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Biomedical subjects

L Hansson

Publications and source records attributed to L Hansson.

At least 433 records · Page 24Linked to original sources
PubMed1983

Treatment of hypertension with beta-blockers with and without intrinsic sympathomimetic activity.

In a randomized double-blind trial 36 patients with essential hypertension were treated with either metoprolol or pindolol for 6 months following a 6-week placebo period. At the end of the placebo period and after 6 weeks and 6 months of active therapy peripheral hemodynamics at rest and during maximal vasodilatation were studied. Exercise heart rate was reduced to the same extent with both metoprolol and pindolol, indicating that the doses used (metoprolol average 179 mg/day; pindolol average 12 mg/day) were equipotent as regards beta-adrenoceptor blocking effect. The antihypertensive effect was identical with both compounds. However, metoprolol caused a significant reduction of heart rate at rest both at 6 weeks and 6 months. With pindolol the reduction in heart rate was not significant at 6 weeks, and it was clearly much less than with metoprolol. On the other hand, no change in calf vascular resistance was seen during metoprolol therapy, whereas a marked and statistically significant reduction was caused by pindolol. Resistance at maximal dilatation in the forearm did not change with metoprolol, but tended to fall with pindolol after 6 weeks and was significantly reduced after 6 months. This indicates that although metoprolol and pindolol have the same antihypertensive potency, the two agents appear to reduce blood pressure through different mechanisms. Thus, cardiac mechanisms seem to play the most important role with metoprolol, whereas pindolol mainly acts by a reduction in vascular resistance. It also seems that treatment with pindolol normalizes the structural arteriolar abnormality present in hypertension as indicated by the reduction in resistance at maximal vasodilation.

Adrenergic beta-Antagonists↗
PubMed1983

Circulatory effects of noise.

Thirteen patients with mild essential hypertension, mean age 44 years (range 21-59), were studied during "stress" before and after postsynaptic alpha-adrenoceptor blockade and combined postsynaptic alpha- and non-selective beta-adrenoceptor blockade. Loud broad band noise (100 dBA for 10 min) was used as the stress stimulus. Exposure to noise caused a significant increase in systolic (7%, p less than 0.05), diastolic (9%, p less than 0.01) and mean arterial pressure (6%, p less than 0.01). The blood pressure elevation was caused by an increase in total peripheral resistance (12%, p less than 0.05). There was no significant change in heart rate, stroke volume or cardiac output. The blood pressure response during noise stimulation was not affected by postsynaptic alpha-adrenoceptor blockade (prazosin, 2 mg orally). The hemodynamic reaction pattern, however, was totally reversed. Thus, the cardiac output increased significantly (9%, p less than 0.05), while the total peripheral resistance tended to decrease. Combined postsynaptic alpha- and non-selective beta-adrenoceptor blockade (labetalol, 200 mg orally) inhibited the increase in systolic blood pressure caused by noise, while the diastolic and mean arterial pressures still increased significantly (5%, p less than 0.01). Labetalol effectively blocked the stress-induced increase in total peripheral resistance and there was no significant increase in cardiac output after combined alpha- and beta-adrenoceptor blockade. Exposure to noise caused a significant increase in circulating noradrenaline (20%, p less than 0.05). Plasma adrenaline and plasma renin activity were not affected by noise stimulation. These results suggest that blood pressure elevation is essential during "stress" but that the hemodynamic pattern causing blood pressure elevation may vary and may be affected by pharmacological blockade of various parts of the sympathetic nervous system.

Adult↗
PubMed1983

Captopril or atenolol in essential hypertension.

