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Biomedical subjects

E B Pedersen

Publications and source records attributed to E B Pedersen.

At least 307 records · Page 17Linked to original sources
PubMed1982

Prostaglandins, catecholamines, renin and aldosterone during hypertensive and normotensive pregnancy.

Urinary excretion of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha), plasma concentrations of renin (PRC), aldosterone (PAC), noradrenaline (PNA) and adrenaline (PA) were determined in the third trimester of pregnancy, 5 days and 3 months after delivery in preeclampsia and normotensive pregnant and non-pregnant control subjects. PGE2 was higher in pregnant control subjects than in non-pregnant subjects, but reduced to non-pregnant level in preeclampsia. PGF2 alpha was the same in preeclampsia and normotensive pregnancy but higher than in the non-pregnant group. PRC and PAC were increased during pregnancy, but considerably lesser in preeclampsia than during normotensive pregnancy. PNA and PA were the same in all three groups. All parameters were normal 3 months after delivery. There were no correlations between any of the hormones and blood pressure in any of the groups. PGE2 was positively correlated to PRC. The lack of renal PGE2 in preeclampsia might be responsible for the decrease in renal blood flow and sodium excretion, and the changes in PRC and PAC are supposed to be secondary to changes in PGE2. It is hypothesised that preeclampsia is a state of prostaglandin deficiency.

Aldosterone↗
PubMed1981

High levels of active 40 000-dalton renin in mouse saliva, but no evidence of inactive or high molecular weight forms.

The presence of renin in parasympathetically elicited mouse saliva was demonstrated by using both the antibody trapping method, which measures renin's enzymatic activity, and a direct radioimmunoassay, which detects the renin molecule by its antigenic properties. Crossed immunoelectrophoresis of saliva samples using an antiserum elicited against pure submaxillary renin showed only one precipitation line, indicating the presence of only one form of renin. The position of the line was similar to that found when submaxillary gland extract was subjected to crossed immunoelectrophoresis. Tandem crossed immunoelectrophoresis showed complete identity between antigenic determinants in submaxillary and salivary renin. An apparent molecular weight of about 35 000 and 38 000 was found when saliva samples were subjected to gel filtration on Ultrogel AcA 44 and Sephadex G-100, respectively. No high molecular weight forms were present and no inactive forms could be demonstrated after limited pepsin or trypsin proteolysis. The specific enzymatic activity of renin in pilocarpine saliva was 0.37 Goldblatt Units (G.U.) . microgram-1, which is identical to that of pure submaxillary gland renin (0.41 G.U. . microgram-1) and to that to the storage form of renin in the submaxillary gland (0.4 G.U. . microgram-1) An identical Km value was found for salivary renin, 1.01 microM, and for pure submaxillary renin, 0.98 microM. It is concluded that renin in pilocarpine-elicited saliva is similar to the storage form of renin in the submaxillary gland with respect to molecular weight, enzymatic and immunological properties.

Animals↗
PubMed1981

Correlation between propranolol in plasma and urine, renin-aldosterone system and blood pressure in essential hypertension.

Thirty patients with mild or moderate essential hypertension, and a fixed elevation of diastolic blood pressure, were randomly allocated to three groups and treated with propranolol 40 mg x 4 (Group 1), 80 mg x 4 (group 2) and 160 mg x 4 (Group 3). Blood pressure (BP), pulse rate (PR), plasma renin activity (PRA), plasma aldosterone concentration (PAC), total plasma propranolol (tPP), free plasma propranolol (fPP), and 24 h urinary propranolol excretion (UP) were determined at the end of four consecutive periods: (A) after four weeks without any treatment; (B) after two to three weeks during which the propranolol dose was gradually increased to the intended level; (C) after four weeks, and (D) after eight weeks of unchanged treatment. The maximum reduction in diastolic BP occurred after period B, and in systolic BP after Period C, for Groups 2 and 3, and for all groups together; for Group 1, however, the maximum diastolic BP reduction was first seen after period C. PR was reduced to the same level in all groups after period B. After period B, PRA an PAC fell in all groups, and remained reduced during C and D Group 1. After periods C and D, PRA and PAC in Groups 2 and 3 did not differ significantly from the levels after period A; tPP, fPP and UP were significantly correlated with the propranolol dose, and were lowest in Group 1 and highest in Group 3; UP was negatively correlated with systolic but not diastolic BP in Periods B, C and D. In contrast neither fPP nor tPP were correlated with systolic or diastolic BP. There was no significant correlation between PRA, PAC and changes in PRA or PAC on the one hand and tPP, fPP, UP, BP or changes in BP on the other. It was concluded that propranolol effectively reduced BP, but diastolic BP reduction was most rapidly obtained at 320 and 640 mg daily, that the activity of the renin -aldosterone system was initially suppressed in all group, but for unknown reasons it increased towards the control level after seven to eleven weeks of therapy with 320 and 640 mg/day, and that the reduction in systolic BP increased with higher doses of propranolol and with increasing urinary propranolol excretion.

