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Biomedical subjects

T Philipp

Publications and source records attributed to T Philipp.

At least 199 records · Page 11Linked to original sources
PubMed1987

Vasopressin is increased in mineralocorticoid-induced blood pressure increase in man.

Vasopressin has been studied intensively in DOCA-salt rats and seems to play an important role in this model of hypertension. In the present study we investigated plasma vasopressin in seven normotensive young volunteers during the early phase of mineralocorticoid-induced hypertension. We administered 0.8 mg/day fludrocortisone for 1 week. Body weight, blood pressure, plasma vasopressin, plasma osmolality and electrolytes, as well as plasma renin activity, were evaluated on days 0, 3 and 7. Blood pressure increased significantly from 117/67 to 121/76 mmHg (P less than 0.05) within 1 week, while plasma osmolality remained unaltered at 284 +/- 3 mOsmol/l. Plasma vasopressin (0.45 +/- 0.1 pg/ml) was increased after 3 days (0.68 +/- 0.5 pg/ml) and rose further to 1.53 +/- 0.27 pg/ml after 1 week (P less than 0.05). Changes in plasma vasopressin concentration were not correlated with alterations in blood pressure. Our results show an increase in plasma vasopressin in the early phase of mineralocorticoid-induced hypertension in man. However, the observed increase is moderate and does not seem to explain the increase in blood pressure alone, but could contribute to the blood pressure increase during mineralocorticoid treatment.

Adult↗
PubMed1987

Platelet intracellular free calcium and hypertension.

Platelet intracellular free calcium concentration was assessed by the quin-2 method in 38 patients with essential hypertension and in 35 normotensive subjects. The concentrations were found to be significantly higher in the hypertensive patients (p less than 0.05); however, there was a wide overlap between the values of both groups. In addition, we determined platelet intracellular free calcium in another model of increased blood pressure, the blood pressure elevation following administration of the synthetic mineralocorticoid fludrocortisone. Administration of 0.8 mg fludrocortisone per day to eight normotensive volunteers resulted in a pronounced increase in intracellular free calcium after the first week and a decrease toward control levels thereafter, while blood pressure remained elevated throughout the period of fludrocortisone administration. Our findings suggest that an increase in intracellular free calcium concentration is a transitory phenomenon and not directly related to the blood pressure elevation.

Adult↗
PubMed1986

Double-blind comparison of the cardioselective beta-blockers bisoprolol and atenolol in hypertension: the Bisoprolol International Multicenter Study (BIMS).

The antihypertensive efficacy and tolerability of bisoprolol and atenolol were compared in the Bisoprolol International Multicenter Study (BIMS). In 104 patients with essential hypertension (21 to 70 years of age and diastolic blood pressures (DBP) of 100-120 mm Hg in the sitting position), after a four-week placebo period, the active drug was given in a random double-blind crossover design (10 to 20 mg bisoprolol, 50 to 100 mg atenolol) for eight weeks each, with a 2 to 6 week placebo wash-out phase between active therapy. All blood pressures were recorded 24 h after drug intake. Of the 104 patients, 10 were withdrawn during the study because of unwanted effects, unsatisfactory blood pressure response, or intercurrent disease, leaving 94 for intraindividual comparisons. After 8 weeks active treatment with individually titrated dose, there were slightly, but significantly greater falls in blood pressure with bisoprolol (p less than or equal to 0.05). Diastolic target pressures of less than or equal to 95 mm Hg were reached in 68% with bisoprolol and 56% with atenolol (p less than or equal to 0.05; Mc Nemar). There was no between treatment group difference in the patients' self-assessed well-being. For both drugs, response rates were greater in patients below the age of 60 years than in those above 60 years. Better antihypertensive responses were observed with bisoprolol in patients regularly smoking cigarettes.

Adrenergic beta-Antagonists↗
PubMed1986

Humoral and blood pressure effects of the angiotensin converting enzyme inhibitor ramipril in essential hypertension.

