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At least 19 recordsLinked to original sources

PubMed1978

Relation between cholinergic and histaminergic components in reflex vasodilatation in the dog.

Previous studies have shown that phentolamine is able to reverse the reflex vasodilatation produced by transitory baroreceptor stimulation by blocking sympathetic, histaminergic, and cholinergic components. A direct anticholinergic action of phentolamine has never been described; however, since it is known that this drug is capable of inhibiting histamine release during the reflex vasodilatation, it is possible that its ability to block the cholinergic component of the reflex is related to the latter property. Therefore, this study was undertaken in an attempt to identify possible relationships between cholinergic and histaminergic components of the reflex vasodilatation. Accordingly, in mongrel dogs the gracilis muscle was isolated and perfused and then loaded with 14C-labeled histamine. A transitory systemic hypertension was induced by intravenous injection of norepinephrine; this produced a reflex vasodilatation, shown by the fall in perfusion pressure, which was accompanied by an increase of histamine release from the muscle. Vagal block induced by atropine pretreatment reduced the fall in perfusion pressure induced by the systemic hypertension and produced a reduction of histamine release during the vasodilatation. In another group of animals a vasodilatation in the perfused muscle was induced by injection of acetylcholine. This response was accompanied by an increase in histamine release from the gracilis muscle. Alpha-receptor blockade, which has been shown to inhibit histamine release, reduced this acetyl-choline-induced vasodilatation. These results, while confirming the participation of the cholinergic system in the reflex vasodilatation elicited by transitory stimulation of the arterial baroreceptors, seem to demonstrate that this component is mediated almost exclusively by histamine release.

Acetylcholine↗

PubMed1975

Dopamine-induced neurogenic vasodilatation in isolated perfused muscle preparation of the dog.

Dopamine, injected into the lumbar aorta of the dog in doses which produce a reversible inhibition of synaptic transmission in the lumbar paravertebral ganglia (0.5-64x10-8 moles), produces a neurogenic vasodilatation in the isolated perfused hindleg or gracilis muscle. This was abolished by acute preganglionic decentralization and by administration into the perfused preparation of alpha-adrenoceptor blocking agents, but not of atropine or diphenhydramine. After decentralization, preganglionic electrical stimulation restored the dopamine-induced indirect vasodilatation. The neurogenic vasodilatation was also seen with intra-aortic injections of epinine (2-32x10-8 moles) and apomorphine (1.2-19.2x10-8 moles) and was preferentially blocked by haloperidol (0.26x10-6 moles). (-)-Noradrenaline, injected into the lumbar aorta in baroreceptor-denervated dogs, was found to be equipotent with dopamine in eliciting the neurogenic vasodilatation; this (-)-noradrenaline-induced effect was preferentially blocked by phentolamine (8x10-6 moles). The possibility that the neurogenic vasodilatation, which occurs upon intra-aortic injection of dopamine in the dog, is due to its gnaglionic-inhibitory effect is discussed.

Acetylcholine↗

PubMed1979

The origin of the hind limb vasodilatation evoked by stimulation of the motor cortex in the cat.

In cats under Althesin anaesthesia, the hind limb area of the motor cortex has been stimulated by means of monopolar, semi-micro-electrodes with careful experimental control so as to avoid reflex effects evoked through stimulation of meningeal afferent fibres or stimulus spread to non-cortical structures. 2. Localized cortical stimulation which elicited muscle contractions in the contralateral hind limb also elicited vasodilation in the same limb: the stimulus threshold was the same for both effects, and the magnitude of the dilatation was related to the strength of contraction. 3. Reduction of the somatic motor response, caused by lesions in the medullary pyramidal tract, was accompanied by a parallel reduction of the vascular response. 4. Prevention of the motor response by gallamine or by spinal cord section at L4--L5 (which leaves the sympathetic outflow to the hind limbs intact) led to abolition of the vascular response. During recovery from gallamine, contraction and vasodilatation returned in parallel. 5. The muscle vasodilatation was insensitive to atropine or guanethidine. 6. It is concluded that the hind limb vasodilatation observed on stimulation of the motor cortex is simply a post-contraction hyperaemia, and that it is independent of the sympathic nervous system. Previous conclusions of a sympathetically mediated vasodilatation probably resulted from inadequate control of the stimulus or a failure to recognize weak muscle contractions.

