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Biomedical subjects

H Ibsen

Publications and source records attributed to H Ibsen.

At least 109 records · Page 6Linked to original sources
PubMed1981

The influence of chronic high alcohol intake on blood pressure, plasma noradrenaline concentration and plasma renin concentration.

1. Sixteen 44-year-old males with chronic high alcohol intake were investigated. Seventeen 44-year-old males with low alcohol intake from the same population served as controls. 2. Plasma noradrenaline concentrations did not differ significantly between individuals with high and low alcohol intake, neither at rest nor after acute stimulation induced by ambulation for 15 min. However, 63% (10 out of 16) of the individuals with high intake showed resting values within the upper quartile range for individuals with low intake. 3. Plasma renin concentration was twice as high (P less than 0.01) in the group with high alcohol intake as in the group with low intake. 4. Systolic as well as diastolic blood pressure was significantly higher (P less than 0.01) in the group with high intake compared with the group with low intake. 5. Sympathetic nerve activity, as defined from measurements of plasma noradrenaline concentration, is not uniformly increased in individuals with chronic high alcohol intake. The mechanism behind the increased plasma renin level as well as the possible role of the renin--angiotensin system in alcohol-induced hypertension remain unsettled.

Adult↗
PubMed1980

Angiotensin II blockade during combined thiazide-beta-blocker treatment.

Sixteen patients (11 M, 5 F), median age 41 years, with essential hypertension insufficiently controlled on hydrochlorothiazide 75 mg/day (DBP greater than or equal to 100 mmHg) were investigated. Plasma renin concentration (PRC), angiotensin II concentration (PA II), aldosterone concentration (PAC), plasma noradrenaline concentration (PNAC), plasma volume (PV) and exchangeable sodium (NaE) were determined and a saralasin-infusion (5.4 nmol/kg/min) was carried out while the patients were on thiazide alone, and in fourteen cases, repeated 3 months later after addition of a beta-blocker (propranolol 6, metoprolol 6 and atenolol 2 patients). On thiazide alone PRC, PA II and PAC was higher than normal in the group as a whole and the angiotensin II-inhibitor, saralasin, caused a significant decrease in MAP in twelve out of sixteen patients. After addition of a beta-blocker SBP and DBP decreased from 164/109 mmHg to 136/94 mmHg. PRC and PA II decreased by 40% and 58%, respectively. At this point saralasin caused no significant change in MAP. No close correlation was found between changes in BP on beta-blocker treatment and either PRC, PA II or saralasin response on thiazide treatment. PV, NaE, PAC and PNAC did not change sigificantly. It is concluded that in pts with thiazide-induced stimulation of the renin-angiotensin system (RAS) addition of a beta-blocker leads to suppression of RAS and the angiotensin II dependence of the blood pressure is nearly abolished. This mechanism might well contribute to the antihypertensive effect of beta-blockade in this particular situation. However, the pharmacological changes induced by beta-blockade are very complex, and most likely other factors are involved in the antihypertensive effect of beta-blocking drugs.

Adrenergic beta-Antagonists↗
PubMed1980

Plasma noradrenaline concentration in hypertensive and normotensive forty-year-old individuals: relationship to plasma renin concentration.

Forty-year-old individuals with labile and with mild sustained essential hypertension, identified during a survey of a population born in 1936, were investigated. None had ever received antihypertensive treatment. In thirty-three individuals (26 M, 7F) with diastolic blood pressure (DBP) greater than or equal to 95 mmHg at the very first examination and in thirty-one (14 M, 17 F) randomly selected normotensive controls plasma noradrenaline concentration (PNAC) was measured at rest supine. In twenty-two patients (16 M, 6 F), with sustained diastolic hypertension (diastolic blood pressure greater than or equal to 95 mmHg on at least three different occasions) and in twenty-four (14 M, 10 F) normotensive controls PNAC and plasma renin concentration (PRC) were measured supine at rest and again 2 h after furosemide and ambulation. Basal and acutely stimulated values for PNAC and PRC were identical in hypertensive and normotensive individuals. A close correlation between PNAC and PRC after acute stimulation (r = 0.77, P < 0.001) as well as between the absolute changes from resting to acutely stimulated values (r = 0.72, P < 0.001) were found in the hypertensive individuals. It is concluded that sympathetic nerve activity, as defined from measurements of plasma noradrenaline concentration, is similar in young patients with mild hypertension and in normotensive controls. We propose that the discrepancies found in the literature might be related to a lack of comparability between hypertensive and normotensive individuals studied, as far as the source of study populations is concerned.

Adult↗
PubMed1980

The use of an angiotensin II antagonist (saralasin) as an adjunct during renal vein catheterization.

