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PubMed1992

Intestinal lymphatic vessels release endothelial-dependent vasodilators.

This study evaluated the possibility that the endothelial cells of microscopic lymphatic vessels can release vasoactive agents which affect the lymphatic vessels and nearby arterioles. Microinotophoresis of acetylcholine (ACh) or bradykinin (BK) onto the wall of quiescent submucosal lymphatic vessels in the rat small intestine had no discernible effects on their diameters but caused spontaneously active mesenteric lymphatic vessels to constrict. Application of ACh or BK to the arteriolar wall caused significant vasodilation. Release of either drug onto the wall of a nearby lymphatic produced arteriolar dilation that was approximately 80% of that observed with direct application to the arteriolar wall; drug application into parenchymal tissue produced a dilation less than 25% of that observed during application to the lymphatic. NG-monomethyl-L-arginine application to the lymphatic blocked all ACh-induced lymphatic-mediated responses but had no effect on the response to direct ACh application to the arteriolar wall or any of the responses to BK application. These results are consistent with the hypothesis that lymphatic endothelial cells are capable of releasing agents that dilate nearby arterioles and cause spontaneously active lymphatic vessels to constrict.

Acetylcholine↗
PubMed1992

Microvascular circulation of the small intestine in horses.

The microvascular anatomic features of the small intestine was described by correlating results of microangiography, light microscopy, gross studies, and scanning electron microscopy of vascular replicas in 14 horses. After heparinization, the horses were euthanatized, a length of jejunum was transected, and blood was flushed free of the circulation, using isotonic NaCl solution. In six horses, the circulatory system was perfused with a modified radiopaque medium and evaluated radiographically. These sections were then evaluated by standard histologic methods. Sections from 8 horses were perfused with 1 of 2 types of plastics and studied grossly or by scanning electron microscopy. The marginal arterial arcade gives rise to vessels that enter the jejunum at the mesenteric angle. These vessels penetrated either directly, by branching and entering on both sides of the mesenteric angle, or supplying only 1 side of the mesenteric angle. All these vessels continued in the submucosa branching extensively, forming a submucosal plexus. This submucosal plexus supplied the tunica muscularis, tunica serosa, and the mucosa. Vessels within the 2 muscle layers ran parallel to the muscle fibers and, consequently, perpendicular to each other. The arterial supply to the mucosa penetrated the muscularis mucosae and branched to supply 2 mucosal capillary networks. An eccentrically placed arteriole penetrated the base of the villus and spiralled to the tip where it "fountained" into a mesh-like capillary network, which descended peripherally in the villus to drain via 1 to 3, but most commonly 2 venules. Venules from adjacent villi united and drained via the submucosal veins.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1981

Evidence that the increased calcium sensitivity of resistance vessels in spontaneously hypertensive rats is an intrinsic defect of their vascular smooth muscle.

We have investigated media thickness and noradrenaline- and calcium-sensitivity of isolated mesenteric resistance vessels from spontaneously hypertensive (SHR) and control Wistar-Kyoto (WKY) rats, which had been treated in various ways. Vessels from untreated SHRs had an increased media thickness and increased noradrenaline- and calcium-sensitivity. Anti-hypertensive treatment of SHRs and WKYs with Felodipine reduced blood pressure, eliminated the difference in vessel media thickness, but did not reduce vessel noradrenaline- or calcium-sensitivity. Chemical sympathectomy of SHRs and WKYs at birth likewise resulted in reduced blood pressure, but did not eliminate the difference in vessel media thickness although again vessel noradrenaline- and calcium-sensitivity remained unchanged. Induction of renal hypertension in WKYs caused an increase in blood pressure and increase in vessel media thickness, but did not affect vessel noradrenaline-sensitivity. The results suggest that while vessel media thickness is influenced by blood pressure, the sensitivity differences of SHR resistance vessels are an intrinsic defect of their vascular smooth muscle, independent both of blood pressure and neurogenic influences.

Animals↗
PubMed1993

Does isoflurane alter mesenteric venous capacitance in the intact rabbit?

