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Biomedical subjects

T Philipp

Publications and source records attributed to T Philipp.

At least 217 records · Page 12Linked to original sources
PubMed1983

Hypotensive action of calcium antagonists as related to plasma noradrenaline and reactivity to noradrenaline.

From animal experiments it has been suggested that calcium antagonists owe their antihypertensive potency to a diminished sensitivity of the resistance vessels to circulating noradrenaline. We studied the effects of two calcium antagonists, nifedipine and verapamil, on blood pressure, reactivity to exogenous noradrenaline and plasma noradrenaline concentration in 10 patients with essential hypertension. In a cross-over comparison the patients were treated with nifedipine and verapamil for four weeks each. Both calcium antagonists led to a similar drop in arterial pressure. Resting plasma noradrenaline did not change during either treatment whereas a slight increase (P less than 0.05) in stimulated noradrenaline levels was observed during nifedipine treatment. The hypotensive effect of nifedipine was associated with a marked reduction (P less than 0.01) in the pressor effect of noradrenaline whereas no change in pressor response could be found during verapamil treatment. The results obtained suggest that an impairment of the pressor response to noradrenaline is not a general prerequisite for the antihypertensive action of calcium antagonists.

Adult↗
PubMed1980

Rôle of sympathetic nervous system in essential hypertension.

Supra-normal supine and stimulated plasma levels of noradrenaline and/or adrenaline, presumably reflecting increased sympatho-adrenal activity, have been found in a proportion of patients with essential hypertension. In established hypertension a disturbed relationship between plasma noradrenaline concentration and pressor response to noradrenaline has been observed. It is suggested that sympathetic nervous activity and pressor response to noradrenaline together form an important determinant of the arterial blood pressure level.

Blood Pressure↗
PubMed1980

Urinary kallikrein in normotensive subjects and in patients with essential hypertension.

Basal 24 hour urinary kallikrein excretion of 20 patients with uncomplicated essential hypertension did not differ significantly from that of 18 normotensive age-matched control subjects. 4 of the 20 hypertensive patients, however, had low kallikrein excretion. Furosemide (40 mg i.v.) caused an increase of urinary kallikrein excretion in the normotensive subjects and in most of the patients with essential hypertension. The stimulating effect of furosemide was less pronounced or even absent in 7 hypertensives. No circadian rhythm of urinary kallikrein excretion was observed. There were weak correlations between 24 hour kallikrein excretion and urinary volume (r=0.59; p < 0.05), and potassium excretion (r=0.51; p < 0.05) in the normotensives. In the hypertensives correlations were found between 24 hour kallikrein excretion and potassium excretion (r=0.51; p < 0.05), aldosterone excretion (r=0.57; p < 0.01), and creatinine clearance (r=0.59; p < 0.01). Our findings do not support the concept that the renal kallikrein-kinin system might play a primary role in the pathogenesis of essential hypertension.

Adult↗
PubMed1979

[Modern methods in localization of pheochromocytomas (author's transl)].

In six patients with adrenal pheochromocytoma the tumors were localized by ultrasonography, phlebography of the adrenal glands and by estimation of plasma catecholamines selectively obtained from the vena cava and the adrenal gland veins. All tumors were localized by selective catecholamine estimation, five by ultrasonography, and four by phlebography. The smallest pheochromocytoma of 1.5 g weight was only localized by selective catecholamine estimation but not by ultrasonography or phlebography. This tumor, however, had been visualized by computed tomography. To avoid diagnostic errors by selective catecholamine estimation, it is important to withdraw blood from the adrenal gland veins prior to the injection of any radiographic contrast media, since this may result in an extremely enhanced secretion of catecholamines from the adrenal medulla.

Adrenal Gland Neoplasms↗
PubMed1979

[Haemodynamic studies on the blood pressure-raising effect of mineralocorticoids (author's transl)].

The effects on systemic haemodynamics of long-term administration of high mineralocorticoid doses were studied in six healthy volunteers. The subjects received the synthetic steroid fludrocortisone in a daily oral dose of 0.8 mg. Central venous and arterial pressures were recorded directly, and cardiac output was determined by dye dilution method before as well as after 1 and 6 weeks of steroid application. Within the first week of steroid administration, mean arterial pressure rose by 5.6 +/- 4.6 (+/- S.D.) mm Hg (p less than 0.025). Body weight increased by 2.5 +/- 1.1 kg (p less than 0.01), and central venous pressure by 1.3 +/- 1.4 mm Hg (p less than 0.05). An increase in cardiac index was observed in all subjects, the average increase was 0.72 +/- 0.47 1/min.m2 (p less than 0.01). Heart rate decreased. After the 6th week of steroid administration, blood pressure had risen in all subjects, the average increase in mean arterial pressure was 17.8 +/- 6.0 mm Hg (p less than 0.001). This pressure rise was the consequence of an increase in total peripheral resistance by 267 +/- 125 dyn.cm-5.s (p less than 0.01) on the average. At that time cardiac index was even lower than at the first study in five of the six subjects. Compared to the second study, heart rate had decreased further, central venous pressure had increased further, and body weight had not changed significantly. This data show that the mineralocorticoid-induced blood pressure rise is initially due to an increase in cardiac output and in its chronic phase due to an elevated peripheral resistance. The mechanism of the increase in peripheral resistance remains unclear.

