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Biomedical subjects

C Su

Publications and source records attributed to C Su.

At least 163 records · Page 9Linked to original sources
PubMed1981

Potentiating effects of 5-hydroxytryptamine and histamine on nerve stimulation-induced contractions of the rabbit mesenteric artery.

Contractions of the rabbit mesenteric artery induced by transmural adrenergic nerve stimulation at a frequency of 8 Hz were augmented by 5-hydroxytryptamine (5-HT), quipazine, methysergide, tolazoline, histamine, angiotensin II and 4-aminopyridine. The potentiating effect of 5-HT was partly reduced by cyproheptadine and by prolonged treatment with methysergide. After treatment with a histamine H1-antagonist, chlorpheniramine, histamine failed to augment but contrarily inhibited the response. This inhibition was reversed after subsequent administration of an H2-antagonist, metiamide. These results indicate that H1- and H2-receptors mediate the potentiation and inhibition, respectively, and that the effect medicated by H1-receptors normally predominates. It seems unlikely that the potentiation by these agents is due to prevention of norepinephrine metabolism, augmentation of norepinephrine release or prostaglandin formation. It is suggested that 5-HT and histamine act on postjunctional 5-HT and histamine receptors, respectively, to modulate the transmitter effect and that norepinephrine, methysergide and tolazoline may also act through the 5-HT receptors.

4-Aminopyridine↗
PubMed1980

Diminished purinergic modulation of the vascular adrenergic neurotransmission in spontaneously hypertensive rats.

The inhibitory effects of adenosine and ATP on the pressor response of the perfused mesenteric vascular bed to perivascular adrenergic nerve stimulation were compared between spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKR). Both adenosine and ATP inhibited the neurogenic vasoconstriction in a dose-dependent manner in WKR, in which the inhibitory effect of adenosine was approximately eight times greater than that of ATP on the basis of 50% inhibitory doses (ID50). In the same preparation isolated from SHR, the inhibitory effects of both adenosine and ATP were significatly smaller than that in WKR. The ID50 values in the SHR for both agonists were approximately six times those found in WKR. These compounds also inhibited the pressor response to norepinephrine (0.3 microgram/ml) infusion, but the degrees of inhibition were markedly less than those with the neurogenic pressor response, and were not significantly different between WKR and SHR. These results suggest that presynaptic inhibition of vascular adrenergic neurotransmission by purine compounds is reduced in SHR.

Adenosine↗
PubMed1980

Potentiative effects of alpha agonistic sympathomimetic amines on vasoconstriction by adrenergic nerve stimulation.

The effects of catecholamines and other sympathomimetic amines with alpha adrenergic activity on vasoconstriction were studied. Short ring segments were prepared from five rabbit blood vessels including the mesoduodenal, brachial, central ear and pulmonary lobar arteries and the saphenous vein. Constriction was elicited by electrical field stimulation of adrenergic neurons. This response was markedly potentiated in the mesenteric preparation by low concentrations of norepinephrine, epinephrine, phenylephrine, methoxamine, naphazoline and oxymetazoline. The potentiation occurred with amine concentrations not sufficient to elevate the spontaneous transmitter release or basal smooth muscle tone. Propranolol, cocaine and metanephrine did not prevent the potentiation. Isoproterenol and dopamine potentiated the response only in high concentrations and tyrosine was without an effect. An unidentified extraneuronal action was probably responsible for the potentiation. The mesenteric artery was unique for its marked potentiation as the brachial artery was potentiated only slightly and the other three vessels were inhibited by the alpha adrenergic agents in the constrictor response to stimulation.

Adrenergic alpha-Agonists↗
PubMed1980

Purine release from vascular adrenergic nerves by high potassium and a calcium ionophore, A-23187.

The effect of high KCl and a Ca++-ionophore, A-23187, on 3H-purine efflux from [3H]adenosine-labeled pulmonary artery and thoracic aortic media of the rabbit was assessed. High KCl (30, 50 and 70 mM) and A-23187 (5 microM) markedly enhanced the efflux from the adrenergically innervated pulmonary artery. The KCl-induced increase of 3H-efflux was greatly diminished by removal of Ca++ from the medium and pretreatment with 6-hydroxydopamine (30 micrograms/ml) and cold storage (4 days), but not by treatment with reserpine and phentolamine. In contrast, the 3H-efflux induced by l-epinephrine was not affected by cold storage or 6-hydroxydopamine but was inhibited by phentolamine. 3H-purine efflux by A-23187 was also significantly reduced by Ca++ removal or cold storage. In the nerve-free aortic medial preparation, the efflux inducing effects of both KCl and A-23187 were very limited. The remaining effect of KCl in this tissue was not Ca++-dependent. From these results the efflux of 3H-purines induced by the high KCl or Ca++-ionophore appears to originate mainly from the amine-containing vesicles in adrenergic nerve terminals, probably through the Ca++-dependent exocytosis. This supports the view that the release of ATP and norepinephrine are coupled in adrenergic neurotransmission.

