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Biomedical subjects

T O Neild

Publications and source records attributed to T O Neild.

At least 37 records · Page 2Linked to original sources
PubMed1989

A study of the phasic response of arterioles of the guinea pig small intestine to prolonged exposure to norepinephrine.

Arterioles of the guinea pig small intestine constricted in response to norepinephrine, but the constriction was not maintained. The duration of constriction was reduced after pretreatment by theophylline, 3-isobutyl-1-methyl-xanthine, bromo-cAMP, or bromo-cGMP, suggesting that the relaxation was related to an increase in cyclic nucleotide levels in the cell. Forskolin also reduced the duration of constriction, suggesting the involvement of cAMP. The duration of constriction was not affected by propranolol or isoprenaline, indicating no involvement of beta adrenoceptors. A scheme to explain these observations, in which alpha 1-adrenoceptor activation stimulates adenylate cyclase, leading to a rise in cAMP and an increased rate of intracellular calcium sequestration is proposed. The resulting fall in intracellular calcium leads to repolarization and relaxation.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Relaxation and hyperpolarization of the smooth muscle of the rat tail artery following electrical stimulation.

1. The smooth muscle of the rat tail artery was made to constrict with noradrenaline or 5-hydroxytryptamine. Electrical stimulation of the contracted artery caused a transient hyperpolarization and relaxation. 2. The hyperpolarization and relaxation could be recorded from denervated arteries, showing that these responses were independent of the perivascular nerves. 3. Removal of the vascular endothelium caused only a small reduction in the relaxation. 4. Raising the external K+ concentration to 20 mM abolished or greatly reduced the relaxation, and caused some reduction of the hyperpolarization. 5. 1 mM-tetraethylammonium chloride abolished both the hyperpolarization and the relaxation. 6. From the membrane potential-contraction relationship for this artery it appeared that the hyperpolarization could account for some but not all of the relaxation.

Animals↗
PubMed1988

Electrophysiological properties of the mesenteric artery of the rabbit with perinephritis hypertension.

Membrane potential and tension were simultaneously recorded in ileal arteries isolated from rabbits with perinephritis hypertension and from sham operated controls. Stimulation of perivascular nerves with single pulses produced excitatory junction potentials, action potentials and contraction. Setting resting tension to levels equivalent to intraluminal pressures of 23, 70 and 114 mm Hg had no effect on the resting membrane potential, excitatory junction potential amplitude, action potential threshold or membrane time constant. The resting membrane potential in arteries from hypertensive rabbits was 3.7 mV less negative than in the shams. There were no significant changes in the action potential threshold or membrane time constant. It is suggested that the changes observed in the membrane potential may contribute to the increased responsiveness found in arteries from this model of hypertension.

Animals↗
PubMed1987

Membrane properties of rabbit basilar arteries and their responses to transmural stimulation.

Changes in membrane potential of rabbit basilar arteries were recorded in response to transmural stimuli applied by means of a suction electrode. Responses to current pulses of long duration and low intensity showed that the passive electrical properties of basilar arteries were similar to those of other vascular smooth muscles. In contrast to peripheral arteries, action potentials were readily evoked by depolarizing currents. Action potentials were graded in amplitude from 17-60 mV according to stimulus strength. Amplitudes and rates of rise of the directly evoked action potentials increased with increasing external calcium and were abolished by cobalt, manganese and magnesium. Brief electrical stimuli which might have been expected to activate perivascular nerves produced slow depolarizing responses whose amplitude and duration increased with increasing stimulus intensity. These responses were not blocked by tetrodotoxin, lowered external calcium, or sympathetic denervation. They do not appear to be due to the release of a conventional neurotransmitter.

Animals↗
PubMed1987

Effects of denervation on the responses of the rat tail artery to alpha beta-methylene ATP.

1. One microM alpha beta-methylene ATP (alpha beta meATP) caused transient contraction and depolarization of the smooth muscle of the rat tail artery. 2. The peak contraction was greater in denervated arteries; the peak depolarization was the same in normal and denervated arteries. 3. This suggests that alpha beta meATP receptors do not increase following denervation. 4. In denervated arteries electrical stimulation produced depolarizing responses that were not due to neurotransmitter release but which were blocked by alpha beta meATP. 5. It is suggested that alpha beta meATP may be a blocker of cation channels.

Adenosine Triphosphate↗
PubMed1987

Actions of neuropeptide Y on innervated and denervated rat tail arteries.

