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Biomedical subjects

C Bell

Publications and source records attributed to C Bell.

At least 271 records · Page 15Linked to original sources
PubMed1978

Effects of renal dopamine receptor and beta-adrenoreceptor blockade on rises in blood angiotensin after haemorrhage, renal ischaemia and frusemide diuresis in the dog.

1. In chloralose-anaesthetized dogs, central venous and arterial angiotensin (AII) levels were monitored by blood-bathed bioassay during venous haemorrhage of 20 ml/kg, acute renal ischaemia induced by suprarenal aortic stenosis and frusemide-induced diuresis. 2. Blockade of intrarenal dopamine receptors with ergometrine reduced markedly the increments in arterial AII associated with haemorrhage or suprarenal aortic stenosis, but did not consistently affect the corresponding increments in venous AII. 3. Ergometrine or renal denervation did not affect the increases of blood AII associated with frusemide diuresis. 4. Blockade of beta-adrenoreceptors with propranolol, by contrast, reduced blood AII increments associated with all three procedures. 5. It is suggested that renin release during moderate haemorrhage and acute suprarenal aortic stenosis is, in the dog, partly due to activation of intrarenal dopaminergic nerves. 6. The possibility is discussed that propranolol may depress renin release in the dog by an action other than that of blocking beta-adrenoreceptors.

Angiotensin II↗
PubMed1978

Localization of vasodilator dopamine receptors in the canine hindlimb.

1 Vascular responses to local injection of dopamine and isoprenaline have been compared in the blood-perfused gracilis muscle and hind paw pads of dogs anaesthetized with chloralose. 2 In the paw pads, dopamine (0.5 to 5.0 microgram) caused a transient vasoconstriction followed by dose-dependent vasodilatation. alpha-Adrenoceptor blockade converted this response to pure vasodilatation, which was attenuated or abolished by the dopamine-receptor antagonist, haloperidol (1 to 2 mg i.a.). In the gracilis, dopamine produced only vasoconstriction. Following alpha-adrenoceptor blockade this was abolished, but only a very small dilator response was revealed. 3 Isoprenaline (0.05 to 0.5 microgram) caused dose-dependent dilatation in both beds, which was attenuated by propranolol (0.1 mg/kg i.v.). 4 Glyceryl trinitrate (0.2 to 5.0 microgram) was used to assess vascular reactivity. When responses to isoprenaline and dopamine were compared with those to glyceryl trinitrate, both beds had approximately equal reactivity to isoprenaline. In contrast the paw pads were 10 fold more responsive to dopamine than was the gracilis. 5 We conclude that the vessels of the paw pads play an important part in the femoral dilator response to dopamine.

Animals↗
PubMed1978

Involvement of uptake1 and uptake2 in terminating the cardiovascular activity of noradrenaline in normotensive and genetically hypertensive rats.

1. In pithed, pancuronium-treated rats, inhibition of Uptake1 with desmethylimipramine (2.5 mg/kg i.v.) increased the time course of the pressor response to vasomotor nerve stimulation (1 and 5 Hz for 5 sec) but not the time course of the pressor response to injected noradrenaline (10 and 50 ng i.v.). 2. Subsequent inhibition of Uptake2 with metanephrine (3 mg/kg, i.v.) did not affect the time course of responses to either vasomotor nerve stimulation or injected noradrenaline. 3. It is concluded that Uptake1 but not Uptake2 is important in terminating the activity of noradrenaline released from rat vasomotor nerves and that neither process inactivates intraluminal catecholamine. 4. By contrast, chronotropic responses of rat atria to adrenergic nerve stimulation were prolonged by blockade of both Uptake1 and Uptake2, in agreement with previous evidence for involvement of both processes in terminating sino-atrial adrenergic responses. 5. Animals from the Otago strain of genetically hypertensive animals were identical to normotensives in their vascular handling of catecholamine. However, they lacked an atrial Uptake2 process. 6. This defect may be related to the high resting heart rate and abnormal cardiac catecholamine turnover observed to exist in the Otago hypertensive rats.

Animals↗
PubMed1978

Observations on the loss of catecholamine fluorescence from intrauterine adrenergic nerves during pregnancy in the guinea-pig.

During unilateral pregnancy in the guinea-pig there is loss of formaldehyde-induced fluorescence from the adrenergic nerves supplying the uterus and its vasculature. This loss occurs initially near the site of implantation at about Day 20 of gestation and spreads progressively. Implantation of wax pellets containing progesterone into the uterine lumen or the gastrocnemius muscle of virgin guinea-pigs for 7 days produced loss of fluorescence from all local adrenergic nerves. No diminution of fluorescence was seen when pellets containing oestradiol were substituted. Chronic denervation studies showed that the adrenergic axons supplying the uterus and its arteries originated from both the ovarian artery and the pelvic region. Our results suggest that loss of adrenergic fluorescence within the uterus during pregnancy is due to an effect of placental progesterone which is localized to the uterus because the high concentration of progesterone necessary to cause fluorescence loss is not attained in the systemic circulation.