Adrenergic Fibers↗
PubMed1978

Modes of vasoconstrictor and vasodilator neurotransmission.

Vasoconstrictor and vasodilator neuroeffector transmission occurs in a variety of modes. Models are presented depicting vascular segments under the direct control of a single or multiple innervation, or an indirect influence via secondary release of a vasoactive substance. The neuroeffector relationship in the rabbit portal vein is described to illustrate the coexistence of several modes of transmission. ATP or its congener is released from the nonadrenergic vasodilator nerves in this vein, possibly as the transmitter. Further, a similar substance is released from the adrenergic vasoconstrictor nerves. It possibly acts directly on smooth muscle cells to relax them, and on the nerve terminals to inhibit the adrenergic transmitter release. Evidence suggests that such purine-mediated feedback mechanism may also occur at many other adrenergic and nonadrenergic neuroeffector synapses.

Adenosine Triphosphate↗
PubMed1978

Neurogenic vasodilation of cat cerebral arteries.

Transmural nerve stimulation (TNS) with 0.3-msec pulses between 1 and 25 Hz dilated cat cerebral artery segments in the presence of active muscle tone. Maximum vasodilatation occurred at 8 Hz. The dilator response to exogenous acetylcholine, but not to TNS, was abolished by atropine. Neither physostigmine nor hemicholinium affected the dilator response to TNS, which persisted after administration of guanethidine, phenoxybenzamine, propranolol, reserpine, and chronic sympathectomy. However, it was abolished by tetrodotoxin and cold storage. When examined histochemically, cat and rabbit cerebral arteries exhibited a rich plexiform distribution of acetylcholinesterase which was not affected appreciably by sympathetic denervation. These results suggest that vasodilation is not mediated through modification of sympathetic activity. They also indicate the existence of a nonadrenergic, possibly noncholinergic, vasodilator innervation in cat cerebral arteries. Preliminary studies suggest that the transmitter is not histamine, ATP, prostaglandins, gamma-aminobutyric acid, dopamine, or serotonin. The cat cerebral artery segments contrast with the isolated rabbit cerebral arteries which predominantly constrict in response to TNS and show a small dilator response.

Acetylcholinesterase↗
PubMed1978

Purinergic inhibition of adrenergic transmission in rabbit blood vessels.

The effect of ATP and its congeners on the adrenergic neuroeffector transmission was evaluated in isolated blood vessels of the rabbit. ATP, ADP, AMP and adenosine inhibited the contractile response of the portal vein to adrenergic nerve stimulation, with a threshold concentration of the order of 0.1 muM and ED50 of about 1 microM. These agents, but not papaverine, inhibited the nerve stimulation-induced response in preference to the norepinephrine- or serotonin-induced response in the portal and saphenous veins and pulmonary and ear arteries. In the portal vein labeled with [3H]norepinephrine, ATP diminished the nerve stimulation-induced efflux of tritiated material. This nucleotide also reduced the KCl-induced tritium efflux but not the tyramine induced-efflux in the [3H]norepinephrine-labeled thoracic aorta. ATP had no significant effect on the uptake of [3H]norepinephrine in the portal vein, ear artery and thoracic aorta. Indomethacin and theophylline partially blocked the inhibitory action of ATP on the neurogenic constrictor response in some of the ear artery and saphenous vein preparations. Desipramine, atropine, propanolol, haloperidol and 2,2'-pyridylisatogen, a blocking agent against ATP in the taenia coli, were without such antagonistic effect. The results are consistent with a proposed negative feedback modulator role of ATP or a related purine compound in adrenergic transmission.

Adenine Nucleotides↗
PubMed1978

Effects of adenosine triphosphate and prostaglandins on vascular adrenergic transmission.

The effects of prostaglandins (PGs) on the adrenergic neuroeffector transmission and their relationship to the action of ATP were investigated. This was in view of the putative negative feedback mediated by ATP or a related purine compound, and the reported stimulation of PG synthesis by adenine nucleotides. The central ear artery and saphenous vein of the rabbit were isolated and their contractile responses to adrenergic nerve stimulation monitored. These responses were markedly reduced by PGE1 and PGE2 and significantly augmented by indomethacin and aspirin, suggesting the occurrence of the PGE-mediated negative feedback. PGF2a facilitated the response of the vein but was without affect on the artery, while arachidonic acid was facilitatory on the former and inhibitory on the latter. Possibly a PGF2a-like substance is formed in the presence of arachidonic acid and, in the vein, masks the effect of any PGE. ATP depressed the arterial and venous contractile response to adrenergic nerve stimulation. This inhibition was not significantly affected by indomethacin or aspirin. It was enhanced in the artery and diminished in the vein by arachidonic acid, but only to the extent of algebraic sum of the effects of ATP and the acid. It seems possible that the purine- and PGE-mediated feedback mechanisms are independent and parallel pathways.

