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Biomedical subjects

H Danielsen

Publications and source records attributed to H Danielsen.

At least 37 records · Page 2Linked to original sources
PubMed1990

Atrial natriuretic peptide and blood volume in patients with chronic glomerulonephritis: effects of albumin and frusemide administration.

Blood volume, blood pressure, plasma concentrations of atrial natriuretic peptide (ANP), cyclic 3',5'-guanosine monophosphate (cGMP), angiotensin II, aldosterone, and arginine vasopressin (AVP), and urinary excretion rates of cGMP, sodium, and water were determined before and after infusion of human albumin 20%, 3.5 ml/kg body-weight to 12 patients with chronic glomerulonephritis and 19 healthy control subjects (Study 1); and before and after frusemide injection, 0.75 mg/kg to 15 patients with chronic glomerulonephritis and 19 healthy control subjects (Study 2). In Study 1 blood volume was expanded to the same degree in patients (8.8 and 7.5%, medians, after 90 and 180 min) and controls (8.6 and 6.1%). ANP was enhanced in the patients (5.9 to 11.0 pmol/l, P less than 0.01) and the controls (4.9 to 7.1 pmol/l, P less than 0.01), but the elevated level was protracted in the patients simultaneously with a delayed sodium excretion. Plasma cGMP increased, aldosterone decreased and AVP was unchanged in both groups, whereas angiotensin II decreased in the patients (P less than 0.01), but not in the controls. In Study 2 blood volume was reduced to a smaller extent in the patients than in the controls (8.9% versus 9.9%, P less than 0.05). ANP an cGMP decreased, and angiotensin II, aldosterone and AVP increased in both patients and controls. In conclusion, patients with glomerulonephritis respond to albumin- and frusemide induced changes in blood volume with essentially the same counter-regulatory changes in ANP, angiotensin II, aldosterone and AVP as do healthy subjects. The more protracted increase in ANP and the decrease in angiotensin II after albumin, and the smaller blood volume reduction after frusemide suggest an abnormal regulation of blood volume in glomerulonephritis.

Adult↗
PubMed1989

Atrial natriuretic peptide and exaggerated natriuresis during acute hypertonic volume expansion in essential hypertension.

In patients with essential hypertension and healthy controls, plasma levels of atrial natriuretic peptide (ANP), angiotensin II (Ang II), aldosterone (Aldo), arginine vasopressin (AVP) and urinary excretion of prostaglandin E2 (PGE2) were measured under basal conditions, and before and after acute volume expansion with a 2.5% hypertonic sodium chloride solution. Tubular sodium handling was assessed by the lithium clearance technique. Under basal conditions ANP was increased in patients compared with controls (9.0 pmol/l versus 7.5 pmol/l, P less than 0.01). In response to acute volume expansion patients exhibited exaggerated increases in ANP (5.3 pmol/l versus 3.0 pmol/l, P less than 0.05), exaggerated natriuresis, and an abnormal decrease in fractional proximal and distal tubular sodium reabsorption (PFRNa and DFRNa, respectively). Furthermore, during comparable urinary flow rates, urinary PGE2 excretion was decreased in patients compared with controls (266 pg/min versus 705 pg/min, P less than 0.05). No differences were found between patients and controls in Ang II, Aldo or AVP under basal conditions. Both groups responded to hypertonic acute volume expansion with comparable decreases in Ang II and Aldo, and an increase in AVP. It is concluded that in essential hypertension ANP is increased under basal conditions and the increase in natriuresis and ANP is exaggerated during acute volume expansion. The exaggerated natriuretic response to acute volume expansion resulted from an altered handling of sodium in both proximal and distal tubules.

Adult↗
PubMed1989

Abnormal glomerular and tubular function during angiotensin converting enzyme inhibition in renovascular hypertension evaluated by the lithium clearance method.

Glomerular filtration rate (GFR) and tubular function were measured by means of the lithium clearance technique in 14 patients with renovascular hypertension (RVH) and eight patients with essential hypertension (EH) before and after oral administration of captopril 25 mg. In RVH captopril reduced 51-Cr-EDTA clearance (67.3 (median) to 47.5 ml min-1, P less than 0.01), proximal absolute reabsorption of fluid (53.9 to 41.5 ml min-1, P less than 0.01) and distal absolute reabsorption of sodium (2195 to 1402 mumol min-1, P less than 0.01), whereas proximal fractional reabsorption increased slightly (77.5 to 80.2%, P less than 0.02). In EH, however, these parameters were practically unaffected by captopril. In both RVH and EH plasma concentrations of angiotensin II and aldosterone were reduced after captopril, but atrial natriuretic peptide in plasma and urinary excretion rate of prostaglandin E2 were unchanged. Blood pressure decreased after captopril in both groups, but the maximum fall in systolic BP was more pronounced in RVH (22%) than EH (13%). It is concluded that angiotensin converting enzyme inhibition markedly reduced absolute reabsorption in both the proximal and distal tubules in RVH, in contrast to EH, predominantly due to fall in the GFR, and that the slight increase in proximal fractional reabsorption may be attributed to a reduction in the hydrostatic pressure in the peritubular vessels.

Adult↗
PubMed1989

Elevated angiotensin II and vasopressin in primary hyperparathyroidism. Angiotensin II infusion studies before and after removal of the parathyroid adenoma.