Adult↗
PubMed1981

Characterization of aggression-provoked renin from an unknown source in male mice.

1. In male mice without kidneys and submaxillary, as well as sublingual, glands aggressive behaviour causes a vast release of renin [J. Bing & K. Poulsen (1979) Acta Physiologica Scandinavica, 107, 251-256]. 2. This resulted in about an 800-fold increase in plasma renin concentration from the control level of 0.52 (range 0.15-0.8) Goldblatt unit (G.U.) x 10(-3)/ml to 430 (range 300-500) G.U. x 10(-3)/ml after aggression. 3. The aggression-provoked renin fulfil all the criteria so far studied for being active renin, identical with normal mouse plasma renin and pure submaxillary mouse renin. 4. It generates angiotensin I with renin substrate and Km (1.2 mumol/l) is the same. It is neutralized by pepstatin but not by inhibitors of metallo-, thiol and serine proteinases, indicating that it is an aspartate proteinase (acidic proteinase). 5. It is a 40 000-mol.wt. renin, which has full enzymatic activity with a specific enzymatic activity of 0.32 G.U./micrograms, identical with that of normal plasma renin. 6. Its enzymatic activity is neutralized by a specific antibody against pure submaxillary renin. It is measureable in the direct renin radioimmunoassay with a dilution curve which parallels that of the standards. It demonstrates complete antigenic identity with pure submaxillary renin in crossed immunoelectrophoresis. 7. Its origin is unknown.

Aggression↗
PubMed1981

Aggression-provoked renin release from an unknown source in male mice.

1. An 800-fold increase in plasma renin occurs after aggressive behaviour in male mice without kidneys and submaxillary glands. 2. The aggression-provoked renin fulfils all the criteria so far studied for being identical with renin. 3. It is an acid proteinase which generates angiotensin I with the same Km and specific enzymatic activity as pure submaxillary renin and normal plasma renin. 4. It is immunologically identical with submaxillary renin in the direct renin assay and in crossed immunoelectrophoresis. 5. It is present in plasma as fully enzymatically active 40 000-mol. wt. renin. 6. It is not likely that it arises from an inactive precursor or binding protein in plasma, since there is no inactive renin present and the high-molecular-weight forms of renin are also present after the fighting. 7. None of many organs so far studied can account for the release. 8. Synthesis of renin de novo during fighting is not likely since it is released also after blockade in vivo of protein synthesis. 9. Origin of the renin is unknown.

Aggression↗
PubMed1981

Responsiveness of the renin-aldosterone system during exercise in young patients with essential hypertension.

The effect of exercise of gradually increased intensity, i.e. 75 W for 20 min followed by 100 W for 20 min, on plasma renin concentration (PRC) and plasma aldosterone concentration (PAC) was studied in young patients with essential hypertension and normotensive control subjects. During exercise without previous sodium loading PRC and PAC increased to the same degree in both hypertensives and normotensives during light exercise; PRC increased further significantly in the normotensives (63 to 72 microIU/ml (medians), P less than 0.01) but not in the hypertensives (46 to 51 microIU/ml) during heavy exercise. PRC and PAC were significantly correlated during both 75 W (rho = 0.633, P less than 0.05) and 100 W (rho = 0.635, P less than 0.05) exercise in the normotensives, but not in the hypertensives. During exercise after loading with 500 ml sodium chloride (0.85 mol/l) PRC and PAC increased in both hypertensives (28 to 42 microIU/ml, P less than 0.01; 0.11 to 0.53 nmol/l, P less than 0.01) and normotensives (22 to 33 microIU/ml, P less than 0.02; 0.12 to 0.34 nmol/l, P less than 0.01), although to a considerably lower degree than without previous loading. PRC and PAC were, however, significantly higher in the hypertensive than in the normotensive group after exercise. It is suggested that the responsiveness of the renin-aldosterone system is abnormal during exercise in young patients with mild essential hypertension, both without and with previous intravenous sodium loading.