1. Neuropeptide Y caused a dose-dependent contraction and depolarization of the smooth muscle of the rat tail artery. 2. 30 nM-neuropeptide Y increased the contraction caused by either nerve-released noradrenaline or smooth muscle action potentials. 3. 30 nM-neuropeptide Y did not change the amplitude or rate of rise of the smooth muscle action potential. It did not change the amplitude of small excitatory junction potentials, suggesting that it did not affect neurotransmitter release. 4. 30 nM-neuropeptide Y increased the contraction caused by exogenous noradrenaline, 5-hydroxytryptamine and K in concentrations that gave submaximal contractions. It did not affect the response to higher concentrations that gave maximal or near-maximal contractions.

Action Potentials↗
PubMed1987

Relation between membrane potential and contractile force in smooth muscle of the rat tail artery during stimulation by norepinephrine, 5-hydroxytryptamine, and potassium.

The relation between smooth muscle membrane potential and contractile force was investigated in the rat tail artery to assess the importance of smooth muscle depolarization in the control of smooth muscle tone. Smooth muscle membrane potential and contractile force were measured simultaneously in isolated pieces of rat tail artery exposed to a range of concentrations of norepinephrine, 5-hydroxy-tryptamine, or raised external potassium. Potassium caused depolarization and contraction when the membrane was depolarized beyond -40 mV. Maximum contraction occurred at -19 mV, and further depolarization gave no increase in contraction. Both norepinephrine and 5-hydroxytryptamine caused contraction and depolarization, but the relation between depolarization and contraction was not the same as when potassium was used. There was significant contraction when the membrane potential was more negative than -50 mV, and the membrane potential was around -30 mV during maximal contractions. Although they acted on pharmacologically different membrane receptors, the relation between membrane potential and contraction was the same for norepinephrine and 5-hydroxytryptamine. Prazosin reduced the responses to norepinephrine but did not change the relation between membrane potential and contractile force. These results indicated that norepinephrine and 5-hydroxytryptamine binding to their respective receptors might activate the same sets of intracellular processes that subsequently caused both depolarization and contraction.

Animals↗
PubMed1986

Effects of alpha beta methylene ATP on membrane potential, neuromuscular transmission and smooth muscle contraction in the rat tail artery.

alpha beta methylene ATP (meATP, 400 nM-1 microM) caused depolarization and constriction of the smooth muscle of the rat tail artery, and block of the excitatory junction potential (e.j.p.). A similar depolarization caused by 25 mM K did not block the e.j.p. Contractions caused by nerve-released noradrenaline acting on alpha-adrenoceptors were potentiated by meATP but this was probably due to the depolarization as 25 mM K had a similar effect. MeATP blocked e.j.p.s recorded in the presence of 3 microM tetrodotoxin, suggesting that meATP was not blocking e.j.p.s by a local anaesthetic action.

Adenosine Triphosphate↗
PubMed1986

Effects of endothelium-derived relaxing factor on the smooth muscle of the rat tail artery.

Simultaneous measurements of smooth muscle membrane potential and tension were made from isolated pieces of rat tail artery. A single electrical stimulus to the perivascular nerves produced a transient contraction of the smooth muscle. The amplitude of the contraction was increased after removal of the endothelium. The excitatory junction potentials and action potentials in the smooth muscle had the same amplitudes before and after removal of the endothelium. Tension obtained by direct stimulation of the arterial muscle in guanethidine-treated arteries was also increased by removal of the endothelium. When the artery was constricted by noradrenaline or 5-hydroxytryptamine, electrical stimulation caused a relaxation that was reduced by removing the endothelium. It was concluded that the electrical stimulus released the endothelium-derived relaxing factor (EDRF) which reduced the amount of contractile force that could be produced by an action potential in the smooth muscle.

Action Potentials↗
PubMed1986

An in vitro study of the pharmacological and electrophysiological properties and the adrenergic innervation of small pulmonary arteries from children with pulmonary hypertension.

A study was made of the pharmacological and electrophysiological properties of pieces of small intrapulmonary arteries (100-450 micron I.D.) taken from children with cardiac defects that caused the pulmonary circulation to be exposed to an abnormally high perfusion pressure. The sensitivity of the arterial smooth muscle to the constrictor agonists acetylcholine and 5-hydroxytryptamine was similar to that reported for adult pulmonary arteries. Norepinephrine or histamine caused little or no constriction, although both these substances have been reported to be powerful constrictors of adult pulmonary arteries. The electrophysiological properties were similar to those of the smooth muscle of systemic arteries. The mean resting membrane potential was -6.12 mV +/- 1.29 (SEM n = 16). Stimulation of the perivascular nerves produced excitatory junction potentials, but no smooth muscle action potentials were recorded. Histochemical investigation revealed catecholamine containing nerve fibres around all intrapulmonary arteries down to 40 micron I.D.