Volatile anesthetics act at a number of sites to alter cardiovascular function and the response of the cardiovascular system to barostatic reflexes. We examined the effects of isoflurane on reflex regulation of mesenteric venous capacitance vessels. To determine whether isoflurane alters mesenteric venous capacitance, continuous direct observations of mesenteric vein diameter, intravenous pressure, and mesenteric sympathetic efferent nerve activity (SENA) were made in 31 chloralose-anesthetized New Zealand white rabbits. Simultaneous measurements were obtained for aortic pressure and heart rate. The responses to changes in baroreceptor activation by means of either bilateral carotid occlusion (BCO) or aortic nerve stimulation (ANS) were studied in one group of 18 rabbits, while the response to direct electric activation by means of celiac ganglion stimulation (CGS) was studied in another group of 13 rabbits. In both groups, isoflurane vapor was administered at levels of 0.75% or 1.5%, and superfused isoflurane was administered directly to the vessel in doses of either 3% or 5% equilibrated with physiologic salt solution. Anesthetic levels were verified by mass spectrometry for expired gas and by gas chromatography for blood and superfusate levels. Inhaled isoflurane reduced hemodynamic variables and SENA in a dose-dependent fashion, but these same variables were unaffected by superfused isoflurane. One and one-half percent inhaled isoflurane abolished all reflex responses to baroreceptor stimulation in mesenteric capacitance veins and in SENA, but superfused isoflurane produced no corresponding attenuation of reflex responses to baroreceptor stimulation. Neither inhaled nor superfused isoflurane suppressed the reflex venoconstriction in response to CGS. Both inhaled and superfused isoflurane dilated the baseline vein diameter before stimulation. These results indicate that isoflurane dose increase the diameter of mesenteric venous capacitance vessels and inhibits reflex-induced constriction of mesenteric veins, whereas mesenteric sympathetic efferent nerve activity decreases and the reflex responses to activation of the carotid sinus and aortic baroreceptors are attenuated by inhaled isoflurane. The mechanism of this action appears to be primarily through the inhibition of central or peripheral sympathetic ganglionic transmission of barostatic control.

Animals↗
PubMed1995

Visualization of endothelial clefts and nuclei in living microvessels with combined reflectance and fluorescence confocal microscopy.

OBJECTIVE: The cellular basis for spatial heterogeneity along postcapillary venules in their response to inflammatory mediators is not understood. To study permeability regulatory processes on an individual cell basis in intact microvessels, we developed methods to delineate individual endothelial cells within living, single perfused microvessels. METHODS: Individual postcapillary microvessels in the mesenteries of frogs and hamsters were perfused with chloride-free Ringer's solutions containing AgNO3 (0.1 g per 100 ml) for 5--10 s. Vessels were immediately flushed with Ringer's solution containing serum albumin and some vessels subsequently perfused with the fluorescent nucleic acid stain YO-PRO-1 (1 microM) for 10-15 min. Vessels were imaged in situ using laser scanning confocal microscopy. A reflectance image from silver precipitate in the endothelial clefts and a fluorescence image of the nuclei were simultaneously recorded. Stacks of confocal images were merged and used to reconstruct the three-dimensional orientation of endothelial cells. Hydraulic conductivity of some frog mesenteric venular vessels, measured before and after perfusion with AgNO3, was used to assess the integrity of the vessels. RESULTS: The endothelial cell clefts were delineated with a very fine, readily imaged precipitate of silver. Hydraulic conductivity measured after AgNO3 perfusion in frog mesenteric venular microvessels was not significantly different from control. Vessels showed a slight reduction in reactivity to inflammatory stimuli. The three-dimensional pattern of endothelial cells in the living vessels was imaged. CONCLUSIONS: Combining confocal microscopy with silver staining in single perfused microvessels was shown to be an effective means to delineate the three-dimensional pattern of endothelial cells forming microvessel walls. It enables further study of the vascular structure and function relationships at the individual cell level in intact microvessels.

Animals↗
PubMed2003

Vasoactive effects of neurokinin B on human blood vessels.

OBJECTIVES: Preeclampsia (PE) is a multisystem disease unique to human pregnancy. Abnormal placentation results in placental hypoperfusion leading to the secretion of a factor(s) by the placenta. Our aim was to investigate whether neurokinin B (NKB) is the circulating factor associated with PE. STUDY DESIGN: Vascular effects of NKB were assessed in blood vessels dissected from myometrial and omental biopsy specimens obtained at caesarean section from normal pregnant women (n = 26) or in mesenteric blood vessels obtained from nonpregnant female Wistar rats (n = 4). RESULTS: Incubation with NKB did not alter endothelial-dependent relaxation of omental or myometrial arteries. NKB produced a dose-dependent relaxation in preconstricted omental arteries and veins. NKB did not affect vasoactive responsiveness of rat mesenteric arteries. CONCLUSION: We conclude from these observations that NKB is not the circulating factor associated with increased vascular resistance in PE.

