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Biomedical subjects

I Eide

Publications and source records attributed to I Eide.

At least 127 records · Page 7Linked to original sources
PubMed1982

The effect on HDL cholesterol of oxprenolol and atenolol.

In 19 healthy men aged 50 with untreated mild essential hypertension (WHO group I classification) randomized into two groups, treatment (18 weeks) with oxprenolol (n = 10) lowered HDL cholesterol by 11.4% (P less than 0.02) and cholesterol ratio (HDL cholesterol X 100/LDL + VLDL cholesterol) by 13.7% (P less than 0.05) whereas atenolol (n = 9) lowered HDL cholesterol by 16.5% (P less than 0.02) and cholesterol ratio by 19.2% (P less than 0.01). In the total material (n = 19) the reduction of HDL cholesterol correlated positively with initial concentration of HDL (r = 0.48, P less than 0.05). Increments of total triglycerides by 20.0 and 17.9%, respectively, for the two drugs and small changes in total cholesterol, LDL + VLDL cholesterol and uric acid were not significant. The HDL cholesterol lowering effect of oxprenolol and atenolol observed in the present study may have clinical importance since such metabolic side effects have been postulated to counteract the beneficial effect of blood pressure reduction on development of atherosclerosis and coronary heart disease in mild essential hypertension.

Adrenergic beta-Antagonists↗
PubMed1982

Antihypertensive drugs and blood lipids: the Oslo study.

The effects on blood lipids and uric acid of six different antihypertensive drugs used alone, and of five different combinations of two antihypertensive drugs, are reported here. Prazosin significantly lowered serum low density lipoprotein and very low density lipoprotein (LDL + VLDL) cholesterol and total triglycerides while maintaining high density lipoprotein (HDL) levels. Atenolol lowered LDL + VLDL cholesterol slightly. Both pindolol and hydrochlorothiazide (HCTZ) were neutral, while oxprenolol increased total triglycerides. Propranolol lowered HDL cholesterol and increased total triglycerides and uric acid. The combination of prazosin plus pindolol has a direct favorable lipid profile, while the combination of propranolol plus HCTZ lowered HDL cholesterol and increased total triglycerides. The combination of propranolol plus prazosin lowered HDL cholesterol, but to a lesser degree than propranolol alone, which suggests that prazosin was not able to completely counteract the negative effects of propranolol on HDL. Methyldopa plus HCTZ, and HCTZ plus amiloride were neutral with regard to effects on blood lipids. It is suggested that the metabolic effects of antihypertensive drugs could be of special importance in the long-term treatment of mild hypertension.

Adrenergic alpha-Antagonists↗
PubMed1982

Evidence of increased peripheral catecholamine release in patients with long-standing, untreated essential hypertension.

In 20 middle-aged men with untreated sustained essential hypertension for more than 5 years, both plasma adrenaline and noradrenaline were positively and significantly correlated with blood pressure. In both hypertensives and 19 normotensive control subjects supine arterial adrenaline concentrations were more than twice the venous concentrations consistent with adrenal production of this catecholamine. Adrenaline a--v(arterial-venous)differences(mean +/- SE) were significantly higher in the hypertensive group (82 +/- 15 pg/ml) than in the controls (50 +/- 5 pg/ml) indicating increased release of adrenaline in the hypertensives (P less than 0.05). Similarly, v-a(venous-arterial) differences of noradrenaline were significantly higher in the hypertensive (44 +/- 20 pg/ml) than in the control group (-10 +/- 16 pg/ml) indicating peripheral noradrenaline release in patients with essential hypertension. The findings are compatible with increased forearm noradrenaline and adrenal adrenaline release in these patients with long-standing untreated essential hypertension.

Arteries↗
PubMed1982

Renal contribution to plasma catecholamines--effect of age.

In 18 subjects undergoing diagnostic cardiac catheterization renal venous noradrenaline during rest (296 +/- 26 ng/l, mean +/- SE) was significantly increased over arterial noradrenaline concentrations (250 +/- 20 ng/l, P less than 0.01) while, in contrast, the arterial adrenaline level (79 +/- 9 ng/l) was higher than the renal venous (41 +/- 4 ng/l, P less than 0.001). Age correlated positively with both renal venous noradrenaline (r = 0.56) and the renal venous-arterial difference of noradrenaline (r = 0.56), and negatively with arterial (r = -0.52) and renal venous adrenaline (r = -0.48). According to our data, a net renal venous secretion of noradrenaline and at the same time an uptake of adrenaline from the renal circulation take place at an extent that may influence plasma concentrations of both. With increasing age renal uptake of plasma adrenaline seems to decrease and net release of noradrenaline to increase. The fall in plasma adrenaline may be due to age-dependent involution of the adrenal medulla. In studies of plasma adrenaline concentrations and of the renal handling of plasma catecholamines the influence of age must be taken into account.