The humoral and antihypertensive activities of the angiotensin converting enzyme (ACE) inhibitor 2-[N-[(S)-1-ethoxycarbonyl-3-phenylpropyl]-L-alanyl]-(1S, 3S, 5S)-2-azabicyclo[3.3.0] octane-3-carboxylic acid (ramipril, Hoe 498) were investigated in 10 patients with essential hypertension (WHO stage I or II). After a 7-day placebo period, the patients were treated with 5 mg ramipril orally once daily for 14 days. Peak serum concentrations of the active metabolite M1 (dicarboxylic acid) of 5.4-62.0 ng/ml were observed 2-6 h after the first oral dose. The maximum ACE inhibition of 95% was reached 2-4 h after the first oral dose, inhibition exceeded 70% 24 h after dosing. The maximum drop in the systolic and diastolic blood pressure (random zero sphygmomanometer) was measured 4 h after ramipril (p less than 0.02, p less than 0.01), but blood pressure on days 7 and 14 of the treatment period was not different from pretreatment values. Automatically recorded blood pressure results showed a marked reduction of both systolic and diastolic blood pressure during treatment compared to placebo. No side effects occurred. From the present data it is concluded that ramipril is a potent ACE inhibitor in hypertensive patients and that further controlled studies are required for the evaluation of the antihypertensive effect of 5 mg ramipril in essential hypertension.

Adult↗
PubMed1985

Free intracellular calcium in essential hypertension. Effects of nifedipine and captopril.

The acute effects of nifedipine (20 mg sublingually) and of captopril (12.5 mg orally) on blood pressure and on platelet intracellular free calcium were investigated in 11 and 12 patients, respectively, with essential hypertension. Platelet calcium was measured by the Quin 2 method. Application of both drugs resulted in a significant fall in blood pressure within 60 min. Platelet calcium, however, was lowered by nifedipine only. There was no correlation between blood pressure reduction and changes in platelet calcium. Platelet intracellular free calcium concentration was 99 +/- 3 nmol in 30 normotensive subjects and 109 +/- 5 nmol (+/- s.e.m.) in 26 patients with essential hypertension (P < 0.05). There was a wide overlap between the values of normotensives and hypertensives. Thus there is no positive evidence of an increased platelet intracellular free calcium concentration in a large proportion of patients with essential hypertension.

Adult↗
PubMed1985

Intracellular free calcium and ionized plasma calcium during mineralocorticoid-induced blood pressure increase in man.

Intracellular free calcium is considered to play a key role in vascular smooth muscle contraction. Platelet-free intracellular and plasma total and ionized calcium were assessed during mineralocorticoid-induced blood pressure increase in eight normotensive subjects receiving 0.8 mg fludrocortisone per day for 6 weeks. Blood pressure rose within 1 week and showed a further increase up to the 6th week. Plasma noradrenaline and renin activity (PRA) showed a decrease after 1 week and remained suppressed throughout the study. Ionized plasma calcium fell during mineralocorticoid treatment without any significant changes in total plasma calcium. Intracellular free calcium markedly increased after 1 week and decreased towards control levels thereafter. Previous studies have shown that after 1 week of fludrocortisone administration total peripheral resistance is still normal or even subnormal, whereas it is increased after 6 weeks. Therefore, the initial increase in intracellular free calcium, if also present in arteriolar smooth muscle cells, does not appear to be directly related to the final elevation of total peripheral resistance.

Adolescent↗
PubMed1985

Sympathetic tone and pressor response to noradrenaline during mineralocorticoid-induced blood pressure rise in man.