Twenty-five patients with essential hypertension were randomly assigned to treatment with either captopril or atenolol. There were 15 males and 10 females and their mean age was 53 years, range 32-66 years. Systolic and diastolic blood pressures were significantly reduced by atenolol 50-100 mg once daily. Captopril 25-50 mg 3 times daily caused a significant decrease in supine diastolic but not in systolic blood pressure. After the addition of hydrochlorothiazide (25-50 mg) to those who did not become normotensive (supine diastolic blood pressure less than 95 mm Hg) on captopril or atenolol alone, blood pressure was further reduced. Captopril combined with hydrochlorothiazide significantly reduced both supine and standing blood pressure by 31/17 mm Hg (p less than 0.01) and 33/18 mm Hg (p less than 0.001) respectively. Atenolol combined with hydrochlorothiazide caused a significant decrease of both recumbent and standing blood pressure by 21/10 mm Hg (p less than 0.01) and 23/13 mm Hg (p less than 0.05 systolic, p less than 0.001 diastolic). The reduction of systolic blood pressure was significantly better with the captopril/hydrochlorothiazide combination, while there was no difference between the groups as regards diastolic blood pressure reduction. Thus, hydrochlorothiazide potentiates the blood pressure lowering effect of captopril more than of atenolol. This could be due to a synergistic interaction between captopril and hydrochlorothiazide.

Adult↗
PubMed1983

Stress and platelet activation.

Severe stress, with increased secretion of adrenaline, is likely to cause platelet activation. The aim of the present study was to investigate if moderate stress, which usually is not accompanied by adrenaline secretion, could induce activation of platelets, as measured by changes in the plasma concentrations of platelet factor 4 (PF-4). Noise stimulation (100 dBA for 10 min) caused a significant increase in the diastolic (10%, p less than 0.01) and mean arterial pressures (4%, p less than 0.01) of 10 healthy male volunteers. The plasma levels of PF-4 and the venous platelet concentrations were, however, unaffected during noise exposure. The results therefore suggest that stress not accompanied by adrenal medullary activation, does not induce platelet activation.

Adrenal Medulla↗
PubMed1983

Maternal hypertension during pregnancy and high blood pressure in children. Preliminary communication.

A group of 29 women with previous pre-eclampsia/hypertension in pregnancy and 37 of their children were investigated. At follow-up 7-12 years later, all mothers had mild to moderate hypertension. The children had a significantly higher blood pressure than age and sex-matched controls. Intracellular Na+ in erythrocytes from the children was normal but potassium was significantly higher compared to normotensive controls. The history of maternal essential hypertension and previous pre-eclampsia/hypertension in pregnancy seems to indicate an increased risk for high blood pressure in children, evident before puberty.

Adolescent↗
PubMed1983

A clinical follow-up study of 260 women with hypertension in pregnancy.

In 1969-73, 260 women had pre-eclampsia or hypertension in pregnancy. 237 were examined 7-12 years later. 172 were found to be normotensive, 24 were classified as having borderline hypertension while 62 had hypertension (antihypertensive treatment or BP greater than or equal to 160/100 mm Hg). Late hypertension was more often found after severe pre-eclampsia and gestational hypertension than after mild pre-eclampsia. Hypertension preceding pregnancy was more common with severe pre-eclampsia. A family history of hypertension and repeated hypertensive pregnancies seem to predispose for later hypertension.

Adult↗
PubMed1983

Antihypertensive mechanism of beta-adrenoceptor antagonism--the role of beta 2-blockade.

We performed this study in order to evaluate the antihypertensive effect of selective beta 2-adrenoceptor blockade. A highly beta 2-selective antagonist (ICI 118.551) was given to 15 male patients with essential hypertension who had previously shown a lowering of blood pressure in response to beta 1-selective or nonselective beta-adrenoceptor blockade. After a four-week placebo period ICI 118.551 was given (50 or 100 mg t.i.d.) for one week (randomized, double-blind). Before and 3 h after the first dose blood pressure, central and peripheral haemodynamics were studied by impedance cardiography and forearm plethysmography respectively. Blood pressure and heart rate were also measured after one week of treatment. After acute administration of drug cardiac output fell 14% (P less than 0.001) due to a fall in heart rate from 69 to 61 beats/min (P less than 0.002). Mean arterial pressure was unchanged (112 mmHg) and total peripheral resistance increased 18% (P less than 0.01). A similar rise in forearm resistance could be seen (14%). There was no reduction in blood pressure after one week of treatment although heart rate remained significantly reduced. Selective beta 2-adrenoceptor blockade does not lower blood pressure in patients previously responding to beta 1-or beta 1/beta 2-adrenoceptor blockade.