Renal vein catheterization was performed in fifteen hypertensive patients with unilateral renal disease. Samples for measurement of plasma renin concentration were obtained from each of the two renal veins and from the femoral artery (or the inferior caval vein)-before and during saralasin infusion. Saralasin infusion induced a significant decrease in blood pressure. In ten patients with lateralization of renin secretion before infusion, saralasin induced a 2-fold increase of the renin gradient across the diseased kidney, whereas there was no significant renin gradient across the contralateral kidney neither before nor after saralasin infusion. Thus, the renal venous renin ratio (diseased/contralateral) increased from a mean value of 2.10 to 4.13. In five patients without lateralization of renin secretion prior to infusion, saralasin induced a significant increase of renin gradient across both kidneys. In consequence, evidence for lateralization did not emerge and the renal vein renin ratio remained unchanged at 1.10. In cases with lateralization of renin secretion, the use of saralasin provides confirmatory evidence for strictly unilateral renin secretion with suppression of renin output from the contralateral kidney. In patients without obvious lateralization of renin secretion before saralasin, the administration of this angiotensin II inhibitor can serve to demonstrate a potential renin for renin secretion, shared by both kidneys.

Angiotensin II↗
PubMed1979

Angiotensin II blockade during combined thiazide-beta-adrenoreceptor-blocker treatment.

1. Sixteen patients (11 male, five female), median age 41 years, with essential hypertension insufficiently controlled by hydrochlorothiazide (75 mg/day; diastolic blood pressure greater than or equal to 100 mmHg), were studied. 2. Plasma renin concentration [renin], plasma angiotensin II concentration ([ANG II]), plasma volume and exchangeable sodium (NaE) were determined, and a saralasin infusion (5.4 nmol min-1 kg-1) was carried out while the patients were on thiazide alone and, in 14 cases, 3 months after addition of a beta-adrenoreceptor blocker (propranolol, six, metoprolol, six, and atenolol, two patients). 3. On thiazide alone, saralasin caused a significant decrease in mean arterial blood pressure in 12 out of 16 patients. The saralasin response was closely related to pre-saralasin plasma [ANG II] (r = 0.73, P less than 0.01). Plasma [renin] and [ANG II] were higher than normal in the group as a whole. 4. After addition of a beta-adrenoreceptor blocker systolic and diastolic blood pressure decreased from 164/109 mmHg to 136/94 mmHg. Plasma [renin] and [ANG II] decreased by 40 and 58% respectively. At this point, saralasin caused no significant change in mean arterial pressure. No close correlation was found between plasma [renin] or [ANG II] or saralasin response on thiazide treatment and changes in blood pressure during subsequent thiazide/beta-adrenoreceptor-blocker treatment. Plasma volume and NaE did not change significantly. 5. In patients with thiazide-induced stimulation of the renin-angiotensin system, addition of a beta-adrenoreceptor blocker leads to suppression of the system and, at the same time, ANG II-dependence of blood pressure disappears. This contributes to the antihypertensive effect of beta-adrenoreceptor blockers in this particular situation.

Adult↗
PubMed1979

Plasma noradrenaline concentration in hypertensive and normotensive 40-year-old individuals: relationship to plasma renin concentration.

1. Forty-year-old individuals with mild essential hypertension, identified during a survey of a population born in 1936, were investigated. Forty-year-old normotensive subjects, drawn from the same population, served as a control group. 2. Plasma noradrenaline concentration and plasma renin concentration at rest supine and after acute stimulation, as induced by frusemide intravenously and ambulation, did not differ from reference values in the 40-year-old normotensive controls. In the hypertensive group a close correlation (r = 0.77, P less than 0.001) was found between plasma noradrenaline and plasma renin concentration after acute stimulation. 3. Sympathetic nerve activity, as defined by measurements of plasma noradrenaline, is normal in mild essential hypertension. Discrepancies described in the literature are probably related to a lack of comparability between hypertensive and normotensive study populations.

Adult↗
PubMed1979

A follow-up study of hypertensive patients after operative treatment of unilateral renovascular or renal disease.

A study of 44 hypertensive patients with unilateral renovascular or renal parenchymal disease is presented. All patients underwent corrective surgery. Out of the 44 operated patients, five did not participate in the follow-up examination. The remaining 39 patients constitute the study population. The effects of surgery on the hypertensive state could be evaluated in 35 patients, whereas four died less than two months after the operation. Follow-up studies were carried out at 8-60 months after the operation. The average period of observation was 32 months; 24 patients were observed for more than two years. As a group, the patients had severe hypertension with extensive target organ damage and widespread atherosclerosis. A fairly rigorous selection process was applied, and an unsatisfactory response to medical management was considered a point of major importance. In the majority of cases, renovascular lesions were atherosclerotic, with only two cases of fibromuscular dysplasia. Unilateral nephrectomy was performed in 32 patients, whereas seven underwent reconstructive vascular surgery. Out of 35 patients, 22 (63%) were cured, 8 (23%) improved and 5 (14%) unaltered. A gratifying regression of hypertensive lesions in target organs was observed in patients who were cured or improved by surgery. The frequency and severity of postoperative complications were related to the presence of extrarenal vascular disease.