Adult↗
PubMed1979

[The diagnosis of phaeochromocytoma: sensitivity of vanillylmandelic acid and urinary catecholamine determination and the Katecult test (author's transl)].

Tumour weight was compared with maximal vanillylmandelic acid and catecholamine excretion in 24-hour urine in 21 patients with phaeochromocytoma. The tumour weight correlated both with vanillylmandelic acid (r = 0.805, P less than 0.001) as well as urinary catecholamine levels (r = 0.725, P less than 0.001). Normal vanillylmandelic acid excretion was found in seven patients; urinary catecholamine levels were abnormal in all patients. The Katecult test was additionally performed in ten patients, with nine positive results.

Adrenal Gland Neoplasms↗
PubMed1979

[Pathogenesis of essential hypertension. Plasma noradrenaline, plasma renin and pressor effects of noradrenaline and angiotensin in normotensive patients and patients with essential hypertension].

Plasma noradrenaline, plasma renin and pressor action of exogenous noradrenaline and angiotensin in normotensive subjects and patients with essential hypertension. In normotensive subjects an inverse correlation was observed between the index of sympathetic nervous activity, the plasma noradrenaline concentration during physical exercise, and reactivity to exogenous noradrenaline. The relationship between the index of sympathetic nervous activity and reactivity to noradrenaline was invariably disturbed in age-matched patients with essential hypertension. A multiple regression analysis revealed a highly significant correlation between the combination of both factors and the height of mean arterial blood pressure (r = 0.91). The data suggest that both factors combined, sympathetic nervous activity and pressor response to noradrenaline, are an important determinant of the arterial blood pressure level. An inverse relationship could also be demonstrated between plasma renin concentration and pressor response to angiotensin II in normotensives and hypertensives. However, this relationship was unaltered in the hypertensives. Therefore angiotensin II does not appear to contribute directly to the high blood pressure.

Humans↗
PubMed1979

Urinary kallikrein in normotensive subjects and in patients with essential hypertension.

1. Excretion of urinary kallikrein was normal in 13 out of 15 patients with uncomplicated essential hypertension. 2. Frusemide increased urinary kallikrein excretion in normotensive subjects and in patients with essential hypertension. The stimulating effect of frusemide on urinary kallikrein was significantly diminished in patients with essential hypertension. 3. No correlations of urinary kallikrein with sodium, potassium, and aldosterone excretion were found. 4. The results do not support the idea that urinary kallikrein plays a primary role in the pathogenesis of essential hypertension.

Adult↗
PubMed1979

Studies on the mechanism of mineralocorticoid-induced blood pressure increase in man.

1. To gain insight into the mechanism of mineralocorticoid-induced blood pressure rise in man we performed haemodynamic studies in six normotensive volunteer subjects before and during administration of the synthetic steroid 9 alpha-fluorocortisol (0.8 mg daily) for a period of 6 weeks. In a further study, performed in seven subjects, plasma noradrenaline concentration and reactivity to exogenous noradrenaline were determined before and during administration of the mineralocorticoid. 2. Within the first week of steroid administration an increase in mean arterial blood pressure could be demonstrated, which was due to an increase in cardiac output. After the sixth week the elevated blood pressure was the consequence of an increased total peripheral resistance. 3. Plasma noradrenaline concentration decreased and reactivity to exogenous noradrenaline increased during steroid administration. 4. The mechanism underlying the increase in total peripheral resistance during long-term mineralocorticoid administration remains unclear. Increased sympathetic tone does not seem to be a factor since plasma noradrenaline decreased considerably. Pressor response to noradrenaline increased probably due to decreased sympathetic tone.

Adult↗
PubMed1978

Sympathetic nervous system and blood-pressure control in essential hypertension.

In normotensive subjects an inverse correlation was observed between an index of sympathetic nervous activity (the plasma-noradrenaline concentration during physical exercise) and reactivity to exogenous noradrenaline. This relationship was invariably disturbed in age-matched patients with essential hypertension. Multiple-regression analysis revealed a highly significant correlation between the combination of both factors and the height of mean arterial blood-pressure (r=0.91). The findings suggest that sympathetic nervous activity and pressor response to noradrenaline together form an important determinant of the arterial blood-pressure level. An inverse relationship could be demonstrated between plasma-renin concentration and pressor response to angiotensin II in normotensives, and this relationship was unchanged in hypertensive patients. Therefore angiotensin II does not appear to contribute directly to high blood-pressure.

Adult↗
PubMed1978

Sympathetic responsiveness and antihypertensive effect of beta-receptor blockade in essential hypertension.