Adult↗
PubMed1981

Effects of exercise on urinary excretion of albumin and beta 2-microglobulin in young patients with mild essential hypertension without treatment and during long-term propranolol treatment.

The effect of exercise on the urinary excretion of albumin, beta 2-microglobulin, renal plasma flow (RPF) and glomerular filtration rate (GFR) was studied in two groups of young patients with mild essential hypertension, one comprising nine untreated patients (1) and one comprising eight patients treated with propranolol (2), and in a group comprising ten normotensive healthy control subjects (3). The urinary excretion of albumin and beta 2-microglobulin, RPF and GFR were measured during four consecutive periods: a control period of 40 min; two exercise periods of 20 min each, with a load of 75 W and 100 W, respectively; and a control period. During exercise group 1 showed an increase in albumin excretion and a decrease in beta 2-microglobulin excretion, while group 2 showed an increase in albumin excretion during heavy exercise only and unchanged beta 2-microglobulin excretion, and group 3 showed unchanged albumin and beta 2-microglobulin excretion. RPF and GFR were reduced during exercise in all groups, most markedly in the hypertensive groups. During both exercise loads albumin excretion was higher and RPF was lower in group 1 than in 3. In group 2 albumin excretion was lower than in 1 during the light exercise load, whereas RPF and GFR were lower during both exercise loads. It is concluded that young patients with mild essential hypertension have both an abnormally high albumin excretion and an abnormally low RPF during exercise. During propranolol therapy urinary albumin excretion was partly normal. The changes in albumin excretion suggest glomerular leakage.

Adult↗
PubMed1980

Comparison of the effects of propranolol and labetalol on renal haemodynamics at rest and during exercise in essential hypertension.

The effect of exercise on renal haemodynamics was examined in young patients with mild essential hypertension. Four groups of subjects were studied: 13 normotensive, healthy control subjects, and 15 untreated, 11 propranolol-treated, and 6 labetalol-treated patients. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were measured during four consecutive periods, a pre-exercise control period, two exercise periods with loads of 450 kpm/min and 600 kpm/min, respectively, and a post-exercise control period. In the untreated patients RPF and GFR were lower during exercise than in the normotensive control subjects, whereas no significant differences were found at rest. In the propranolol-treated patients the reduction in RPF and GFR during exercise was more pronounced than in the untreated hypertensives. In the labetalol-treated patients however, RPF and GFR were reduced only to the same degree as in the untreated hypertensives. The reduced renal blood flow in propranolol-treated patients may be attributed to a compensatory increase in sympathetic activity caused by an impaired cardiac response to exercise. The lack of reduction in renal blood flow during labetalol therapy could partly be related to alpha-adrenergic blockade in the renal vascular bed induced by labetalol, and partly to the smaller reduction in cardiac output during labetalol than during propranolol therapy.

Adult↗
PubMed1980

Plasma catecholamines, renin and aldosterone during combined alpha- and beta- adrenoceptor blockade in patients with severe arterial hypertension.

Arterial blood pressure and plasma catecholamines, renin activity and aldosterone concentration in 12 patients with severe essential hypertension were studied before and after combined alpha- and beta- adrenoceptor blockade induced by oral labetalol treatment for 2 months. Frusemide in a fixed dose was employed as a basic antihypertensive agent throughout the study. Blood pressure was adequately controlled in only 6 patients. Mean body weight increased by 1.8 kg and there was a rise in body weight which was inversely correlated with the fall in standing mean blood pressure. The mean plasma noradrenaline concentration decreased from 0.30 to 0.20 ng/ml, whereas plasma adrenaline did not change significantly. Plasma renin activity and aldosterone concentration varied greatly, but the mean values did not change significantly. Change in body weight was correlated inversely with changes in plasma noradrenaline and renin. The results suggest that labetalol, through its combined alpha- and beta- adrenoceptor blocking action, induces a rise in body weight, probably due to sodium and fluid retention, which partly counterbalances its anti-hypertensive effect and partly modifies both renin and sympathetic nervous activity.