Adrenergic Fibers↗
PubMed1977

Is the renal vasodilatation induced by beta-adrenoceptor stimulants in the dog mediated through dopamine receptor?

In chloralose-anaesthetized dogs the renal vasodilator effect of isoprenaline is depressed by blockade of either dopamine or beta-adrenoceptors but the renal vasodilator effect of dopamine is depressed only by blockade of dopamine receptors. This suggests that the vasodilatation induced by beta-stimulants within the canine kidney is due in part to activation of dopamine receptors.

Acetylcholine↗
PubMed1977

Rabbits possess conventional T lymphocytes.

Rabbit lymphocytes have been analyzed as to surface Ig markers in relation to the function of the cells. A battery of specific anti-Ig reagents as well as supposed B and T cell-specific mitogens were used, and DNA synthesis as well as high-rate Ig synthesis in vitro were recorded. Using cells from spleen lymph node or blood, surface Ig-negative lymphocytes expressed the expected behavior of T lymphocytes. No evidence was found of significant expression of allotypic markers on the surface of such nonactivated rabbit T lymphocytes. Lymphoid cells from bone marrow constituted an exception to the rule in the sense that they contained a high proportion of cells being surface Ig-negative at the time of anti-Ig column fractionation. They did, however, rapidly express surface Ig molecules as well as B cell markers as judged by B cell mitogenic stimulation shortly after in vitro explanation. In conclusion, we failed to find any constant region Ig markers on rabbit lymphocytes, which in every sense behave like conventional T lymphocytes.

Animals↗
PubMed1977

Release by vasopression of E-type prostaglandins from the rate kidney.

1. In order to test whether the release of E-type prostaglandins from the kidney by various vasoconstrictor stimuli is related specifically to adrenoreceptor activation, we have compared release of prostaglandin E-like material from perfused rat kidneys during infusion of noradrenaline or vasopressin. 2. Concentrations of noradrenaline or vasopressin that produced comparable rises in renal perfusion pressure also released comparable amounts of prostaglandin E-like material. This effect was abolished by infusion of an inhibitor of prostaglandin synthesis into the kidney. 3. We conclude that liberation of E-type prostaglandins during renal vasoconstriction is probably related to the activation of intrarenal smooth muscle and odes not involve any specific hormonal receptor. Stimulation of release of prostaglandin E may explain certain reported renal actions of vasopressin.

Animals↗
PubMed1977

Dopamine-induced depression of adrenergic nerve-mediated contraction of smooth muscle.

1 Dopamine (0.25-1.0 micrometer) applied extraluminally depressed vasoconstrictor responses of the perfused rabbit ear artery to low frequency adrenergic nerve stimulation. 2 The depressant effect of dopamine was prevented in the presence of haloperidol (0.1 micrometer) but not in the presence of phentolamine (0.03-0.14 micrometer). 3 Extraluminal dopamine (1 micrometer) or intraluminal injection of dopamine in amounts up to 0.025 micronmol had no dilator effect on arteries partially constricted by infusion of noradrenaline. 4 Dopamine also depressed contractile responses of guinea-pig vas deferens to low frequency adrenergic nerve stimulation. However, in this tissue the effect of dopamine was prevented by phentolamine but not affected by haloperidol. 5 In neither the rabbit ear artery nor the guinea-pig vas deferens did haloperidol increase the magnitude of responses to nerve stimulation or affect muscle sensitivity to noradrenaline. 6 We conclude that the adrenergic axons in the rabbit ear artery, but not the guinea-pig vas deferens, possess specific receptors for dopamine whose activation depresses axonal conduction or transmitter release. However, our results do not favour the view that these receptors are activated during normal transmission at physiological frequencies.

Animals↗
PubMed1976

Contribution of prostaglandins to the renal vascular supersensitivity to vasoconstrictor agents exhibited by New Zealand genetic hypertensive rats.

1. Studies were made of the effects on responses to vasoconstrictor agents of prostaglandins released from Krebs perfused isolated kidneys of genetic hypertensive and normotensive rats. 2. Prostaglandin E-like activity, detected by bioassay, was released from kidneys of both groups of rats during the vasoconstriction produced by noradrenaline, angiotensin or prostaglandin F2alpha. 3. In preparations obtained from hypertensive rats, responses to higher doses of noradrenaline or angiotensin were initially greater than those from normotensive rats and these were then reduced to a greater extent by infusion of indomethacin, which abolished release of prostaglandin E-like activity. Thereafter, in kidneys of either group, vasoconstriction to noradrenaline was potentiated by infusion of prostaglandin E2. 4. We conclude that, in rats, renal prostaglandins released in response to vasoconstrictor agents could augment the effect of such agents and in genetic hypertensive rats release of renal prostaglandins could contribute to the disease.

