Biomedical subjects

R Bültmann

Publications and source records attributed to R Bültmann.

41 records · Page 3Linked to original sources

PubMed1991

Noradrenaline-ATP corelease and cotransmission following activation of nicotine receptors at postganglionic sympathetic axons.

In rabbit mesenteric arteries, nicotine-evoked vasoconstrictor responses were markedly reduced by prazosin, slightly reduced after desensitization by alpha, beta-methylene ATP, and abolished by combined treatment with prazosin and alpha, beta-methylene ATP. In guinea-pig vasa deferentia preincubated with [3H]noradrenaline, nicotine elicited contractions as well as an overflow of tritium and of ATP. The contractions were greatly reduced by prazosin and abolished after additional desensitization by alpha, beta-methylene ATP. The nicotine-induced overflow of tritium was not changed by either treatment. The overflow of ATP was decreased by prazosin but not diminished further after additional desensitization by alpha, beta-methylene ATP. Activation of prejunctional nicotine receptors elicits a corelease of noradrenaline and ATP which leads to cotransmission in both tissues.

Adenosine Triphosphate↗

PubMed1991

Adrenergic and purinergic cotransmission in nicotine-evoked vasoconstriction in rabbit ileocolic arteries.

The possible involvement of ATP, in addition to noradrenaline, in nicotine-evoked vasoconstriction was studied in branches of the ileocolic artery of the rabbit. For measurement of vasoconstrictor responses, the arteries were simultaneously incubated and perfused. For measurement of the release of [3H]-noradrenaline, they were preincubated with [3H]-noradrenaline and then superfused. Prazosin (0.1 mumol/l) antagonized the constrictor effect of exogenous noradrenaline but not that of exogenous ATP. Desensitization of P2X-receptors by alpha, beta-methylene ATP markedly attenuated the effect of exogenous ATP but not that of noradrenaline. The presumed P2-purinoceptor antagonist suramin (100 mumol/l) reduced the maximal contraction obtainable with noradrenaline and shifted the concentration-response curve for the constrictor effect of alpha, beta-methylene ATP to the right, but did not change the effect of ATP. Nicotine elicited monophasic vasoconstrictions which faded while nicotine was still in the medium. The concentration-response curve was bell-shaped with an EC50 of 50 mumol/l and a maximal effect at 180 mumol/l, and the exposure time-response curve indicated that responses were maximal after 5 s of contact of nicotine (180 mumol/l) with the tissue. Neither prazosin 0.1 mumol/l nor desensitization by alpha,beta-methylene ATP changed the time course of the response to nicotine, but both depressed the magnitude of the responses over the whole concentration- and exposure time-response curves. The depression was greater with prazosin than with alpha,beta-methylene ATP. Desensitization by alpha,beta-methylene ATP or addition of suramin 100 mumol/l practically abolished the prazosin-resistant part of the response. The effect of nicotine was blocked by hexamethonium as well as by sympathetic denervation by 6-hydroxydopamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1991

Contraction-mediating alpha 2-adrenoceptors in the mouse vas deferens.

The question of the existence of postjunctional, contraction-mediating alpha 2-adrenoceptors, in addition to the known alpha 1-adrenoceptors, was studied in the mouse isolated vas deferens. Both the alpha 1-selective agonist phenylephrine and the alpha 2-selective agonist 5-bromo-6-(2-imidazolin-2-ylamino)-quinoxaline (UK 14,304) caused contraction of the vas deferens. In the presence of the alpha 1-selective antagonist prazosin (added in order to prevent an alpha 1 component in the effect of high concentrations of UK 14,304), the alpha 2-selective antagonist yohimbine and idazoxan shifted the concentration-response curve of UK 14,304 to the right in a manner compatible with competitive antagonism and with dissociation constants KB indicating the involvement of alpha 2-adrenoceptors. The maximal contraction elicited by UK 14,304 (in the presence of prazosin) was much lower than the maximal contraction elicited by phenylephrine. The effect of UK 14,304 was not changed by the P2-purinoceptor agonist alpha,beta-methylene-ATP and was reduced by neuropeptide Y, but was markedly enhanced by relatively low concentrations of phenylephrine. When the sympathetic fibres of the vas deferens were stimulated by trains of ten widely spaced (0.5 Hz) electric pulses, the tissue responded with ten separate twitches in which purinergic and adrenergic components were isolated by prazosin and suramin, respectively. Prazosin reduced the first adrenergic twitch in these trains at concentrations close to its KB value at alpha 1-adrenoceptors, whereas yohimbine and idazoxan reduced the first adrenergic twitch at concentrations far lower than their KB values at alpha 1-adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1990

