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Biomedical subjects

M Henning

Publications and source records attributed to M Henning.

At least 55 records · Page 3Linked to original sources
PubMed1980

Central cardiovascular and biochemical effects of baclofen in the conscious rat.

Baclofen (beta-D-chlorophenyl-GABA, 1.25-10 mg kg-1 i.p.) elicited dose-dependent increases in blood pressure and heart rate in conscious rats. similar responses were observed after intracisternal or intracerebroventricular injections of baclofen 0.125-1 microgram kg-1. Baclofen i.p. was largely ineffective after spinal transection at C7. Pretreatment with phenoxybenzamine, bethanidine or hexamethonium antagonized the cardiovascular effects of i.p. baclofen. These actions were significantly attenuated after catecholamine depletion and synthesis inhibition by means of alpha-methyl-m-tyrosine and alpha-methyl-p-tyrosine. The responses to baclofen were not affected by bilateral adrenal demedullation but abolished by pentobarbitone anaesthesia. Hence, the cardiovascular effects of baclofen are probably evoked from central nervous structures and mediated via the sympathetic nervous system. In doses corresponding to those used in the circulatory studies i.p. baclofen increaed endogenous concentrations of brain DA and decreased DA utilization but only slightly affected brain NA concentrations and utilization.

Anesthesia↗
PubMed1980

Pre- and postsynaptic alpha-adrenoceptor antagonists: differentiated cardiovascular effects in the rat.

Intravenous (i.v.) injections of yohimbine, phentolamine, prazosine and phenoxybenzamine lowered blood pressure and increased heart rate in conscious rats. Intracerebroventricular (i.c.v.) injections of yohimbine and phentolamine increased blood pressure and heart rate; this was antogonized by pretreatment with clonidine. Phenoxybenzamine and prozosine had no effect or gave hypotension and tachycardia on i.c.v. injection. Pentobarbitone anaesthesia partly antagonized the cardiovascular effects of all alpha-adrenoceptor antagonist. Synthesis and utilization of central noradrenaline was increased by i.v. or i.c.v. yohimbine; anaesthesia partly antagonized this effect. In peripheral tissues others have found that yohimbine, tolazoline, piperoxan and phentolamine are potent blockers of the presynaptic alpha-adrenoceptors while phenoxybenzamine and prazosine act preferentially on postsynaptic alpha-adrenoceptors. The differentiated cardiovascular response to i.c.v. injection of these blockers may reflect their different affinity to central pre- and postsynaptic alpha-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1980

Effect of chronically administered nicotine on axonal transport of dopamine-beta-hydroxylase in peripheral adrenergic neurons and on blood pressure and heart rate in the rat.

Nicotine was given to rats of about 200 g b.wt. in the drinking water for up to 2 months. Different doses of nicotine, from 25 mg to 100 mg per litre water, were tested with respect to their reducing effect on the normal increase in body weight. No effect was found on the normal accumulation of dopamine-beta-hydroxylase (DBH) proximal to a ligation of peripheral adrenergic neurons. This indicated a normal turnover of amine storage granules. This was interpreted as nicotine being without effects on the activity of the adrenergic neurons. In agreement with this lack of effect no changes of blood pressure or heart rate were found in rats receiving 50 mg nicotine per litre of drinking water.

Animals↗
PubMed1978

Noradrenaline receptor sensitivity after chronic ethanol administration.

The effects of the central noradrenaline receptor stimulating agent clonidine on blood pressure, heart rate, and flexor reflex activity were studied in intact rats and in rats chronically treated with ethanol. The clonidine-induced changes were similar in ethanol-treated animals and in animals never subjected to ethanol. The results suggest that the sensitivity of central noradrenaline receptors involved in the mediation of the circulatory changes and of the flexor reflex activity after clonidine is not altered by chronic administration of ethanol.

Animals↗
PubMed1978

On the disulfiram-like effect of coprine, the pharmacologically active principle of Coprinus atramentarius.