In order to evaluate the role of calcium metabolism in blood pressure regulation, 15 patients with primary hyperparathyroidism and 9 healthy control subjects were studied before and during angiotensin II infusion. The patients were re-investigated 2-5 months after removal of the parathyroid adenoma. Blood pressure, plasma levels of angiotensin II, aldosterone, arginine vasopressin, and atrial natriuretic peptide, and creatinine clearance were determined. Blood pressure and the blood pressure response to angiotensin II infusion were both the same before and after the operation. Angiotensin II and arginine vasopressin during basal conditions were significantly higher before than after the operation (angiotensin II: 17 (median) to 10 pmol/l, P less than 0.02; arginine vasopressin: 2.9 to 1.9 pmol/l, P less than 0.01), whereas aldosterone, atrial natriuretic peptide, and creatinine clearance were unchanged. During angiotensin II infusion, aldosterone, arginine vasopressin, and atrial natriuretic peptide increased to approximately the same levels before and after the operation. Blood pressure was not correlated to any of the hormones measured. Thus, patients with primary hyperparathyroidism have elevated plasma levels of angiotensin II and arginine vasopressin which may be compensatory phenomena counteracting volume depletion owing to a decreased renal concentrating ability induced by hypercalcemia, and owing to PTH-induced inhibition of renal sodium reabsorption.

Adenoma↗
PubMed1988

Atrial natriuretic peptide, angiotensin II and aldosterone in plasma in chronic glomerulonephritis during basal conditions and during exercise.

Atrial natriuretic peptide (ANP), angiotensin II (AII) and aldosterone (Aldo) in plasma were determined at supine rest in 16 normotensive and 9 hypertensive patients with chronic glomerulonephritis and in 18 control subjects (Study 1). In addition, 12 of the normotensive, 7 of the hypertensive patients and 11 of the control subjects were studied with the same parameters after an exercise test (Study 2). Study 1 showed that supine ANP, AII and Aldo did not differ significantly between the groups. In Study 2, ANP increased after exercise in the normotensive patients (8.4 vs. 11.4 pmol/l (median), p less than 0.05) and control subjects (7.6 vs. 9.3 pmol/l, p less than 0.02) but not in the hypertensives (7.6 vs. 7.9 pmol/l, p greater than 0.10), and after exercise ANP was increased in the normotensive patients compared with the controls (p less than 0.02). After exercise, an enhanced increase of Aldo was found in the hypertensives but not in the normotensive patients compared with the controls, whereas the increase of AII did not differ significantly between the groups. It is concluded that patients with chronic glomerulonephritis and relatively well preserved renal function do not have major abnormalities of ANP at rest or during exercise. In the normotensive patients, however, ANP increased to a higher level than in the controls, but the difference was small and further studies are needed to define the role of ANP in blood pressure regulation of early stage chronic glomerulonephritis.

Adult↗
PubMed1988

Urinary prostaglandin E2 and F2 alpha excretion in nephrotic syndrome during basal conditions, after water loading, and after remission of the syndrome.

The urinary excretion rate of prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) was determined in patients with the nephrotic syndrome both before and after an oral water load in 21 patients and 17 control subjects, and before and after remission of the syndrome in 8 of the patients. In the nephrotic syndrome PGE2 excretion rate varied considerably during basal conditions, remission was accompanied by an increase in the PGE2 excretion, and both basal PGF2 alpha excretion rate and the normal response in PGF2 alpha water loading were reduced. A significant, positive correlation was found between urine flow rate and excretion rate of PGE2 in the periods with the largest urine flow rate in both patients and control subjects. It is suggested that a relatively suppressed renal prostaglandin production may be a pathogenetic factor for sodium and water retention in the nephrotic syndrome, although it cannot be excluded that the abnormal prostaglandin excretion pattern is secondary, at least partially, to the reduction of urine flow rate.

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

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

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

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

A method for determining ploidy distributions in liver tissue by stereological analysis of nuclear size calibrated by flow cytometric DNA analysis.

A method is presented for determining ploidy distributions in mouse liver from image analysis with stereological estimations of nuclear size in tissue sections. Nuclear profile distributions obtained from profile measurements were subjected to a mathematical unfolding procedure in order to obtain the nuclear size distributions. Based on the assumption that nuclear size increases monotonically with nuclear DNA content, flow cytometric DNA analysis of suspensions of liver cell nuclei was used to calibrate the method, thus yielding the mean nuclear size of each ploidy class, i.e., diploid, tetraploid, and octaploid nuclei. After the size interval for each of the ploidy classes was determined, the method allowed determination of ploidy distributions in mouse liver by stereological image analysis alone. The method was established from combined stereological and flow cytometric measurements on liver tissue representing two different stages of liver regeneration after two-thirds partial hepatectomy, and it was tested against an independent set of data representing a marked increase in the portion of S-phase cells.

Animals↗
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

Direct preparation and G-banding of chromosomes of mouse liver cells.

A method has been developed for the direct preparation and G-banding of chromosomes of mouse liver cells by combining the techniques of liver perfusion and preparation of G-banded chromosomes with partial hepatectomy and colcemid treatment of the animal. The results indicate that cytogenetic investigations of isolated preneoplastic liver cells are possible. The method offers an increased possibility for the use of the liver as an in vivo test system for mutagens and carcinogens.

Animals↗