Adult↗
PubMed1978

Radioimmunoassay for saralasin by means of anti-angiotensin II sera.

A radioimmunoassay for the angiotensin II-inhibitor saralasin has been developed. The assay is based upon an exploitation of the cross-reactivity of antisera raised against angiotensin II, with radioiodinated saralasin as the tracer peptide. Performance data for the assay and results obtained in clinical infusion studies are presented.

Angiotensin II↗
PubMed1978

Different secretion patterns of active and inactive renin in man.

1. In plasma samples from normal subjects and patients with untreated essential hypertension, the concentration of inactive renin (as measured after acidification) was on average 4-5 times higher than the concentration of active renin (as measured without acidification).2. Plasma angiotensin II concentration was correlated to active renin but not to inactive renin. 3. A hyperacute stimulation induced by infusion of saralasin resulted in a marked rise of active renin, whereas inactive renin remained unchanged. 4. An acute stimulation induced by frusemide and ambulation led to a considerable rise in active renin and a slight, but significant, rise of inactive renin. 5. Stimulation with oral thiazide over 5 days induced a seven-fold rise of active renin, with a doubling of inactive renin. Thiazide treatment for 3 months led to a four-fold rise of active renin and a three-fold rise of inactive renin. 6. There was no difference between the concentrations of inactive renin in systemic plasma, ipsilateral and contralateral renal venous plasma in 12 patients with renovascular hypertension, neither before nor after infusion of saralasin with the associated fall in blood pressure. 7. We conclude that the time constants pertinent to secretion or release of active and inactive renin in man are of different orders of magnitude.

Benzothiadiazines↗
PubMed1978

Changes in plasma volume and extracellular fluid volume after addition of prazosin to propranolol treatment in patients with hypertension.

In fifteen patients with hypertension, inadequately controlled during treatment with propranolol alone (mean dosage 333 mg/day), plasma volume (PV) and extracellular fluid volume (ECV) were determined. After addition of prazosin for 3 months (mean dosage 9 mg/day) there was a significant increase in PV and ECV, on average 8 and 5%, respectively. The decrease in supine blood pressure, systolic as well as diastolic, was very modest, on average 11 mmHg (SD +/- 12) and 4 mmHg (SD +/- 7), respectively. The changes in standing blood pressure were more pronounced. It is assumed that the expansion of PV and ECV contributes to the inadequate blood pressure response found in the present study.

Adult↗
PubMed1978

Changes in plasma volume and extracellular fluid volume and after addition of hydralazine to propranolol treatment in patients with hypertension.

In 16 patients with hypertension, BP could not be controlled satisfactorily by treatment with propranolol alone (mean dosage 325 mg/day). Plasma volume (PV) (T-1824) and extracellular fluid volume (ECV) (82Br-distribution space) were determined in these patients before and after the addition of hydralazine for three months (mean dosage 135 mg/day). After the addition of hydralazine, PV and ECV increased significantly, by 9% and 3%, respectively. Systolic and diastolic BPs decreased, by 15% and 13%. The mechanisms inducing fluid retention during treatment with hydralazine and the clinical significance of the problem are discussed. It is concluded that the addition of a diuretic to propranolol-hydralazine treatment is often well indicated.

Adult↗
PubMed1978

Effect of selective goitre resection on absent thyrotrophin response to thyrotrophin releasing hormone in idiopathic euthyroid goitres.

Absent thyrotrophin (TSH) response to thyrotrophin releasing hormone (TRH) was found in ten of fifty consecutive nodular goitrous patients who were clinically and biochemically euthyroid. These ten patients together with a reference group engaging fifty-eight healthy individuals matched for sex, age, and geographic region form the basis of the present study. Patients with autonomously functioning single adenomata were excluded from the investigation. In the patient group, values of serum thyroxine (T4), free T4-index, and serum TSH did not differ significantly from those recorded in the reference group, whereas serum triiodothyronine was found to be significantly higher in the patients, although within the normal range. After selective resection of the goitre, the TSH responsiveness to TRH recovered completely. Routine indices of thyroid function, however, demonstrated no major deviation from pre-operative levels. During a follow-up period of 1 year, no systematic alterations were recorded in TSH response to TRH nor in the thyroid function tests, indicating maintenance of euthyroidism with restored normality within the pituitary-thyroid axis. The present study lends support to the view that increasing functional autonomy apparently is a common trend in goitre evolution in a non-endemic area.

Adult↗