Coprine or disulfiram was given to rats in various doses at various time intervals before the administration of 2 g/kg ethanol. The ratio acetaldehyde/ethanol in the alveolar air was measured by gas chromatography and was taken as an index of the aldehyde dehydrogenase (ALDH) activity. The activity of dopamine beta-hydroxylase (DBH) was estimated in the same animals by measuring the amount of 14C-octopamine formed from 14C-tyramine in the heart. Coprine and disulfiram both caused an increase in the acetylaldehyde/ethanol ratio, coprine being more potent than disulfiram. Disulfiram, but not coprine, reduced the net yield of 14C-octopamine. In rats pretreated with either coprine or disulfiram, blood-pressure and heart-rate were recorded before and after intraperitoneal injections of 0.4 g/kg ethanol. In both cases ethanol caused a marked and rapid fall in blood-pressure. However, this effect was accompanied by tachycardia only in animals treated with coprine. It is concluded that coprine like disulfiram inhibits ALDH, but only disulfiram causes an additional inhibition of DBH. This difference may account for differences in the cardiovascular response to ethanol.

Agaricales↗
PubMed1978

Interaction of alpha- and beta-adrenergic receptor blocking agents: circulatory effects in the conscious rat.

The alpha-receptor blockers phenoxybenzamine and phentolamine produced similar circulatory effects, e.g. hypotension and tachycardia in the conscious rat. The hypotension was more pronounced than that seen after an acute cervical transection of the spinal cord or after hexamethonium treatment. The tachycardia was blocked by drugs with beta 1-receptor blocking capacity while the hypotensive response was blocked by drugs with beta 2-receptor blocking capacity. The pronounced hypotension and tachycardia was absent after spinal transection, hexamethonium pretreatment or adrenal demedullation. In adrenal demedullated rats substitution with adrenaline after alpha-receptor blockade produced tachycardia and hypotension of the same degree as seen in intact rats after alpha-receptor blockade. There was no correlation between the degree of beta-blocker induced decrease in heart frequency and increase in blood pressure after alpha-receptor blockade, while a significant correlation was found between the alpha-blocker induced decrease in blood pressure and the subsequent beta 2-blocker induced increase in blood pressure. In spinal rats, pretreated with phentolamine, adrenaline caused a depressor response. This depressor response was converted into a pressor response by administration of beta-blockers at doses which seemed to correlate well with the doses of beta-blockers needed to effectively block the alpha-blocker induced hypotension in intact animals. It is concluded that acute administration of phentolamine or phenoxybenzamine, by blocking alpha-receptors causes a reflex increase in adrenaline output, which subsequently further decreases the blood pressure and increases the heart frequency by stimulation of beta-receptors.

Adrenergic alpha-Antagonists↗
PubMed1977

New trends in pharmacology.

Among the factors influencing the arterial blood pressure the neural control through the autonomic nervous system is of paramount significance. The sympathetic division of this system holds a key position in this regard and its neural transmission mechanisms represent a well established target for pharmacological interference aimed at lowering blood pressure. This presentation will first deal with the morphological and physiological basis for blood pressure control through the sympathetic nervous system and the various possibilities for antihypertensive drug action through this system. Special attention will be drawn to recent advances in catecholamine research which may offer new leads in the development of blood pressure lowering agents. A second topic in this review will be some remarks on other pharmacological principles for interference with vascular control apart from the sympathetic system, particularly the vasodilator principle.

Animals↗
PubMed1977

Reduced adrenal amine synthesis in spontaneously hypertensive rats after long-term treatment with propranolol.

Male spontaneously hypertensive rats were either fed a diet containing 3 mg/g of (+/-)-propranolol, giving a mean daily intake of 178 +/- 4.2 mg/kg, or a control diet from 7 weeks of age for 6 months. Three days after cessation of propranolol-treatment, the arterial blood pressure of the treated group was about 10% lower than that of the control group. Adrenal dopamine content and tyrosine hydroxylase activity were reduced to 76% and 71% of the control values, respectively. The results indicate that propranolol causes a reduced sympathetic discharge through its central action, although blockade of beta-adrenoceptor-mediated local regulatory mechanisms cannot be excluded.

Adrenal Glands↗
PubMed1976

Gammahydroxy butyric acid: cardiovascular effects in the rat.

Gammahydroxybutyric acid (GHBA) 1 g/kg i.p. induced a marked and sustained increase in heart frequency and blood pressure in the rats. These effects of GHBA were abolished by a high spinal transection. In biochemical experiments GHBA in the same dose increased the turnover of brain noradrenaline but decreased the turnover of dopamine. The cardiovascular effects of GHBA are suggested to be of central origin, and possibly involve central noradrenergic mechanisms.

Animals↗