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Biomedical subjects

A Distler

Publications and source records attributed to A Distler.

At least 199 records · Page 11Linked to original sources
PubMed1983

Sympathetic nervous activity and the pressor effect of noradrenaline under chronic alpha-beta-adrenoceptor blockade with labetalol in hypertension.

In 14 patients with essential hypertension, the influence of the alpha- and beta-adrenoceptor blocking drug labetalol on blood pressure, heart rate, plasma renin, plasma noradrenaline and pressor effect of exogenous noradrenaline was investigated during long-term treatment. During the initial four weeks of treatment, labetalol at a dose of 400 mg/day showed a slight effect only on supine blood pressure, whereas upright blood pressure was already lowered effectively after the second week of treatment (p less than 0.01). An increase in the mean dose to 850 mg/day had an additional blood pressure-lowering effect (p less than 0.001), whereby a preferential decrease of the orthostatic blood pressure was no longer apparent. Further increase in the mean dose to 1,000 mg/day at the end of the 12th week did not have an additional blood pressure-lowering effect. Body weight, plasma renin and plasma noradrenaline remained unchanged on labetalol treatment in the lowest and the highest dose. There was, however, an increased pressor effect of exogenous noradrenaline, i.e. an alpha-adrenoceptor antagonistic effect of labetalol was not detectable under these conditions. The cause of the increased pressor effect was a reduced elimination of noradrenaline from plasma, which is probably the consequence of an inhibition of the uptake 1 process by labetalol. During long-term treatment with the doses administered, the blood pressure-lowering effect of labetalol appears essentially to be the expression of the beta-adrenoceptor blocking properties of the drug.

Adult↗
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↗
PubMed1981

[Errors in the treatment of hypertension (author's transl)].

Errors in the treatment of hypertension may occur at any level of the therapeutic concept. They can, however, largely be avoided by considering the following suggestions. A hypertension requiring treatment is usually only detectable by several blood pressure measurements taken on different days. A diagnostic confirmation of the hypertensive disease should precede the onset of the antihypertensive therapy. General measures and dietetic restrictions and indispensable to any hypertensive therapy. Drug therapy can only be successful if it is individual, if side-effects are avoided and if contraindications are taken into consideration. In addition the frequency of taking the drug and the necessary number of tablets to regulate the blood pressure must be kept as low as possible.

Adrenergic beta-Antagonists↗
PubMed1980

Antihypertensive effect of guanfacine: a double-blind cross-over trial compared with clonidine.

1. Sixteen patients with essential hypertension were treated with guanfacine and with clonidine for 5 weeks each in a double-blind, placebo-controlled, cross-over trial. Dosage ranged from 2 to 6 mg guanfacine and from 0.3 to 0.9 mg clonidine daily in two or three divided doses. 2. Both compounds caused a significant and comparable decrease in blood pressure. Patients whose blood pressure was not reduced to normal by 2 to 3 mg guanfacine daily did not respond better to an increase in the dose. 3. Dryness of the mouth and constipation occurred with about equal frequency with both agents, but sedation and orthostatic circulatory effects were considerably more frequent with clonidine. 4. A withdrawal syndrome was observed on discontinuation of clonidine in one patient as opposed to no rebound hypertension on stopping guanfacine treatment. 5. Guanfacine caused a significant decrease in plasma noradrenaline and adrenaline, suggesting a decrease in sympatho-adrenal activity.

Adolescent↗
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

[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

[Renal kallikrein-kinin system and control of blood pressure (author's transl)].

Kallikrein excreted with the urine appears to be formed in the kidney. The kallikrein-kinin system in the kidney is localized in the distal nephron from the juxtaglomerular apparatus to the collecting duct. It has been shown that intrarenal infusion of kinins produces an increase in renal blood flow as well as diuresis and natriuresis. Part of the effect of kinins appears to be mediated by the release of prostaglandins. However, the precise role of the renal kallikrein-kinin system in sodium and volume homeostasis and in blood pressure regulation still remains to be determined. Mineralocorticoids as well as the diuretics furosemide, bumetanide and bendroflumethiazide increase, spironolactone decreases kallikrein excretion. Urinary kallikrein has been shown to increase acid-as well as cryoactivation of prorenin in vitro. It is unclear as yet, however, whether the renal kallikrein-kinin system takes part in converting inactive prorenin into active renin in vivo. There are reports on subnormal, normal as well as increased kallikrein excretion in spontaneously hypertensive rats. In rats susceptible to the hypertensive effect of salt a substantially decreased excretion of kallikrein has been observed. Kallikrein excretion has been described to be increased in primary aldosteronism and to be reduced in a proportion of patients with established essential hypertension. In patients with labile hypertension, however, kallikrein excretion appears to be normal suggesting that decreased urinary kallikrein in essential hypertension is a consequence rather than a cause of hypertension. The renal kallikrein-kinin system does not appear to play a primary role in the pathogenesis of hypertension.

Angiotensin II↗
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↗