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Biomedical subjects

H Grobecker

Publications and source records attributed to H Grobecker.

At least 73 records · Page 4Linked to original sources
PubMed1976

[Specific and non-specific effects of beta-adreno-receptor blocking drugs in man (author's transl)].

The effect of tyramine infusion or exercise on catecholamine concentration and dopamine-beta-hydroxylase activity in plasma of normal volunteers has been studied. Whereas the increase in plasma catecholamine concentrations by tyramine infusion was not changed 90 min after oral application of a single dose of beta-adrenoceptor blocking drugs (penbutolol, practolol, I.C.I. 66082), the increase in blood pressure was diminished. However, the increase in plasma catecholamine, concentration, i.e. the adrenergic response to exercise was significantly enhanced during beta-adrenoceptor blockade. On the other hand, dopamine-beta-hydroxylase activity was not further increased during beta-adrenoceptor blockade. - The non-specific membrane activity of the beta-adrenoceptor blocking drugs wass assessed by the degree of inhibition of serotonin uptake by human platelets in vitro. Their order of potency, according to IC 50 values estimated from the dose response curves was: propranolol less than penbutolol less than practolol less than I.C.I. 66082. The inhibitory activity of these drugs in vivo was also studied by measuring serotonin uptake by platelets isolated 90 min after oral administration. Due to the high dose only propranolol showed a marked membrane activity.

Adrenergic beta-Antagonists↗
PubMed1976

Adrenaline-forming enzyme in brainstem: elevation in genetic and experimental hypertension.

The adrenaline-forming enzyme (phenylethanolamine N-methyltransferase) was elevated in the A1 and A2 regions of the brainstem of 4-week-old spontaneously (genetic) hypertensive rats and in the A1 region of adult experimentally (deoxycorticosterone acetate and sodium chloride) hypertensive rats. The administration of a phenylethanolamine N-methyltransferase inhibitor to experimentally hypertensive animals caused a reduction of the elevated blood pressure to normal values. These results implicate adrenaline-containing neurons in the brainstem in the development of hypertension.

Blood Pressure↗
PubMed1976

Peripheral and central catecholaminergic neurons in genetic and experimental hypertension in rats.

1. Activity of peripheral and central catecholaminergic neurons was studied in spontaneously hypertensive rats (SHR) and deoxycorticosterone (DOCA)-salt hypertensive rats. 2. In young SHR (4 weeks) the plasma values of bpth noradrenaline and dopamine-beta-hydroxylase activity were increased compared with those of normotensive rats of the Wistar/Kyoto strain. Total catecholamines (mostly adrenaline) were not significantly different. 3. In the adrenal glands of 2-weeks-old and 4-weeks-old SHR activities of tyrosine hydroxylase, dopamine-beta-hydroxylase, phenylethanolamine-N-methyl transferase were decreased, compared to Wistar/Kyoto rats. 4. The adrenaline-forming enzyme was elevated in the A1 and A2 regions of the brain stem of 4-weeks-old SHR and in the A1 region of adult DOCA-salt hypertensive rats. 5. In the adrenal glands of adult DOCA-salt hypertensive rats tyrosine hydroxylase activity was increased. 6. These results implicate peripheral noradrenaline-containing neurons and central adrenaline-containing neurons in the development of genetic and experimental hypertension in rats.

Adrenal Glands↗
PubMed1976

[On the mode of action of heptaminol (author's transl)].