Adrenergic beta-Antagonists↗
PubMed1983

Ketanserin in hypertension. Early clinical evaluation and dose finding study of a new 5-HT2 receptor antagonist.

Ketanserin, a new 5-hydroxy-tryptamine antagonist, was given at three different dosage levels (double-blind, randomized) in a dose finding study for 2 months to 31 patients with mild to moderately severe essential hypertension. Treatment with ketanserin was then continued until 9 months had been completed. A significant antihypertensive effect was demonstrated at daily dosages of 20 mg t.i.d. or 40 mg t.i.d. The antihypertensive effect was similar to that of previous multiple drug treatment with conventional drugs. However, 60 mg t.i.d. was not acceptable, at least not as initial dosage. At this dose level, 8 out of 10 patients had to be withdrawn from the study during the initial phase due to unwanted effects. It is conceivable that alpha 1-adrenoceptor blockade may have played a role at this dose level, since postural reactions were observed which was otherwise not the case during this study. Ketanserin is a new and interesting alternative in the treatment of hypertension. At the same time it offers a tool by which the role of 5-hydroxy-tryptamine in the regulation of arterial pressure can be investigated.

Adult↗
PubMed1983

Prediction of later hypertension following a hypertensive pregnancy.

The aim of the present study was to identify factors predicting later hypertension following a hypertensive pregnancy. In the years 1969-1973, 261 out of a total of 17 000 pregnancies were complicated by pre-eclampsia or hypertension in pregnancy. In a follow-up study seven to 12 years later, 238 (91.2%) of these women were investigated. It was discovered that 26.4% of the women had hypertension and 10.1% had borderline hypertension compared with 2 and 6.5% respectively in a group of matched control subjects. A stepwise regression analysis was performed in order to evaluate the association between nine different variables and blood pressure at follow-up. We found that systolic blood pressure in early pregnancy was the single most important factor predicting systolic blood pressure at follow-up (r2 = 0.28). When highest recorded blood pressure before delivery and age were entered into the statistical model, r2 was increased to 0.35 (P less than 0.0001). Unlike previous studies, parity and proteinuria did not add to the predictive power of the analysis. Late hypertension was found in more than 25% of women seven to 12 years after a hypertensive pregnancy. The most important factor associated with later hypertension was blood pressure before pregnancy.

Blood Pressure↗
PubMed1982

Effects of treatment with nifedipine and metoprolol in essential hypertension.

In a double-blind trial 26 patients with essential hypertension were treated with nifedipine or placebo for 8 weeks, following a 4-week run-in-placebo period in all patients. The daily dosage of nifedipine during this phase was 10 mg 3 times daily. Metoprolol was then added to the therapeutic regimen of both groups for a further 12 weeks. Both nifedipine and metoprolol used as mono-therapy caused statistically significant reductions of arterial pressure. The addition of metoprolol to nifedipine tended to reduce blood pressure further, but blood pressures were not significantly lower than during nifedipine mono-therapy. Side-effects were few and only two patients had to be withdrawn during active therapy, one for headaches during nifedipine therapy, and another for asthma during metoprolol treatment. Combined therapy with a beta-adrenoceptor blocking agent, such as metoprolol, and a calcium antagonist with vasodilation properties, such as nifedipine, offers a theoretically interesting approach in the treatment of hypertension, even though the practical outcome in the present study probably suffered from an inadequate dose of nifedipine during the period of combined therapy.

Adult↗
PubMed1982

Effect of noise on blood pressure and 'stress' hormones.

1. Noise stimulation (95 dBA) for 20 min caused a significant increase in diastolic (12%, P less than 0.001) and mean arterial pressure (7%, P less than 0.001) in 15 healthy normotensive male subjects. 2. There was no significant change in systolic blood pressure or heart rate during exposure to noise. 3. Adrenaline, noradrenaline, prolactin, cortisol and growth hormone concentration in venous plasma were not affected during noise stimulation.

Adult↗