To gain insight into the role of the sympathetic nervous system in the development of mineralocorticoid hypertension, we determined noradrenaline and adrenaline in plasma and urine before, during and after administration of the synthetic steroid, fludrocortisone, for a period of 6 weeks in normotensive volunteer subjects. In addition, pressor reactivity to exogenous noradrenaline, platelet alpha 2- and lymphocyte beta 2-receptors, and platelet intracellular free calcium were determined. Fludrocortisone induced a fall in free and sulpho-conjugated plasma noradrenaline and after 6 weeks, a rise in free and sulpho-conjugated noradrenaline excretion. The number of alpha 2- and beta 2-adrenergic binding sites decreased. A marked increase in platelet free intracellular calcium was found after the first week of fludrocortisone administration followed by a decrease in the following weeks. Reactivity to exogenous noradrenaline was found to be enhanced and this could be a factor contributing to the development of hypertension. Whereas the decrease in plasma noradrenaline observed would suggest a diminution in sympathetic tone, the finding of a rise in urinary noradrenaline excretion after 6 weeks of steroid administration in the presence of suppressed plasma levels points to an increased renal sympathetic drive. The decreased number of platelet alpha 2- and lymphocyte beta 2-receptors observed would also be consistent with the assumption of an increased sympathetic tone.

Adult↗
PubMed1985

Compliance with salt restriction as a limiting factor in the primary prevention of hypertension.

It is an important but still unresolved question whether reduction of salt intake in the offspring of hypertensives (a high risk group) prevents the development of the disease. Therefore, 178 offspring (14-26 years old) of hypertensives were enrolled in a 2-year pilot trial aimed mainly at a reduction in salt consumption. For the intervention group (n = 99) a behavioural approach was chosen with extensive counselling by experienced dietitians. The controls (n = 79) received no continuous dietary advice. Both groups showed a small decline in sodium intake over time, but the differences between the two groups were not significant. Division into subgroups with and without sodium reduction revealed no differences in blood pressure. We conclude that the inherent resistance to any change of lifestyle among healthy subjects may require new and more comprehensive motivational approaches.

Adolescent↗
PubMed1984

Crossover comparison of nitrendipine with propranolol in patients with essential hypertension.

The antihypertensive effect of nitrendipine (2 X 10 to 2 X 20 mg/day) was compared with that of propranolol (2 X 80 to 2 X 160 mg/day) in a randomized crossover study. Twenty-five patients were treated over two 4-week periods following a placebo period of 2 weeks. Three patients dropped out of the study because of side-effects (two on nitrendipine and one on propranolol). Arterial pressures decreased in a comparable manner from 171/107 mm Hg (measured in a sitting position) to 147/91 mm Hg after 4 weeks on nitrendipine and to 145/93 mm Hg after 4 weeks on propranolol. The frequency of side-effects possibly related to treatment was comparable for both drugs, but decreased with the duration of therapy with nitrendipine only. The antihypertensive effect of nitrendipine, but not of propranolol, correlated positively with age and plasma noradrenaline.

Adult↗
PubMed1984

Effect of nifedipine and verapamil on alpha-receptor-activation in patients with essential hypertension.

The question of whether the hypotensive effect of calcium entry blockers involves an interaction with alpha-adrenergic receptors was examined. The effect of nifedipine subl. (20 mg, n = 9) and of verapamil p.o. (160 mg, n = 9) on the pressor effect of the unselective alpha-adrenergic agonist noradrenaline, as well as on 3H-yohimbine binding to platelet alpha 2-adrenoceptors was studied in patients with essential hypertension. In addition, the effect of nifedipine on reactivity to the selective alpha 1-adrenergic agonist phenylephrine was investigated (n = 9). Nifedipine caused a significant reduction of reactivity to noradrenaline (P less than 0.01), along with a significant decrease in binding sites (P less than 0.01). Affinity to the alpha 2-receptors was unchanged. Verapamil, although equally effective in lowering blood pressure, had no effect on the pressor response or binding sites. The pressor effect of the alpha 1-agonist phenylephrine was reduced (P less than 0.01) by nifedipine. Nifedipine may therefore affect both alpha 1- and alpha 2-adrenoceptors in patients with essential hypertension. Since verapamil did not affect the pressor response to noradrenaline or yohimbine-binding, the interaction with alpha 2-adrenoceptors does not appear to be a general prerequisite for the hypotensive action of calcium entry blockers.

Adult↗
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↗