatinine clearance (Ccr) increased significantly after remission (63 ml/min to 88 ml/min, P less than 0.01), and the fractional excretion of sodium was enhanced. AVP was higher in the nephrotic syndrome both before (2.9 pmol/l) and after remission (2.9 pmol/l) compared with the control group (1.8 pmol/l). ANG II and Aldo did not change after remission and remained at the same level as in the control group. The elevation in delta C water max. after remission was accompanied by an increase in Ccr in all patients and delta C water max. and Ccr were significantly correlated (rho = 0.600, n = 16, P less than 0.05). No relationship was found between the change in delta C water max. and ANG II and Aldo.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