Animals↗

PubMed1975

Possible mechanism of histamine release during active vasodilatation.

Continuous electrical stimulation of the cut synpathetic innervation to perfused gracilis muscles restored vasoconstrictor tone and active dilatation resulted when stimulation was terminated. This dilatation was unaffected by cholinergic blockade but was blocked by the antihistamine tripelennamine. Prior vasoconstriction was not required to produce active dilatation since sympathetic stimulation applied during infusion of xylocholine (betaTM10) produced no vasoconstrictor response yet an antihistamine-sensitive vasodilatation appeared when stimulation ceased. This dilatation was also blocked by the alpha-adrenergic receptor blocker phentolamine even though adrenergic vasoconstrictor tone was absent. These results suggest that the release of histamine from its storage site is mediated by an alpha-receptor mechanism. Since betaTM10 abolished adrenergic vasoconstriction but preserved histamine-mediated vasodilatation that could be prevented by alpha-adrenergic blockade, it is proposed that histamine release may be under the control of separate adrenergic fibers without a vasoconstrictor function. This mechanism may underlie the process of active reflex vasodilatation since upon reflex withdrawal of tonic sympathetic activity an antihistamine-sensitive vasodilatation occurs.

Animals↗

PubMed1975

The influence of imipramine on dopamine-induced ganglionic inhibition and neurogenic vasodilatation in the dog.

Imipramine potentiates the dopamine-induced inhibition in the paravertebral lumbar ganglia of the dog. Potentiation by imipramine of the dopamine-induced neurogenic vasodilatation in the isolated perfused gracilis muscle, is seen in cross-circulation preparations only, where imipramine is injected into the perfusion circuit of an isolated perfused gracilis muscle, it antagonizes the dopamine-induced neurogenic vasodilatation. When imipramine is injected intravenously into a dog with an autoperfused gracilis muscle, the peripheral antagonism masks the potentiating effect at the ganglionic level, and the dopamine-induced neurogenic vasodilatation is abolished.

Action Potentials↗

PubMed1976

Activation of sustained sympathetic vasodilatation in dog by spinal cord stimulation.

Electrical stimulation in lateral sites of the upper cervical spinal cord evoked vasodilatation after adrenergic blockade. Sympathetic fibres mediating sustained vasodilatation were shown to be separate from adrenergic sympathetic fibres since the adrenergic vasoconstrictor response in the paw evoked by vasomotor stimulation in the medulla was not reversed to vasodilatation after bretylium.

Animals↗

PubMed1979

Absence of sympathetic cholinergic vasodilatation in cats during early stages of affective behaviour elicited by stimulation of central amygdala, postero-lateral hypothalamus and locus coeruleus.

1. Stimulation of the central amygdala, postero-lateral hypothalamus and locus coeruleus in cats resulted in a sustained increase in arterial pressure, an increase in heart rate, with a poststimulation bradycardia and an increase in peripheral resistance (vasoconstriction in the vessels of the hindlimbs). The behavioural pattern was characterized by an alerting reaction. Increased stimulus intensities resulted in rage reactions if the amygdala or the hypothalamus were stimulated. 2. Stimulation of the basal amygdala resulted in a cardiovascular pattern characterized by a sympathetic cholinergic vasodilatation. The concomitantly observed behaviour was characterized by alerting, anxious behaviour, eventually resulting in defence. 3. Alerting was not necessarily linked to sympathetic cholinergic vasodilatation. 4. The cardiovascular pattern including sustained vasoconstriction of the vessels of the hindlimbs was supposed to be of greater importance for the induction of hypertension than the cardiovascular pattern, including sympathetic cholinergic vasodilatation.

Affect↗

PubMed1978

Comparison of beta-adrenoceptors mediating vasodilatation in canine subcutaneous adipose tissue and skeletal muscle.

