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  • 1
    Electronic Resource
    Electronic Resource
    British Diabetic Association Abstracts Medical and Scientific Section, Spring Meeting (1968)
    Springer
    Diabetologia 4 (1968), S. 375-380 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01211775
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  • 2
    Electronic Resource
    Electronic Resource
    Plasma concentration of α-methyldopa and sulphate conjugate after oral administration of methyldopa and intravenous administration of methyldopa and methyldopa hydrochloride ethyl ester (1975)
    Springer
    European journal of clinical pharmacology 8 (1975), S. 381-386 
    Details
    ISSN: 1432-1041
    Keywords: α-methyldopa ; plasma concentration ; hypertension ; sulphate conjugation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The plasma concentrations of free α-methyldopa and methyldopa sulphate conjugate were measured in 7 hypertensive patients with normal renal function following α-methyldopa (1 g) orally. Five of these patients subsequently received α-methyldopa ethyl ester (250 mg) (methyldopate) intravenously and two further patients received 250 mg of α-methyldopa intravenously. After oral administration a large amount of total plasma α-methyldopa was present as sulphate conjugate. There were wide interindividual differences in the ratio of free: conjugated α-methyldopa in plasma (ratio at 4 hours ranged from 3.73 – 0.83) suggesting that individual differences in the extent of sulphate conjugation may occur. There was no close correlation between the degree of conjugation and the fall in arterial pressure. At all time intervals examined, plasma concentrations were higher following intravenous α-methyldopa than α-methyldopate. The plasma concentration of α-methyldopa (free and esterified) 60 minutes after i.v. α-methyldopate was 1.7±0.3 µg/ml wile at the same time after the same dose of methyldopa by the same route the mean concentration was 5.9 µg/ml. Although small amounts of sulphate conjugate were detected after i.v. α-methyldopate, insignificant quantities of conjugate were found after i.v. α-methyldopa. The average fall in mean arterial pressure was 27 mm Hg following i.v. α-methyldopa but only 2.7 mm Hg following α-methyldopate. These results suggest that sulphate conjugation of α-methyldopa occurs in the gastrointestinal tract during absorption. Hydrolysis of α-methyldopa ethyl ester does not appear to be instantaneous and pharmacokinetic differences between the ester and free α-methyldopa have been demonstrated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00562310
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  • 3
    Electronic Resource
    Electronic Resource
    A bleak outlook for placebos (and for science) (1979)
    Springer
    European journal of clinical pharmacology 15 (1979), S. 219-221 
    Details
    ISSN: 1432-1041
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00618508
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  • 4
    Electronic Resource
    Electronic Resource
    Pharmacokinetic and concentration-effect relationships of clonidine in essential hypertension (1977)
    Springer
    European journal of clinical pharmacology 12 (1977), S. 463-469 
    Details
    ISSN: 1432-1041
    Keywords: Essential hypertension ; clonidine ; plasma levels ; concentration-effect
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effect of oral doses of 300 µg of clonidine hydrochloride on blood pressure, sedation and saliva production in 5 essential hypertensives were qualitatively similar to the effects in normotensive subjects. Peak plasma clonidine concentration (1.34±0.28 ng/ml) and plasma half-life (10.0 ±0.8 h) were similar to normotensives. During chronic oral dosing there was no evidence of drug accumulation. Some tolerance to the sedative and salivary flow effects occurred but no tolerance to the hypotensive effect was observed. There was a linear relationship between reduction in saliva flow and plasma levels of clonidine. The hypotensive effect was also related to plasma level at low concentrations. At plasma levels 〉1.5 ng/ml the hypotensive effect was diminished. This loss of effect at high plasma concentration may be related to the peripheral, post-synaptic alpha-adrenoceptor agonist action of the drug.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00561067
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  • 5
    Electronic Resource
    Electronic Resource
    The effects of nifedipine and hydralazine induced hypotension on sympathetic activity (1982)
    Springer
    European journal of clinical pharmacology 23 (1982), S. 479-482 
    Details
    ISSN: 1432-1041
    Keywords: nifedipine ; hydralazine ; blood pressure ; sympathetic activity ; calcium antagonism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary To determine whether inhibition of sympathetic activity is a factor in calcium antagonist induced hypotension, plasma noradrenaline was measured after intravenous infusion of hydralazine (25 mg) and the calcium antagonist nifedipine (4 mg) in 6 hypertensive males. The resultant reduction in mean blood pressure (12.4% and 14.2% respectively) was accompanied by similar increases in heart rate and plasma noradrenaline concentration. These results suggest that calcium slow channel blockade does not inhibit noradrenaline release from sympathetic nerves and that nifedipine induced hypotension is independent of such a mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00637492
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  • 6
    Electronic Resource
    Electronic Resource
    A crossover comparison of clonidine and methyldopa in hypertension (1972)
    Springer
    European journal of clinical pharmacology 4 (1972), S. 222-227 
    Details
    ISSN: 1432-1041