The effect of heptaminol, an aliphatic amine with an alcoholic group on carbon 2, on sympathetic nerves and on isolated chromaffine granules was infestigated. In cats, heptaminol caused long-lasting, dose-dependent pressor effects accompanied by tachycardia and contractions of the nictitating membrane. In comparison with tyramine, heptaminol was 100 times less potent in increasing blood pressure and 10 times less effective in inducing contractions of the nictitating membrane. The rise in blood pressure as well as tachycardia and contraction of the nictitating membrane were diminished by cocaine. After pretreatment with cocaine, heptaminol in high doses caused short-lasting depressor effects. Also in rats the pressor effect of heptaminol was weaker but of longer duration than that of tyramine. The dose-response curve was depressed by pretreatment with reserpine. The tachycardia induced by heptaminol was markedly diminished after pretreatment with reserpine. After repeated injections heptaminol reduced the norepinephrine content of the rat heart by 20-40%, Tyramine and hexylamine were more effective than heptaminol in depleting the norepinephrine stores of the heart (50-60%). In fluorescence microscopic investigations on sympathetic nerves (rat iris) depleted of norepinephrine by reserpine, the uptake of alpha-methylnorepinephrine could be inhibited or prevented by heptaminol. The spontaneous release of catecholamines from isolated bovine chromaffine granules was enhanced (+30%) by heptaminol or methamphetamine in high concentrations. In lower concentrations, however, both drugs reduced the uptake of 14C-epinephrine in isolated medullary granules by 20-40%. In addition a non-specific papaverine-like spasmolytic effect of heptaminol could be demonstrated. The results suggest that heptaminol exerts its pharmacological action by interfering with release and uptake of norepinephrine.

Adrenal Medulla↗
PubMed1975

Excretion of norephedrine by man after oral administration of oxyfedrine.

After oral administration of oxyfedrine to healthy volunteers, norephedrine was identified in the urine by thin layer chromatography and gas liquid chromatography and mass spectrography. 30 hours after single oral doses of 8, 16 or 24 mg of oxyfedrine, about 4, 8 and 9 mg, respectively, of norephedrine were found in the urine, i.e. on a molar base 75-100% of the dose was excreted as norephedrine. The peak of excretion occurred within 2-4 hours after administration of the drug. No accumulation of oxyfedrine and/or its metabolite was observed after administration of 16 mg of oxyfedrine t.i.d. for three days. It could not be decided whether oxyfedrine was metabolized to norephedrine by liver enzymes, as in rats, or was spontaneously degraded to norephedrine, e.g. in duodenal fluid before absorption. 30-150 min after oral oxyfedrine (24 mg) norephedrine was demonstrable in duodenal fluid. Thus, in addition to the direct beta-sympathomimetic effects of oxyfedrine, it may also have indirect sympathomimetic effects because of the noradrenaline-releasing properties of its metabolite norephedrine.

Administration, Oral↗
PubMed1975

Correlation between increased dopamine-beta-hydroxylase activity and catecholamine concentration in plasma: determination of acute changes in sympathetic activity in man.

In 11 healthy untrained volunteers the increase in plasma dopamine-beta-hydroxylase (DBH) activity during graded physical exercise has been examined as a true measure of increased activity of the sympathetic nervous system. The correlation between DBH activity, catecholamine concentration (CA) in plasma and heart rate was studied. When work on an electrically braked bicycle ergometer was gradually increased from 12.5 to 100, 200 and 300 watts there was a linear increase in DBH activity and heart rate; the increase in CA concentrations followed an exponential function. The peak values for DBH activity and CA concentration in plasma after the 300 watt work load (as percentages of the resting levels) were 130+/-3% and 820+/-71%, respectively; the adrenaline concentration in plasma increased only to 150+/-19% (p less than 0.05). There were significant correlations between heart rate and work load, DBH and work load and log CA and work load. The data imply direct correlations between heart rate and DBH, heart rate and log CA and DBH and log CA. The exponential increase in noradrenaline concentration in plasma might be due either to a greater net ""overflow'' from sympathetic nerve endings, and/or to increased secretion by the adrenal medulla. In the latter case, the release of noradrenaline would not be accompanied by secretion either of adrenaline or DBH. After work ceased there were sharp falls in heart rate and CA concentration, which indicate an immediate drop in sympathetic activity. DBH activity in plasma returned to normal very slowly; it reached half maximum values after 20-22 min. It is concluded that increased sympathetic activity in man can be estimated in vivo as changes in DBH and/or CA concentration in plasma. In contrast, a rapid decrease in sympathetic activity is directly reflected only by a rapid fall in the plasma concentrations of CA.

Epinephrine↗