Blood flow changes in response to various drugs in simulataneously autoperfused canine subcutaneous adipose tissue and gracilis muscle were compared to study the vascular beta-adrenoceptors. Compared to isoprenaline the beta 2-selective agonist salbutamol was 4--6 times more potent as a vasodilator in the muscle than in adipose tissue. Furthermore two beta 1-selective agonists (Tazolol and H80/62) caused vasodilatation in adipose tissue but not in the gracilis muscle. When given by close i.a. injection after beta-adrenoceptor blockade, adrenaline was a more potent vasoconstrictor than noradrenaline in both tissues. Before beta-blockade, however, noradrenaline was the more potent vasoconstrictor in the gracilis muscle whereas adrenaline was more potent in adipose tissue. Intravenous infusion of adrenaline in doses causing vasodilatation in the muscle caused vasoconstriction in adipose tissue whereas intravenous infusion of noradrenaline caused vasoconstriction in both tissues. The present findings suggest that the beta-adrenoceptors mediating vasodilatation in skeletal muscle are mainly ose tissue. Since adrenaline is a much more potent beta2- than beta1-agonist, these differences point to different roles of intravascular adrenaline in the two sites. In skeletal muscle circulating adrenaline is mainly a vasodilator whereas in subcutaneous adipose tissue it mainly acts as a vasoconstrictor.

Adipose Tissue↗

PubMed1977

Histamine mediation in muscular vasodilatation induced by beta adrenoceptor stimulation in dogs.

This study was designed to investigate the possibility of a histamine mediation in muscular vasodilation induced by beta adrenoceptor stimulation. Accordingly, in seven dogs the effects of isoproterenol administration on the release of 14C-histamine from the perfused gracilis muscle were studied. Beta adrenoceptors stimulation induced a vasodilatation, as shown by a decrease in perfusion pressure(-43 +/- 12 mm Hg); simultaneously, a significant increase of the radioactivity measured in the venous blood effluent from the gracilis muscle was observed. Both these events were blocked by propranolol. In the other five dogs, chlorpheniramine was able to reduce the vasodilatation induced by the injection in the gracilis muscle of isoproterenol. Under control conditions, isoproterenol induced a fall in perfusion pressure of 44 +/- 5 mm Hg while, after chlorpheniramine, perfusion pressure decreased by only 24 +/- 4 mm Hg. The results of this study seem to confirm the possibility of a histamine mediation in isoproterenol-induced vasodilatation. However, further investigation is needed in order to identify the exact role of histamine in the geneis of this phenomenon.

Animals↗

PubMed1979

Mechanism of the cerebrocortical vasodilatation during anoxia.

The possible role of cerebrocortical ion homeostasis, NAD/NADH redox state and of cortical oxygen tension was investigated in the initiation of hypoxic cortical vasodilatation. In addition, changes in cerebrocortical extracellular concentrations of Na+, K+, and Cl- during anoxia were studied. The results were as follows. a) The cerebrocortical reflectance decrease, e.g. cerebral vasodilatation, lagged behind the cortical pO2 decrease by 1-2 sec, but preceded the decrease of arterial blood pressure and ECoG as well as the extracellular Na+, K+, Cl- increases by 20-30 sec. Since the cortical pO2 decreased first and the ion changes lagged behind the onset of vasodilatation by 20-30 sec, it is suggested that the CBF increase in hypoxia is mediated via the cortical pO2 decrease. b) A significant NAD reduction was already present after 20 sec. of nitrogen breathing. Since the ECoG and MABP decreased, and K+ activity increased much later than this, it is presumed that the NAD reduction during the first 30-40 sec of anoxia indicates an increased rate of glycolysis, but not mitochondrial hypoxia. c) In the predepolarization phase a 17% K+, 4% Na+, 5% Cl- increase is probably the result of a reduction of the extracellular spaces caused by water movement and by the migration of Na+ and Cl- from the extracellular to the intracellular space. The large K+, Na+, Cl- changes during terminal depolarization can be interpreted as a result of the failure of the membrane bound Na+ -K+ pump and of the altered ion permeability of the cell membranes.

Action Potentials↗

PubMed1977

Effects of guanethidine on histamine release during reflex vasodilatation in the dog.