Acetylcholine↗
PubMed1985

Measurements of the membrane potential of arterial smooth muscle in anesthetized animals and its relationship to changes in artery diameter.

Intracellular recordings of membrane potential were made from the smooth muscle of small (90-200 micron i.d.) arteries in the ears of anaesthetized guinea pigs and rabbits. Perivascular nerve stimulation evoked excitatory junction potentials and action potentials in the smooth muscle. No spontaneous muscle action potentials were recorded. Local block of perivascular nerve activity with tetrodotoxin caused a vasodilatation and a small hyperpolarization of the smooth muscle. Prazosin caused a smaller vasodilatation and no hyperpolarization. It was concluded that some of the nerve-mediated arterial tone may be caused by noradrenaline acting alpha 1-receptors, and some by some other mechanism.

Anesthesia↗
PubMed1985

Images of arterioles in unfixed tissue obtained by acoustic microscopy.

A scanning acoustic microscope operating at 600 MHz was used to observe arterioles in a thin sheet of collagenous connective tissue dissected from the submucosa of the guinea-pig small intestine. The arterioles were clearly defined in images made using transmitted ultrasound, and the acoustic attenuation (alpha) of the arteriolar wall was estimated to be 120 cm-1. Images made using reflected ultrasound did not show the arterioles clearly.

Animals↗
PubMed1983

The relation between the structure and innervation of small arteries and arterioles and the smooth muscle membrane potential changes expected at different levels of sympathetic nerve activity.

The membrane potential changes in arterial smooth muscle due to natural sympathetic nerve activity have been calculated. The electrical properties of the smooth muscle syncytium were taken into account and various assumptions made concerning the release of noradrenaline by the perivascular nerves. The depolarization that would result from asynchronous nerve activity at various mean frequencies was calculated for arterioles and small arteries of various diameters up to 150 micron. The calculations suggested that the depolarization would be irregular and that discrete excitatory junction potentials as evoked by synchronous nerve stimulation would not be recorded during natural nerve activity. The irregularity of the depolarization would be greater in small arterioles and would cause them to reach threshold for action potential generation at lower frequencies of nerve activity than larger arteries.

Action Potentials↗
PubMed1983

Effects of nifedipine on nerve-evoked action potentials and consequent contractions in rat tail artery.

The effects of nifedipine on the electrical and mechanical activity recorded from the rat tail artery were examined. Intracellular recordings were obtained from the smooth muscle and vessel diameter monitored during nerve stimulation. Nifedipine (0.1-10 microM) depressed contractions elicited by single and repetitive (2 Hz) stimulation by 32-100% but was ineffective in decreasing the amplitude of the associated action potentials. Concentrations greater than or equal to 10 microM caused a slowly developing membrane depolarization. No change in the amplitude of subthreshold excitatory junction potentials was observed at concentrations of nifedipine less than 50 microM when the membrane depolarization was less than 8 mV. At all concentrations examined nifedipine lowered the stimulus intensity required to initiate an action potential. The amplitude of the nerve-evoked action potential recorded in lowered external Ca2+ (1 mM) was slightly increased (5-10%) by nifedipine. However, nifedipine readily reversed the increased amplitudes of the nerve-evoked action potentials and contractions caused by the addition of 20 mM tetraethylammonium chloride in the tail artery. The action potential recorded in normal solution from the guinea pig vas deferens was selectively abolished by nifedipine.

Animals↗
PubMed1982

Lack of alpha-adrenoreceptor binding of [125I]BE2254 to rat basilar artery membranes.

Rat basilar arteries do not contain classical alpha- or beta-adrenoreceptors as assessed by electrophysiological techniques even though these arteries are innervated by catecholamine-containing perivascular nerves. These arteries were therefore examined for their ability to selectively bind an alpha-adrenoceptor radioligand, [125I]BE2254 (2/beta/4-hydroxyphenyl)-ethylaminomethyl)-tetralone). For comparison, rat tail arteries were also studied as these are known to contain functional alpha-adrenoreceptors. It was found that basilar artery membranes had only one-third of the specific binding of tail artery membranes and this finding collaborates the electrophysiological data.

Animals↗