Interaction of adenine nucleotides, UTP and suramin in mouse vas deferens: suramin-sensitive and suramin-insensitive components in the contractile effect of ATP.

Effects of various nucleotides, nucleosides and noradrenaline on smooth muscle tension were studied in the isolated mouse vas deferens. alpha, beta-Methylene-ATP, ATP gamma S, noradrenaline, ATP and UTP elicited contraction, with potency decreasing in that order; there was no contractile response to adenosine or uridine (up to 100 mumol/l). Prolonged incubation with alpha, beta-methylene-ATP (concentration increased stepwise from 0 to 15 mumol/l) selectively reduced contractions induced by ATP and UTP but not those induced by noradrenaline, and there was cross-tachyphylaxis between ATP and UTP. Suramin (10-300 mumol/l) did not alter the response to noradrenaline but shifted the concentration-response curves for alpha, beta-methylene-ATP, ATP gamma S, UTP and lower concentrations of ATP (0.1-1 mumol/l) to the right. The pA2-values of suramin were 5.2 against alpha, beta-methylene-ATP, 4.8 against ATP gamma S, 5.1 against UTP and 5.4 against lower concentrations of ATP. The effects of higher concentrations of ATP were largely resistant to suramin. The results indicate that the mouse vas deferens possesses contraction-mediating smooth muscle P2x-receptors. UTP also acts at this receptor, and there is no evidence for a separate UTP receptor. The selective inhibition of nucleotide- but not noradrenaline-induced contractions by suramin confirms the view that suramin is a selective P2-antagonist. The resistance against suramin of part of the effect of ATP suggests that ATP activates a suramin-insensitive site in addition to the P2x-receptor.

Adenine Nucleotides↗

PubMed1989

Effects of suramin and alpha, beta-methylene ATP indicate noradrenaline-ATP co-transmission in the response of the mouse vas deferens to single and low frequency pulses.

Vasa deferentia from mice were field-stimulated by trains of 10 pulses delivered at 0.5 Hz. The pulses elicited separate twitches, the first of which (corresponding to a single pulse) exceeded the following ones in height and width and often was clearly biphasic. alpha, beta-Methylene-ATP 1 mumol/l and suramin 100 mumol/l caused almost identical changes. They reduced the height of the first twitch in the train by about one half and also reduced its width in a manner indicating that only the second, slow phase remained, but reduced much more markedly the following twitches in which now a small second, slow phase also became detectable. Idazoxan 0.1 mumol/l or yohimbine 0.1 mumol/l, when added in the presence of alpha, beta-methylene-ATP or suramin, further decreased the first twitch but enhanced twitches No. 2 to 10. These responses were then almost abolished by prazosin 0.1 mumol/l. Successive addition of prazosin 0.1 mumol/l and idazoxan 0.1 mumol/l to previously untreated vasa deferentia depressed the response to the first pulse by about one half in a manner indicating that only the first, rapid phase remained, but had comparatively little effect on the responses to the subsequent pulses. Suramin 100 mumol/l almost abolished the contractions remaining in the presence of prazosin and idazoxan. The results indicate that the first, rapid phase of the neurogenic contractions elicited by single or low frequency pulses is mediated by ATP which substantially contributes to all responses in a train. The second, slow phase is mediated by noradrenaline which substantially contributes to the response to the first pulse only.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