1 The effects of guanethidine pretreatment on the release of [14C]-histamine during the reflex vasodilatation induced in the atropinized gracilis muscle by rapid intravenous administration of noradrenaline, were studied in dogs. 2 After guanethidine treatment the haemodynamic reflex response was completely abolished and no appreciable modification of [14C]-histamine release from the gracilis muscle following intravenous noradrenaline was observed. 3 These results suggest the hypothesis that the withdrawal of the sympathetic discharge represents the mechanism of histamine release during the reflex vasodilatation. Therefore, guanethidine would suppress both the passive and the histaminergic component of the baroreceptor reflex through the abolition of the sympathetic tone.

Animals↗

PubMed1977

[The influence of vasodilatators on intraocular pressure and blood pressure (author's transl)].

The influence of different vasodilatators on blood pressure and intraocular pressure has been tested in animal experiments. For that purpose substances with alphasympathicolytic effect (Hydergin, Trental) have been tested as well as substances which are of direct influence on the muscles. In all cases a decrease of the blood pressure was noticed. Furthermore in most of the cases an increase of the intraocular pressure could be seen. This is due to a direct dilatation of ocular vessels. The effects were short-lived and reversible. We tried to find an explanation for the variations of intraocular pressure during the decrease of blood pressure. The low transmural pressure (PTM) and the corresponding low starting point of the muscle tonus seemed to be responsible for this phenomenon. Without doubt the starting point of the blood pressure, the dose, and the cardiac ability for compensation are of great influence in the development of the curve. Only a sufficiently high blood pressure is able to dilate the ocular vessels, so that one has to draw therapeutic conclusions from the constellation blood pressure/intraocular pressure before deciding on treatment.

Animals↗

PubMed1978

Does normoxic pulmonary vasodilatation rather than hypoxic vasoconstriction account for the pulmonary pressor response to hypoxia?

A mediator of the pulmonary pressor response to hypoxia has not been found. The pressor phenomenon could be explained if the pulmonary vasodilatation present during normoxia were maintained by a vasodilator substance such as bradykinin. Ventilation of the lungs with air or oxygen causes the release of bradykinin which is rapidly inactivated in the lungs. Inhibition of the inactivating enzyme prevents the development of pulmonary hypertension in response to chronic hypoxia. Bradykinin is formed in the blood and is also present in alveolar macrophages, which arise from precursors in haematopoietic tissue. Formation of bradykinin by granulocytes is critically dependent on the local oxygen tension. The enzyme which inactivates bradykinin also converts angiotensin I to angiotensin II and thus provides a mechanism for interaction between the pulmonary and systemic vasculatures. The rate of inactivation of bradykinin may be altered by small changes in pH. It is postulated that when bradykinin production is reduced during hypoxia the higher tone of the pulmonary vascular smooth muscle, maintained by numerous constrictor stimuli, asserts itself.

Bradykinin↗

PubMed1979

SK&F 92657, a novel antihypertensive acting by precapillary vasodilatation and beta-adrenoreceptor blockade.

1. The properties of a new antihypertensive agent, SK&F 92657, DL-3-[2-(3-t-butylamino-2-hydroxypropoxy)phenyl]-6-hydrazinopyridazine, have been studied. 2. The compound caused a sustained fall in blood pressure in several species as a result of precapillary vasodilatation, particularly in the renal and coronary vasculatures. 3. The beta-adrenoreceptor-blocking actions of SK&F 92657 prevent reflex cadiac stimulation.

Adrenergic beta-Antagonists↗

PubMed1977

Autonomic neuroeffector junctions--reflex vasodilatation of the skin.

A general model of the autonomic neuroeffector junction is proposed. In this model, emphasis is placed on the muscle effector bundle with electrotonic coupling between individual cells via gap junctions (or nexuses) and en passage release of transmitter from autonomic nerve varicosities. This release results in transmission to effector cells across junctional clefts ranging from about 20 nm in the vas deferens and iris to as much as 2000 nm in some large arteries. The ultrastructural identification of different autonomic nerve types is described. Current theories on the synthesis, storage, release, and inactivation of transmitter during cholinergic, adrenergic, and purinergic transmission are summarized. Some speculations are made about the possible involvement of purinergic nerves in the innervation of vessels and mast cells in the skin, and whether this involvement results in a functional link between ATP, histamine, bradykinin, and prostaglandin in cutaneous vasodilatation. Another possibility considered as the basis for this reflex is the release of substance P from sensory (pain) nerve collaterals in the skin.