Adenosine Triphosphate↗
PubMed1977

Development of neuroeffector mechanisms in the carotid artery of the fetal lamb.

A survey has been made of mechanisms associated with vascular adrenergic neuroeffector transmission in the lamb fetuses between 53 days and term gestation. The common carotid artery was isolated for studies of enzymic activities, uptake of norepinephrine (NE) and reactivity to vasoactive agents. The extra-neuronal NE uptake, monoamine oxidase and catechol-O-methyltransferase activities were present in the carotid artery of the youngest fetuses. The contractile responses to NE and serotonin and neuronal NE uptake preceded the response to adrenergic nerve stimulation during fetal growth. These results suggest that the mechanisms for adrenergic transmitter inactivation, transmitter action on vascular smooth muscle cells, and neuronal transmitter delivery develop in that sequence.

Animals↗
PubMed1977

Uptake of 3H-norepinephrine in rabbit mesenteric blood vessels.

The uptake of traited norepinephrine in isolated rabbit mesoduodenal blood vessels was measured. Neuronal uptake was estimated utilizing the inhibitory effect of cocaine, and expressed on the basis of wet and dry tissue weights as well as circumferential area of the vascular wall. This area was presumed to approximate the area of the adrenergic nerve terminal plexus. The wet weight of smaller tissues was apt to be underestimated due to excessive drying during weighing; dry weight was more consistent over a wide range of tissue size. Either on the basis of weight or circumferential are, neuronal uptake in arteries increased as the diameter diminished, but uptake was practically constant in all segments of the veins. Arterial uptake per unit circumferential area was greater than in the accompanying veins, but this was not necessarily the case when uptake was expressed per unit weight. Neuronal norepinephrine may be a useful index of adrenergic nerve density. On this basis it is suggested that the adrenergic neural vasoconstriction increases with decrease in diameter of both arteries and veins in rabbit mesoduodenum.

Adrenergic Fibers↗
PubMed1976

Changes in the contractile response of arteires and veins from hypertensive rabbits to sympathetic nerve activity: assessment of some postsynaptic influences.

Contractile responses to field stimulation of intramural nerves of arteries and veins taken from rabbits made hypertensive by partial constriction of the abdominal aorta have been related to the carotid artery pressure. The increase in contraction of cephalic and short saphenous veins with rise in carotid artery pressure can be accounted for by an increase in sensitivity of the alpha-adrenergic receptor. The neurogenic contraction of the ear artery increased with carotid artery pressure rise. Changes in some of the extraneuronal factors that influence transmitter distribution and disposition in the tunica media were examined. In hypertensive animals, the percentage of released adrenergic transmitter entering the vessel wall might be expected to decrease due to an increase in medial thickness. However, this percentage was not significantly altered in the ear artery probably due, in part, to a concomitant increase in medial permeability to the transmitter. Extraneuronal transmitter disposition factors, i.e. extraneuronal uptake, monoamine oxidase, and catechol-O-methyltransferase activity are directly related to the wet weight of the vessel wall. Thus, their contribution to transmitter disposition would be expected to increase with increase in vessel wall thickness and tend to reduce the response to sympathetic activity. As the contractile response increased in the hypertensive vessels despite such changes, the increase in effector cell mass and density of neuronal terminal plexus, shown previously to increase with hypertension, are more important than these other considerations.

Animals↗
PubMed1976

Neurogenic sympathetic vasoconstriction of the rabbit basilar artery.

When examined by fluorescence microscopy the rabbit basilar artery contains a rich adrenergic-like plexus at the adventitiomedial junction. The fluorescence disappears upon chronic reserpinization and bilateral superior cervical ganglionectomy. Transmural stimulation of intramural nerves a results in a response which is predominantly constrictor but also contains a small, inconstant dilator component. The constrictor response is abolished by chronic reserpinization, bilateral superior cervical ganglionectomy, and cold storage of the preparation. The constriction is prevented by the adrenergic neuron blocking agents guanethidine and bretylium but not by such alpha-adrenergic receptor blocking agents as phenoxybenzamine (PBZ), phentolamine, and tolazoline. Our results show that doses of the three latter agents sufficient to abolish contractions to norepinephrine (NE) in concentrations of up to 10(-2) M only potentiate and prolong the contractile response to nerve stimulation. The beta-adrenergic receptor blocking agent, propranolol, and inhibitors of NE neuronal uptake, such as desipramine (desmethylimipramine, DMI) and cocaine, do not influence the size of the neurogenic response. These results suggest that the vasoconstrictor component of the rabbit basilar artery response to transmural nerve stimulation (TNS) is mediated via sympathetic adrenergic-like neurons, but at the same time also raise the question whether the transmission process is typical of classic adrenergic neuroeffector mechanisms.

Animals↗