    Keywords: Antihypertensive agents ; clonidine ; methyldopa ; hypertensive rebound ; side effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The results of a titrated-dose cross-over comparison of clonidine with methyldopa are reported. Only one third of those entering the trial completed it. The blood pressure lowering effect of the two drugs is seen to be very similar. Patients experienced significantly more dry mouth whilst on clonidine but sedation was equally distributed over the two treatments. A hypertensive rebound occurred in some patients after sudden withdrawal of clonidine. The place of this new compound in routine management of hypertension is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00635800
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  • 7
    Electronic Resource
    Electronic Resource
    Introduction (1985)
    Springer
    European journal of clinical pharmacology 28 (1985), S. 1-1 
    Details
    ISSN: 1432-1041
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00543702
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  • 8
    Electronic Resource
    Electronic Resource
    Central nervous system mechanisms in blood pressure control (1985)
    Springer
    European journal of clinical pharmacology 28 (1985), S. 3-11 
    Details
    ISSN: 1432-1041
    Keywords: α2-adrenoceptors ; antihypertensives ; β-receptors ; α-methyldopa ; β-Blockers ; catecholamines ; clonidine ; CNS ; noradrenaline ; opiates
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Much of our knowledge about the CNS control of blood pressure is derived from animal studies using techniques such as intracerebroventricular administration of drugs, stereotactic ablation of specific brain nuclei, and biochemical analysis of these nuclei. These methods have identified numerous specific brain nuclei in the brain stem and a meshwork of interconnecting neurones involved in cardiovascular control. The main neurotransmitter involved is noradrenaline but recent interest has focused on several laterally situated nuclei which are capable of synthesizing adrenaline. Centrally acting antihypertensive drugs are thought to act by stimulating central α2-adrenoceptors either by the parent drug itself (clonidine) or via the formation of an active metabolite (α-methyldopa). This leads to decreased peripheral sympathetic activity and a hypotensive response but the latter is often attained at the expense of central side-effects such as drowsiness or dry mouth. The mechanism of the antihypertensive effect of β-Blockers remains uncertain although the balance of evidence is against a central effect. The central administration of propranolol causes decreased peripheral sympathetic activity in animals, but plasma catecholamine levels are little altered by β-Blockers in man. In equipotent antihypertensive doses, central α-agonists cause a much greater reduction in plasma noradrenaline than β-Blockers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00543703
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  • 9
    Electronic Resource
    Electronic Resource
    The pharmacodynamics and metabolism of propranolol in man (1970)
    Springer
    European journal of clinical pharmacology 2 (1970), S. 127-133 
    Details
    ISSN: 1432-1041
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary 1. The metabolic fate of intravenous and oral propranolol has been studied after single doses in man using 14C labelled propranolol. — 2. After oral administration there is virtually complete absorption and peak blood levels of propranolol and 4-hydroxy propranolol (a beta blocking metabolite) are seen at about 1 1/4 h after administration. Studies in normal subjects confirm that the maximum degree of beta blockade occurs at this time. — 3. Following intravenous administration, no 4-hydroxy propranolol is seen and the possible reasons for this are discussed. — 4. Excretion of the administered radio-active dose is mainly in the urine, with only 1%–4% of the administered radio-activity appearing in the faeces after both intravenous and oral dosing. — 5. The major metabolite so far identified in the urine is naphthoxylactic acid, which accounts for approximately 20% and 40% of oral and i.v. doses respectively. — 6. The greater proportion of radio-activity excreted in the urine (30–60% of the administered dose) is as yet unidentified although it may be a conjugate of propranolol. The level of total blood radio-activity following both intravenous and oral propranolol is very much higher than that of either propranolol or 4-hydroxy propranolol. The major portion of this blood radio-activity appears to be the same as the unidentified urinary metabolite. — 7. Following intravenous doses the decline of pharmacological response roughly parallels that of propranolol concentration in the plasma, and does not correlate with the plasma concentration of the unidentified metabolite.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00420338
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  • 10
    Electronic Resource
    Electronic Resource
    Evidence for a peripheral component in the sympatholytic actions of clonidine and guanfacine in man (1984)
    Springer
    European journal of clinical pharmacology 27 (1984), S. 23-27 
    Details
    ISSN: 1432-1041
    Keywords: hypertension ; alpha2-adrenoceptors ; blood pressure ; clonidine ; guanfacine ; healthy volunteers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The time courses of the changes in plasma growth hormone and noradrenaline concentrations in response to 15 min infusions of clonidine 0.2 mgs and guanfacine 2 mgs, were studied in six normal volunteers, in a double-blind, randomised, crossover study. Plasma noradrenaline fell within 15 min of the commencement of drug administration, by 36±14% after clonidine (p〈0.05) and by 32±11% (p〈0.05) after guanfacine. Plasma growth hormone was not significantly elevated until the 30th minute to 12.0±4.7 lU/ml (p〈0.05) after clonidine and 14.7±11.5 lU/ml (p〈0.05) after guanfacine, having been undetectable prior to both drugs. The reduction in plasma noradrenaline by these α2-adrenergic agonists, prior to activation of central adrenoceptors as detected by changes in plasma growth hormone, is evidence for a peripheral component in their sympatholytic effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00553149
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