Acetylcholinesterase↗

PubMed1978

Guanethidine-induced vasodilatation in the rabbit, mediated by endogenous histamine.

1 The effects of guanethidine (0.5-4 mg/kg i.v.) on arterial pressure, hindlimb blood flow and hindlimb vascular resistance (HVR) were studied in unanesthetized rabbits subjected to "total" autonomic block. 2 Evidence that this response was mediated by histamine release was that (a) 3H-labelled histamine levels in the hindlimb venous blood rose substantially after guanethidine; (b) infusion of exogenous histamine caused an inhibition of the guanethidine-induced vasodilatation; and (c) competitive antagonism of the response was obtained with the H2-antagonist burimamide. 3 There was good correlation between the [3H]-histamine ;elease and the time course of the vasodilator response. Glyceryl trinitrate infusions that lowered HVR substantially, did not cause release of histamine. 4 Reserpine, desipramine and indomethacin pretreatment did not alter the vasodilator response to guanethidine. 5 The guanethidine vasodilator response was not influenced by the H1-antagonist mepyramine or by the other H2-antagonists, metiamide or cimetidine. The vascular receptors stimulated by endogenous histamine may be distinctive from those stimulated by exogenous histamine, or the action of guanethidine may involve greater production of histamine at an intracellular site that is more readily reached by burimamide than by the other H2-antagonists.

Animals↗

PubMed1978

Vasodilatation and modulation of vasoconstriction in canine subcutaneous adipose tissue caused by activation of beta-adrenoceptors.

The present experiments were undertaken to study the balance between vascular alpha- and beta-adrenoceptors in canine subcutaneous adipose tissue during sympathetic nerve stimulation and noradrenaline injections. Propranolol potentiated and prolonged the vasoconstrictor response to close i.a. injections of noradrenaline. The vasoconstriction induced by brief nerve stimulation (0.5 to 8 Hz) was, however, unaltered by the beta-adrenoceptor blockade. During prolonged nerve stimulation the vasoconstrictor response was well maintained at 1.5 Hz but at 4 Hz there was a gradual escape. The escape phenomenon at 4 Hz was diminished by propranolol. The beta1-selective antagonist practolol, like propranolol, potentiated and prolonged the vasoconstriction induced by noradrenaline injections and reduced the vasoconstrictor escape during prolonged nerve stimulation at 4 Hz. Furthermore, the vasodilatation induced by noradrenaline injection or nerve stimulation during alpha-adrenoceptor blockade was diminished by practolol. Practolol also blocked the lipolytic response to noradrenaline and nerve stimulation. The beta2-selective antagonist H35/25 blocked the effects of the beta2-selective agonist salbutamol but failed to alter noradrenaline as well as nerve stimulation induced vascular and lipolytic beta-adrenoceptor responses. The present results provide further support for the hypothesis that vascular beta-adrenoceptors in adipose tissue are humoral (noninnervated), preferentially activated by circulating noradrenaline. Moreover, both vascular and lipolytic beta-adrenoceptors activated by noradrenaline in adipose tissue are best classified as beta1-adrenoceptors.

Adipose Tissue↗

PubMed1979

The effect of vasodilatation and sympathetic nerve activation on net water absorption in the cat's small intestine.

The rate of net water uptake from the feline small intestine has been investigated during control conditions, during graded infusions of the vasodilator drug isopropylnoradrenaline, and during electrical stimulation of the regional sympathetic nerve fibres to the gut. Net water absorption rate was largely unaffected by intestinal vasodilatation. The fraction of the absorbate transported via the lymphatics remained also constrant at 20-40% of the total absorption regardless of blood flow rate. Stimulating the sympathetic nerve fibres to the small intestine increased, however, net water absorption rate. The increase was particularly pronounced when blood pressure was kept constant during the period of stimulation. The absorption rate was on an average almost doubled at a stimulation frequency of 8 Hz during constant pressure conditions. The mechanism(s) explaining this nervous control of water absorption are tentatively discussed.

Adrenergic Fibers↗