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Biomedical subjects

J Giese

Publications and source records attributed to J Giese.

At least 91 records · Page 5Linked to original sources
PubMed1983

Generation and elimination of angiotensins I and II in the kidney, liver and lung.

Inflow and outflow concentrations of angiotensins I (AI) and II (AII) from both kidneys, the liver and the lung were measured in 30 hypertensive patients, the majority having lateralization of the renin secretion. In the renin secreting kidney the data indicated a high generation rate of AI. In the contralateral kidney and splanchnic region both AI and AII were 'eliminated', and in the lungs the results confirmed previous evidence of converting enzyme activity.

Adolescent↗
PubMed1983

Pulmonary angiotensin II production in respiratory failure.

Plasma angiotensin II concentration gradients across the pulmonary vascular bed, plasma renin concentration and serum converting enzyme activity were measured in 19 patients. The majority of the patients were critically ill. Nine patients had septicemia with acute respiratory failure, six patients had severe chronic lung disease and four patients had other serious disorders requiring haemodynamic monitoring. Pulmonary angiotensin II generation rates were calculated as the products of the pulmonary plasma flow and the angiotensin II concentration gradient across the lung. Several patients had a highly activated renin-angiotensin system. There was a strictly linear correlation between the plasma angiotensin II concentrations in mixed venous blood and in systemic arterial blood across a wide range, the concentration in arterial blood being 1.4-1.5 times that in mixed venous blood in each of the three groups of patients. Serum converting enzyme activity was not different from the level observed in a group of control patients above 50 years of age, but lower than in younger normal individuals. The maximal angiotensin II production rates in the pulmonary vascular bed of patients with life-endangering pulmonary disease were similar to the rates previously measured in hypertensive patients with renovascular or renal parenchymal disease. In conclusion, the process of angiotensin I conversion in the lung operates without impediment in spite of severe pulmonary injury.

Adolescent↗
PubMed1983

Postpartum renal failure and malignant hypertension treated with captopril.

A case of postpartum renal failure and malignant hypertension in a 24-year-old woman is reported. The condition occurred three weeks after caesarian section following a normotensive pregnancy. Treatment with a converting enzyme inhibitor, captopril, for one year normalized the blood pressure, with concurrent reduction of plasma angiotension II concentration and markedly improved glomerular filtration rate. It is suggested that activation of the renin-angiotensin system may cause the hypertension and impairment of renal function in postpartum renal failure, and that use of drugs blocking the renin system may be of particular clinical value in this situation.

Acute Kidney Injury↗
PubMed1982

Double-antibody solid-phase radioimmunoassay for blood bradykinin.

A solid phase radioimmunoassay for the determination of blood bradykinin has been developed. Highly specific antibodies against bradykinin were raised in rabbits after coupling the peptide to thyroglobulin. Iodination of [Tyr8]-bradykinin was carried out with a chloramine-T procedure resulting in a tracer with high specific activity. Bradykinin was isolated in the following way: blood was sampled directly into acetone, and lipids were removed by extraction with petroleum either (40-60 degrees C). The final purification was made on QAE-Sephadex A-25 at pH 7.4. The mean recovery of added [125I-Tyr8]-bradykinin was 28% with a sample volume of 6 ml whole blood. The sensitivity of the radioimmunoassay was 1.25 pg/tube or 3 pg/ml blood. The reproducibility of the method is satisfactory with a between-assay coefficient of variation below 16%. Levels found in venous blood were below 3 pg bradykinin/ml in normal persons.

Adult↗
PubMed1981

Captopril combined with thiazide lowers renin substrate concentration: implications for methodology in renin assays.

1. We have measured plasma concentrations of renin, renin substrate and angiotensins I and II as well as plasma renin activity in nine patients with severe or malignant hypertension during treatment with captopril, hydrochlorothiazide and propranolol. 2. On captopril and hydrochlorothiazide the plasma concentrations of renin substrate and angiotensin II decreased markedly, while renin and angiotensin I levels were increased. 3. The changes in renin substrate concentration suggest a consumption of substrate induced by an increased renin release. Further, the positive feedback of angiotensin II on hepatic renin substrate synthesis may be inhibited. 4. The sequential changes in renin release during captopril treatment should be monitored by measuring plasma renin concentration since plasma renin activity measurements will be profoundly influenced by the marked changes in plasma renin substrate concentration.

Angiotensinogen↗
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↗
PubMed1981

Simple screening procedure for the diagnosis of primary aldosteronism.

A simple screening protocol for the diagnosis of primary aldosteronism was applied to 149 hypertensive patients. The diagnostic criterion for possible primary aldosteronism was the combination of supine plasma renin concentration less than 15 mIU/l (normal range 6-54) and plasma aldosterone concentration greater than 11 ng/100 ml (normal range 3-18). None of 63 persistently normokalaemic hypertensive patients fulfilled this criterion. Seventeen (20%) of 86 hypokalaemic patients showed hormonal values consistent with primary aldosteronism. The presence of an adrenal adenoma was verified in eight of these patients. Thus screening for primary aldosteronism can be restricted to hypokalaemic patients. The prevalence of primary aldosteronism in a hypertensive population was calculated to be less than 1%.

Adenoma↗
PubMed1980

Localization of aldosterone-producing tumours in primary aldosteronism by adrenal and renal vein catheterization.

Regional venous plasma aldosterone concentrations were determined and assessed against concurrent arterial levels in 16 patients with primary aldosteronism. The results obtained by sampling from the left adrenal vein or the left renal vein allowed correct side prediction of the presupposed adenoma in each patient. The problems caused by intermittent secretion of aldosterone by the tumour and the importance of correct positioning of the catheter are emphasized. Repeated sampling and continuing reference to systemic, arterial aldosterone levels proved valuable.

Adenoma↗
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↗