Adult↗
PubMed1980

Effect of propranolol and labetalol on renal haemodynamics at rest and during exercise in essential hypertension.

The effect of exercise on renal haemodynamics was studied in young patients with mild essential hypertension. Four groups of subjects were studied: thirteen normotensive, healthy control subjects, fifteen untreated, eleven propranolol-treated, and six labetalol-treated patients. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were measured during four consecutive periods, a pre-exercise control period, two exercise periods with loads of 450 kpm/min and 600 kpm/min, respectively, and a postexercise control period. In the untreated patients RPF and GFR were lower during exercise than in the normotensive control subjects, whereas no significant differences were found at rest. In the propranolol-treated patients the reduction in RPF and GFR during exercise were more pronounced than in the untreated hypertensives. In the labetalol-treated patients however, RPF and GFR were reduced only to the same degree as in the untreated hypertensive patients. The reduced renal blood flow in propranolol-treated patients could be attributed to a compensatory increased sympathetic activity caused by an impaired cardiac response to exercise. The lack of reduction in renal blood flow during labetalol therapy could partly be related to alpha-adrenoceptor blockade in the renal vascular bed induced by labetalol, and partly to a lesser degree of reduction in cardiac output during labetalol than propranolol therapy.

Blood Pressure↗
PubMed1979

Effect of nifedipine on plasma renin, aldosterone and catecholamines in arterial hypertension.

Acute sublingual administration of nifedipine 10--20 mg to 13 hypertensive patients caused a rapid decrease in blood pressure (BP) and a concomitant increase in heart rate (HR), plasma noradrenaline (NA) and plasma renin activity (PRA); there was no significant change in plasma adrenaline (A) or aldosterone (ALDO). Basal PRA was the major determinant of the rise in PRA, as a close correlation was present between the basal value and the increase caused by nifedipine (r = 0.92), p less than 0.001). The rise in PRA was also correlated with the plasma concentration of nifedipine after 60 min (r = 0.80, p less than 0.01), but it was not correlated with the decrease in BP, the rise in HR or the increase in NA. Nifedipine 30--60 mg daily for 6 weeks caused a reduction in mean BP from 133 to 113 mmHg (p less than 0.001). Body weight and serum potassium decreased but no consistent change was noted in NA, PRA, ALDO or 24 h-excretion of catecholamines. A significant correlation was present between the change in NA and that in PRA (r = 0.74, p less than 0.01). The alterations in the various parameters in the acute and chronic studies were not correlated. The findings indicate that different regulatory mechanisms are activated during acute and chronic administration of nifedipine. It is suggested that an initial rise in sympathetic activity gradually decreases during prolonged therapy, but it still remains a determinant of PRA.

Adult↗
PubMed1979

Effect of oral labetalol on plasma catecholamines, renin and aldosterone in patients with severe arterial hypertension.

Arterial blood pressure and plasma catecholamines, renin activity and aldosterone concentration in 12 patients with severe essential hypertension were studied before and after combined alpha- and beta-adrenergic receptor blockage induced by oral labetalol treatment for 2 months. Furosemide in a fixed dose was employed as a basic antihypertensive agent throughout the study. Blood pressure was adequately controlled in only 6 patients. Mean body weight increased by 1.8 kg and there was a rise in body weight which was inversely correlated with the fall in standing mean blood pressure. The mean plasma noradrenaline concentration decreased from 0.30 to 0.20 ng/ml, whereas plasma adrenaline did not change significantly. Plasma renin activity and aldosterone concentration varied greatly, but the mean values did not change significantly. Change in body weight was correlated inversely with changes in plasma noradrenaline and renin. The results suggest that labetalol, through its combined alpha- and beta-adrenergic receptor blocking action, induces a rise in body weight, probably due to sodium and fluid retention, which partly counterbalances the antihypertensive effect of labetalol, and partly modifies both renin and sympathetic nervous activity.

Adult↗