Adolescent↗
PubMed1981

Increased peripheral release of noradrenaline and uptake of adrenaline in essential hypertension?

1. Twenty middle-aged men with untreated sustained essential hypertension for more than 5 years and 19 comparable normotensive controls were investigated. Both groups were derived from The Oslo Study, where they had served as control hypertensive and normotensive subjects. 2. Supine venous and arterial plasma catecholamines were increased in the hypertensive subjects compared with the normotensive subjects. The mean arterial--venous difference for adrenaline in the hypertensive (0.45 +/- SE 0.08 nmol/l) was increased compared with the normotensive group (0.27 +/- 0.03 nmol/l, P less than 0.05). Similarly, the venous--arterial difference for noradrenaline was increased in the hypertensive (0.29 +/- 0.13 nmol/l, P less than 0.05) compared with the normotensive group (-0.07 +/- 0.11 nmol/l). 3. The results are consistent with an increased release of adrenaline from the adrenal medulla and noradrenaline from the peripheral vascular beds (forearm) in essential hypertension. The increased arterial--venous difference for adrenaline in the hypertensive group also suggests an increased uptake of adrenaline in the peripheral vascular beds.

Epinephrine↗
PubMed1981

Conditions for humoral alpha-adrenoceptor stimulation of renin release in anaesthetized dogs.

To examine whether an alpha-adrenergic agonist, methoxamine, influences renin release solely by its haemodynamic effect, experiments were performed in anaesthetized dogs with denervated kidneys. Methoxamine was infused intrarenally at rates which reduced renal blood flow (RBF) by 30-40%. At control blood pressure, renin release rose during infusion of methoxamine from 1.4 +/- 0.7 to 31 +/- 11 microgram/min. A beta-adrenergic stimulator, isoproterenol, did not increase renin release significantly when administered alone into the renal artery, but doubled the effect of methoxamine infusion: at control blood pressure renin release rose from 0.5 +/- 0.3 to 71 +/- 17 microgram/min during combined infusion of isoproterenol and methoxamine. Mechanical constriction of the renal artery left RBF unaltered down to a renal perfusion pressure of 90 +/- 4 mmHg during methoxamine infusion, whereas the lowest autoregulating pressure in control experiments averaged 60 +/- 5 mmHg. At renal infusion pressure below the range of autoregulation, renin release was not further increased by intrarenal infusion of methoxamine. Isoproterenol infusion at low renal perfusion pressure doubled renin release, which was not significantly altered by additional infusion of methoxamine. The stimulatory effect of methoxamine on renin release at control blood pressure could be diminished but not prevented by infusing 2.9% NaCl intravenously in large amounts. These data indicate that methoxamine induces autoregulated dilation of afferent arterioles by disproportionate vasoconstriction on pre-afferent arteries. Thereby afferent arterioles are conditioned for stimulation of renin release by isoproterenol.

Animals↗
PubMed1981

Conditions for stimulation of renin release by cyclic AMP in anaesthetized dogs.

Cyclic AMP (cAMP) is the intracellular mediator of beta-adrenergic stimulation in most tissues. Stimulation of beta-adrenoceptors increases renin release much more at low than at control arterial perfusion pressure. If beta-adrenergic stimulation is mediated by cAMP, this nucleotide should also potentiate renin release at low perfusion pressure. In anaesthetized, propranolol treated dogs, the dibutyryl derivative of cAMP (DB-cAMP), which penetrates cell membranes more readily than cAMP, increased renin release significantly during renal arterial constriction at a perfusion pressure below the range of autoregulation, but no significant effect was observed at control blood pressure. A dose-response relationship could be demonstrated in propranolol treated dogs by administering DB-cAMP at 10, 100 and 1000 micrograms/min at low but not at control blood pressure. Since sodium excretion increased, stimulation of a macula densa mechanism is unlikely, whereas arteriolar dilation, caused by autoregulation at low blood pressure, may condition the juxtaglomerular apparatus for renin release. Infusion of cAMP had no effect on renin release either at control or low blood pressure, whereas 5'AMP exerted a marked inhibitory effect at low blood pressure. We conclude that infusion of DB-cAMP rather than cAMP stimulates renin release at low but not at control blood pressure and that this effect is not mediated by beta-adrenergic receptors; cAMP may be an intracellular mediator of renin release.

Adenosine Monophosphate↗
PubMed1981

Mechanism of renin release during renal nerve stimulation in dogs.