Animals↗
PubMed1976

Innervation and responses to vasoactive drugs of the extrinsic uterine artery of the macaque.

The responses of isolated, perfused uterine arteries from two species of macaques to perivascular nerve stimulation and to vasoactive drugs have been compared with those previously obtained using similar preparations from men. Uterine arteries from nonpregnant monkeys exhibited dilator responses to nerve stimulation and to acetylcholine, and contained few, if any, beta-adrenoceptors. These properties are not shared by the uterine artery of man and cast doubt on the widely held premise that the physiological characteristics of sub-human primates are similar to those of humans.

Acetylcholine↗
PubMed1976

PHA-induced activation of suppressor cells in normal human peripheral blood lymphocytes.

Normal human peripheral blood and tonsil lymphocytes can be stimulated to proliferate by phytohemagglutinin (PHA). When cells cultured with this mitogen for 3 days were transferred fo fresh autologous lymphocytes in fresh medium with PHA, the mitogen response of the fresh lymphocytes was suppressed. The suppression required the presence of viable cells, in that culture supernatants alone were not inhibitory and cell extracts showed only marginal inhibition. Approximately equivalent numbers of previously stimulated cells were required to produce optimal suppression of the PHA response of fresh cells. Cells irradiated after PHA stimulation were as effective as nonirradiated cells is causing suppression. PHA-stimulated cells also inhibited concanavalinA-induced proliferation and a mixed lymphocyte reaction. However, PHA-stimulated cells only partially inhibited the response to pokeweed mitogen. The suppressive effects were fully retained by a nylon-wool-enriched T-cell fraction but not by a B-cell-enriched fraction.

Cell-Free System↗
PubMed1976

Involvement of uptake2 in the termination of activity of neurogenic noradrenaline in the rat isolated atrium.

1. An examination has been made of the relative effect of drugs which affect Uptake1 and Uptake2 on the mechanical responses to adrenergic nervous stimulation (0-5-5 Hz for 5 sec) in rat isolated atrium. 2. Inhibition of Uptake1 with desmethylimipramine (2 muM) prolonged by 50-90% the time taken for recovery of normal heart rate after a five sec train of nervous stimulation. Inhibition of Uptake2 with metanephrine (4 muM) prolonged by 20-40% the time taken for recovery of normal heart rate. 3. Neither desmethylimipramine nor metanephrine had any consistent effect on the time course of the inotropic response to stimulation or on the amplitudes of either inotropic or chronotropic responses. 4. After administration of desmethylimipramine, metanephrine had a somewhat greater effect on chronotropic responses than when given alone. After administration of metanephrine, desmethylimipramine still further prolonged chronotropic responses to low frequency stimulation (0-5, 1 Hz) but had no effect at 5 Hz. These results agree with the known affinities of each uptake process for different concentrations of noradrenaline in the rat heart. 5. It is concluded that both Uptake1 and Uptake2 participate in the termination of physiological activity of neurogenic noradrenaline in rat isolated atrium even at low frequencies of nervous activation. 6. No evidence was obtained to indicate that manipulation of circulating oestrogen levels by oöphorectomy and oestrogen-priming of female rats had any effect of the efficiency of the cardiac Uptake2 process.

Animals↗
PubMed1976

Cutaneous and muscular rasodilation in the canine hindlimb evoked by central stimulation.

Using stereotaxic procedures, we electrically stimulated specific sites in the hypothalamus and midbrain of anesthetized dogs pretreated with guanethidine and atropine methonitrate. A tract in which stimulation caused noncholinergic dilator responses in the hindlimbs was identified. The course of this trace was different from that subserving cholinergic vasodilation in the hindlimb musculature. In a number of experiments we studied the proportional distribution of blood flow to leg and paw. Responses restricted to the paw were regarded as occurring mainly in cutaneous vessels; those restricted to the leg were regarded as occurring mainly in the skeletal muscle vessels. Some dilator responses in both beds were abolished by intra-arterial administration of antihistamines: other dilator responses were abolished by intra-arterial injections of dopamine antagonists. Centrally evoked dilation of leg and paw vessels by noncholinergic pathways suggests physiological roles for these fibers in the regulation of cardiovascular function.

Animals↗
PubMed1976

The HMOs: new models for practice.

New areas of practice are open to innovative social workers in an existing and expanding comprehensive health care delivery system--the health maintenance organization (HMO). In this article, four health plan models are described that document the experience of social workers in established HMOs. These illustrations demonstrate the necessity and opportunity for expanded social work roles in humanizing and corrdinating patient services in complex multidisciplinary health care delivery systems.

Health Maintenance Organizations↗