The relationship between sympathetic responsiveness and the blood pressure reduction induced by long-term beta-blockade was assessed in patients with essential hypertension. The increase in plasma noradrenaline concentration during physical exercise was used as an index of sympathetic responsiveness. The cardioselective beta-blocker, atenolol, was given to 16 patients with sustained benign essential hypertension for five weeks at a dose of 200 mg/day. Atenolol induced a marked decrease in blood pressure and pulse rate during recumbency, orthostasis and exercise concomitant with a marked increase in plasma noradrenaline concentration (p less than 0.0125) and a pronounced decrease in plasma renin concentration (p less than 0.01). The ratio of plasma noradrenaline during exercise to the base line concentration correlated significantly with the subsequent decrease in mean arterial blood pressure induced by beta-blockade (r = 0.840; p less than 0.001). A less significant correlation was observed between the plasma renin concentration and the subsequent decrease in mean arterial pressure (r = 0.542; p less than 0.05). The results obtained indicate that sympathetic responsiveness is an important determinant of blood pressure response to beta-blockade induced by atenolol.

Adrenergic beta-Antagonists↗
PubMed1978

Plasma noradrenaline and the pressor action of exogenous noradrenaline in normotensive subjects and patients with essential hypertension.

1. An inverse relationship was found between plasma noradrenaline and reactivity to exogenous noradrenaline in normotensive subjects. 2. The relationship between plasma noradrenaline and reactivity was distrubed in age-matched patients with essential hypertension. 3. A multiple-regression analysis showed a highly significant correlation between adrenergic activity and reactivity to noradrenaline and the mean arterial blood pressure level (r = 0.91). The results suggest that adrenergic activity and pressor response to noradrenaline combined are important determinants of arterial blood pressure. 4. An inverse relationship could also be demonstrated between plasma renin activity and reactivity to exogenous angiotensin II. No difference was observed between normotensive and hypertensive subjects.

Adult↗
PubMed1978

The phlebographic diagnosis of phaeochromocytomas.

The diagnosis of phaeochromocytomas is based on the clinical features and on the hormone findings in the peripheral blood. Localisation, however, depends on radiological methods. Pneumoperitoneum was abandoned, because of its low accuracy, in favour of arteriography; lately, suprarenal phlebography has been available for the localisation of phaeochromocytomas. Our experience in nine patients with operatively confirmed phaeochromocytomas is described. Together with venous sampling from the caval system and the suprarenal veins for catecholamine estimations, it was possible to localise all tumours correctly. One tumour lying in the sympathetic chain in the thorax was correctly localised by hormone estimation. Our experience suggests that suprarenal phlebography represents a reliable method for localising phaeochromocytomas which carries a low risk and is to be preferred to arteriography.

Adrenal Gland Neoplasms↗
PubMed1977

[Hemodynamic effects of sar1-ala8-angiotensin in patients with renovascular hypertension (author's transl)].

In 7 hypertensive patients with renal artery stenosis and in 1 patient with hypertension and unilateral pyelonephritic nephrophthisi the influence of the angiotensin II antagonist, saralasin on systemic hemodynamics was studied. In the patients with normal renin infusion of saralasin produced an increase in total peripheral resistance, in patients with elevated renin a decrease in peripheral resistance was observed. In 3 patients who had extremely high renin levels while under sodium saralasin produced a dangerous drop in blood pressure concomitant with a marked decrease in cardiac output and in central venous pressure, heart rate remained unchanged or increased just slightly. The findings suggest that in patients with high plasma renin peripheral resistance, venous tone, venous retrun, and cardiac output are to a large extent controlled by circulating angiotensin II.

Adult↗
PubMed1977

[Sympathetic responsiveness and antihypertensive effect of beta-receptor blockade in essential hypertension: the effect of atenolol (author's transl)].

Plasmin noradrenaline concentration after bicycle exercise (200 W for 2 min), compared with base line concentration, was used as an index of sympathetic responsiveness in patients with essential hypertension. Atenolol (JCI 66082, a "cardioselective" beta-blocker) was given in a daily dose of 200 mg to 16 patients for five weeks. This caused a decrease in supine blood pressure of 37/23 and, on standing, of 36/25 mm Hg compared with the placebo period. There was a significant correlation between the ratio of the increase in plasma noradrenaline concentration on exercise over its base line concentration and the subsequent fall in mean arterial pressure (r=0.840; P less than 0.001). There was a less significant correlation between plasma renin concentration and subsequent decrease in mean arterial pressure (r=0.542; P less than 0.05). Administrations of atenolol caused a rise in plasma noradrenaline both on lying and after exercise (P less than 0.0125), and a fall in plasma renin concentration (P less than 0.01). The results suggest that the antihypertensive effect of atenolol is related to the responsiveness of the sympathetic nervous sytem. Adrenergic activity is apparently an important determinant of blood pressure response to beta-blockade.

Adrenergic beta-Antagonists↗