During renal nerve stimulation, a predominant vasoconstrictory effect on small arteries would lower blood pressure in the afferent arterioles and induce arteriolar dilation and renin release by the autoregulation mechanism. This hypothesis was examined in anaesthetized dogs by stimulating renal nerves at 4 Hz which permitted continuous reduction of renal blood flow (RBF) by 30-40%; renin release increased almost equally at control and low blood pressure, and in the non-filtering kidney during ureteral occlusion. Examinations of the relationship between RBF and arterial perfusion pressure during mechanical constriction of the renal artery showed that the lowest autoregulating pressure was 25-35 mmHg higher during nerve stimulation than in control experiments, consistent with the hypothesis of arteriolar dilation. Phenoxybenzamine, an inhibitor of alpha-adrenoceptors, abolished vasoconstriction and the effect of nerve stimulation on renin release at control blood pressure; renin release rose from 0.9 +/- 0.4 to 17 +/- 5 microgram/min before, and from 1.7 +/- 0.5 to 4.6 +/- 1.4 microgram/min after phenoxybenzamine infusion. At pressures below the range of autoregulation, phenoxybenzamine did not alter renin release response to nerve stimulation. Propranolol, a Beta-adrenergic inhibitor, attenuated the effect of nerve stimulation on renin release both at control and low blood pressure. We conclude that during renal nerve stimulation (1) renin release is caused by beta-adrenergic stimulation provided the afferent arterioles are dilated and (2) that alpha-adrenergic stimulation dilated the afferent arterioles as a consequence of a predominant vasoconstrictory effect on small arteries. Hence, by inhibiting the beta-adrenergic effect by propranolol, renin release does not increase during renal nerve stimulation. Phenoxybenzamine prevents renin release at control blood pressure because afferent arterioles are not dilated during nerve stimulation. In contrast, phenoxybenzamine does not reduce renin release during nerve stimulation at low blood pressure because afferent arterioles are dilated by the autoregulating mechanism.

Animals↗
PubMed1981

Hypernephroma and hypertension. Two case reports.

Evaluation for hypertension revealed a hypernephroma in two patients and increased plasma renin concentrations (PRC) of 2.8 and 3.1 GU . 10(-4)/ml, respectively. In one of the patients, bilateral renal venous catheterization showed lateralization of PRC toward the tumor side in the ratio 10:3. She had secondary hyperaldosteronism with a plasma aldosterone concentration (PAC) of 738 pmol/l, and hypokalemia with a serum potassium level of 3.0 mmol/l. In the other patient, who had malignant hypertension, PAC was not measured but serum potassium was subnormal (3.3 mmol/l). After nephrectomy, blood pressure (BP), PRC and serum potassium returned to normal in both as did PAC in one of the patients. At regular follow-ups through one year after nephrectomy, BP, PRC, PAC and serum potassium remained normal and metastases were not discovered. The increased incidence of hypernephroma in hypertensive patients underscores the importance of acknowledging this possibility during evaluation for hypertension.

Adenocarcinoma↗
PubMed1980

Comparison of metabolic and clinical effects of four oral contraceptive formulations and a contraceptive vaginal ring.

A group of 100 women desiring OC received one of the following four formulations on a randomized basis: (1) mestranol 50 micrograms and norethindrone 1 mg, , (2) ethinyl estradiol 50 micrograms and norethindrone 1 mg, (3) ethinyl estradiol 35 micrograms and norethindrone 1 mg, and (4) ethinyl estradiol 30 micrograms and levonorgestrel 150 mg. An additional 10 women received a CVR containing levonorgestrel and estradiol. Measurement of a large number of serum chemistries, lipids, proteins, clotting factors, and liver enzymes was obtained before and 3 and 6 months after starting medication. Clinical factors such as weight, blood pressure, bleeding or spotting, or any adverse side effects were also recorded. There was no significant difference in the metabolic parameters measured among the four oral contraceptives except the increase in angiotensinogen was slightly less in the groups receiving the compounds with 30 or 35 micrograms estrogen and the groups receiving the norgestrel compound had no increase in triglycerides and a slight decrease in cholesterol levels. When the CVR was compared with all oral contraceptives it was found to produce no change in angiotensinogen levels and a decrease in triglycerides. Some of each group of OC users had a lowering of antithrombin III to abnormal levels but none of the CVR users had his amount of decrease. As oral steroids with 30 or 35 micrograms of estrogen do not produce significantly less metabolic alteration than do compounds with 50 micrograms of estrogen, it is unlikely that their use will reduce the incidence of the uncommon serious adverse effects associated with OC use. However, since the CVR's did not increase angiotensinogen, their use as contraceptives will most likely not produce hypertension and possibly the other serious circulatory problems which are increased in some OC users.

Adolescent↗
PubMed1980

Cage culture turbidostat: a device for rapid determination of algal growth rate.

