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Biomedical subjects

M J Rand

Publications and source records attributed to M J Rand.

At least 217 records · Page 12Linked to original sources
PubMed1966

The inhibitory innervation of the taenia of the guinea-pig caecum.

1. The inhibitory innervation of the taenia of the guinea-pig caecum has been studied, after blocking the responses to stimulation of excitatory cholinergic nerves with atropine.2. Stimulation of the perivascular nerves supplying the taenia caused relaxations. These nerves had properties which were typical of sympathetic post-ganglionic adrenergic nerves. The relaxations caused by stimulation were maximal at frequencies of stimulation above 30 pulses/sec and they were abolished by bretylium, guanethidine and 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP).3. The taenia is also innervated by intramural inhibitory nerves with their cell bodies in Auerbach's plexus. These nerves can be excited by electrical stimulation of the taenia or by the application of ganglion-stimulating drugs.4. The intramural inhibitory nerves have different properties from sympathetic adrenergic nerves. Relaxations in response to stimulation were maximal with frequencies of stimulation of about 5 pulses/sec and they were not blocked by bretylium, guanethidine or DMPP.5. Preganglionic cholinergic fibres in the caecal wall make synaptic connexions with the intramural inhibitory neurones.6. The role of the intramural inhibitory neurones in intestinal activity and their possible connexions with the central nervous system have been discussed.

Anesthetics, Local↗
PubMedDate not supplied

Adrenaline-induced hypertension in rats.

Rats were given a slow-release depot implantation containing adrenaline (0.33 mumole/kg). Adrenaline was released from the implant, giving a plasma level of 1.0 nmole/liter the day after implantation. Adrenaline-treated rats had elevated blood pressures compared to control rats from 1 day to 8 weeks after treatment. However, 8 weeks after treatment no adrenaline from the implant was found in the plasma, suggesting that at this time factors other than the adrenaline were responsible for maintaining the rise in blood pressure. In rats given metoprolol tartrate (5 mg/kg/day, p.o.), adrenaline treatment did not increase the blood pressure.

Animals↗
PubMedDate not supplied

Adrenaline activation of prejunctional beta-adrenoceptors and hypertension.

Rats implanted with osmotic minipumps containing adrenaline (0.2 ml, 2.9 mM) developed increased systolic and diastolic blood pressures, whereas blood pressures in rats implanted with osmotic minipumps containing the same amount of noradrenaline did not differ from those of sham-operated control rats. Heart rates did not differ from control in either treatment group. Concomitant administration of metoprolol (2.5 mg/kg, i.p., twice daily) abolished the effect of adrenaline-treatment on blood pressure. Plasma concentrations of adrenaline and noradrenaline released from the minipumps were 17 nM and 2.4 nM, respectively The atria accumulated 56 pmol/g of adrenaline released from the minipump. In isolated atria, adrenaline (10 nM) increased noradrenergic transmitter release by acting on prejunctional beta-adrenoceptors. Incubation of isolated atria with adrenaline led to the accumulation of 46 pmol/g. This adrenaline was released as a cotransmitter and mediated a positive feedback effect on transmission which was disrupted by metoprolol (0.1 micro M). It is suggested that the increase in blood pressure produced in rats by chronic treatment with adrenaline is due to facilitation of noradrenergic transmission to cardiovascular effector tissues. Such an effect may be involved in the development of stress-induced hypertension.

Animals↗
PubMedDate not supplied

Effects of serotonin on sympathetic noradrenergic transmission in rabbit isolated ear artery.

The amplifying effect of serotonin in subconstrictor concentrations on steady-state vasoconstrictor responses to norepinephrine (NE; 0.001-3 microM) and to stimulation of periarterial sympathetic nerves (SNS; 0.3-ms pulses, 0.1-3 Hz) has been studied in rabbit isolated ear artery. Ketanserin (30 nM by itself had no effect on responses to NE or SNS; however, the amplifying effect of serotonin (10 nM) on responses to NE was abolished; ketanserin also markedly reduced the amplifying effect of serotonin on responses to SNS. Idazoxan (100 nM) had no effect on responses to NE or SNS; furthermore, idazoxan had no effect on the amplifying effect of serotonin. Prazosin (10 nM) reduced responses to NE and SNS; however, prazosin had no effect on the amplifying effect of serotonin on responses to NE and SNS. Intraluminally applied serotonin increased responses to intraluminal and extraluminal NE and to SNS. Extraluminally applied serotonin increased responses to extraluminal NE but not to intraluminal NE or SNS; however, in the presence of cocaine (1 microM), an amplifying effect of extraluminal serotonin on responses to intraluminal NE and to SNS was also observed. It thus appears that the amplification by serotonin of the alpha 1-adrenoceptor-mediated responses to NE and SNS in rabbit ear artery involves postjunctional 5-HT2-receptor activation. Moreover, the neuronal uptake process appears to modify the amplifying effect of serotonin.

Animals↗