The present cage culture turbidostat consists of a growth chamber and a control unit. The microorganisms (photoautotrophic algae) are kept in the growth chamber by porous membranes (pore size 1 to 3 mum) which retain the algae but allow efficient exchange of the growth medium. Flow rate and composition of the medium can therefore be varied independently of algal population density. A reciprocating pumping mode of the medium is introduced to obtain more gentle clearance of membranes than that provided by rotation or stirring in other membrane fermentors. Pulsed light and a light-emitting diode/light-sensitive transistor couple are used to monitor the turbidity of the culture, independent of external light needed for growth. The control unit keeps the turbidity constant by frequent activation of the dilution pump. Theoretical analysis of growth in the turbidostat shows that integrated activation time of the dilution pump is proportional to the growth rate of the organism. Theoretical analysis was also used to determine minimum flow-rate and nutrient concentration of medium to cover the requirement of the algae. Experiments with three different marine diatoms were carried out, and they demonstrated that the growth rate could be determined every hour and that the cultures could be kept at constant turbidity over 10 to 14 days at least.

Journal Article↗
PubMed1978

Enhanced hypothalamic noradrenaline biosynthesis in Goldblatt I renovascular hypertension.

1. Hypertension was induced in rats by renal artery clip with the contralateral kidney removed (Goldblatt I) or left intact (Goldblatt II). 2. Plasma noradrenaline was increased 62% in the Goldblatt I animals after 3 weeks. 3. Hypothalamic tyrosine hydroxylase and dopamine beta-hydroxylase activities, and the concentration of noradrenaline were increased in the Goldblatt I animals after 3 weeks. 4. Enhanced hypothalamic noradrenaline synthesis may be a pathogenic factor in Goldblatt I renovascular hypertension.

Animals↗
PubMed1978

Clinical assessment of sympathetic tone: orthostatic blood pressure responses in borderline primary hypertension.

Orthostatic changes of systolic, diastolic and pulse pressure, and pulse rates were evaluated as clinical indicators of sympathetic nerve tone in 28 patients with uncomplicated primary hypertension. After sixty minutes in the upright position, systolic blood pressure increased in 13 and decreased in 15 of the patients, while pulse pressure diminished in 19, was unchanged in 4 and increased in 5 of the patients. The changes of both systolic blood pressure and pulse pressure showed a significant positive correlation with basal (supine) levels of norepinephrine (r = 0.40, p less than 0.05 and r = 0.54, p less than 0.01, respectively). In the total sample of patients, 25% had basal plasma norepinephrine concentrations above the normal range. Of the patients with increased systolic blood pressure after standing, 38% had elevated basal norepinephrine. Similarly in patients with increased orthostatic pulse pressure or in those with pulse pressure reductions less than 10 mm Hg, 45% had elevated basal norepinephrine. On the other hand, of patients with reductions of pulse pressure of more than 10 mm Hg, only 6% had elevated basal norepinephrine. Of the patients with similar systolic blood pressure reductions, none had increased plasma norepinephrine. Both diastolic blood pressures and pulse rates always rose during orthostatic stress, but they did not correlate with basal sympathetic tone. In conclusion, hypertensive patients with orthostatic increases of systolic and pulse pressure are more likely to have elevated basal sympathetic tone than unresponsive patients. The former may comprise a subset of hypertensives who have a causal neurogenic component. They may be more sensitive to drugs which suppress sympathetic nerve function.

Adolescent↗
PubMed1977

Mechanism of renin release during acute ureteral constriction in dogs.

The relationship between renal arterial pressure and renin release was examined in anesthetized dogs during complete or partial ureteral constriction. During complete ureteral occlusion ureteral pressure rose to 95+/-4 mm Hg and renin release increased from 1.7+/-0.7 to 22.3+/-3.1 mug/min; renal blood flow (RBF) was not significantly changed. Renin release was not further increased during subsequent renal arterial constriction; RBF fell in proportion to perfusion pressure, indicating maximum autoregulated arteriolar dilation. During partial ureteral constriction to a ureteral pressure of 65+/-6 mm Hg, renin release was moderately raised but release mechanisms became fully stimulated when renal arterial pressure was reduced to 104+/-3 mm Hg. By further constricted of the renal artery, RBF fell in proportion to perfusion pressure and renin release remained high and constant. In control experiments without ureteral constriction, renal arterial pressure had to be reduced to below 65+/-8 mm Hg to fully stimulate renin release (22.0+/-3.8 mug/ml which is not different from 22.3+/-3.1 mug/min during ureteral occlusion). During partial ureteral constriction, saline infusion (0.9% NaCl at 40 ml/min) raised urine flow, sodium excretion, renal pelvic pressure, and renin release. Thus, the stimulatory effect on renin release of a rise in ureteral pressure exceeded the inhibitory effect of increased sodium excretion. This observation, together with maximum renin release coinciding with complete arteriolar dilation during various combinations of renal arterial and ureteral constriction, is compatible with the conclusion that arteriolar dilation is predominating stimulus to renin release during ureteral constriction.

Animals↗