Animals↗
PubMed1988

Effect of pinacidil on norepinephrine- and potassium-induced contractions and membrane potential in rat and human resistance vessels and in rat aorta.

The effect of pinacidil on contractile responses to norepinephrine, potassium, and membrane potential was examined in rat and human resistance vessels. In some experiments rat aorta was also used. Pinacidil (0.1-30 microM) caused a concentration-dependent relaxation of norepinephrine-induced contractions in all vessels studied. In the same concentration range, pinacidil had only little effect on potassium (125 mM) activated rat mesenteric and femoral resistance vessels. In denervated rat mesenteric resistance vessels, a depolarization with potassium (125 mM) before superimposing a norepinephrine tone markedly diminished the effect of pinacidil. In resting rat mesenteric resistance vessels, pinacidil (1-10 microM) caused a hyperpolarization of 10-15 mV. In rat aorta, pinacidil (10 microM) caused a significant (p less than 0.001) increase in 86Rb+ efflux rate constant whereas 1 microM had no effect. The results of these experiments indicate that the vasodilating effect may be caused by a hyperpolarization of the vascular smooth muscle cell membrane.

Aged↗
PubMed1985

Effect of ouabain on tone, membrane potential and sodium efflux compared with [3H]ouabain binding in rat resistance vessels.

To investigate the mechanism by which ouabain causes acute increase in peripheral resistance, the effect of ouabain on vessel tone, 22Na efflux and membrane potential has been compared with the binding of [3H]ouabain in rat isolated mesenteric resistance vessels (lumen diameter approximately 200 microns). Ouabain at concentrations between 1 X 10(-8) and 1 X 10(-3) M had no effect on the tone of resting vessels but caused potentiation of the tone of vessels which were submaximally contracted with noradrenaline. In the entire concentration range, these acute potentiating effects of ouabain on vessel tone correlated well with an acute inhibitory effect on 22Na efflux and with acute [3H]ouabain binding, consistent with the vasoconstrictor effect of ouabain being associated with inhibition of the Na-K pump. At all concentrations, in both resting and activated vessels, ouabain exposure caused an acute concentration-dependent depolarization of the membrane. At low ouabain concentrations (1 X 10(-6) and 1 X 10(-5) M) the potentiating effect on vessel tone and the inhibitory effect on 22Na efflux were transient, so that after 10 min no effect of ouabain was seen. This was consistent with these ouabain concentrations failing to cause a measurable increase in the intracellular Na concentration ([Na]i) after longer term (up to 2 h) exposure. The recovery of 22Na efflux was due to a recovery of the ouabain-sensitive part of the 22Na efflux, suggesting that the transitory nature of these effects is due to stimulation of uninhibited Na-K pumps. The transient effects of low ouabain concentrations contrasted with binding experiments where, with 1 X 10(-6) M-ouabain, the binding first peaked after 30 min with only a small decline thereafter. With higher concentrations of ouabain (1 X 10(-4) and 1 X 10(-3) M), the potentiating effect was also transitory, but 22Na efflux was permanently inhibited and the [Na]i rose. The possibility of there being two populations of ouabain binding sites having different affinities, was supported by the observation of shoulders in the ouabain concentration-effect characteristics obtained with respect to the mechanical potentiation of noradrenaline responses, the 22Na efflux and the acute ouabain binding. In all cases a shoulder was seen between 1 X 10(-6) and 1 X 10(-5) M-ouabain. The results are consistent with the vasoconstrictor effect of ouabain being due to depolarization of the membrane as a consequence of inhibition of the Na-K pump.

Animals↗
PubMed2002

Endothelin receptor function in mesenteric veins from deoxycorticosterone acetate salt-hypertensive rats.

OBJECTIVES: To identify the receptors by which endothelin-1 (ET-1) increases venomotor tone in hypertension. METHODS: Vascular reactivity to ET-1 and the selective endothelin receptor subtype B (ET(B)) agonist, sarafotoxin 6c (S6c), was studied in mesenteric blood vessels from deoxycorticosterone acetate (DOCA-salt) hypertensive and normotensive control rats. The diameter of small (< or = 280 microm) mesenteric arteries and veins was monitored in vitro using computer-assisted video microscopy. Contractions of mesenteric arteries (< or= 250 microm diameter) were also studied, using a myograph. ET-1 mRNA levels were measured in mesenteric arteries and veins using real-time RT-PCR techniques. RESULTS: ET-1-induced contractions were reduced in arteries of DOCA-salt hypertensive rats compared with those of normotensive control rats; S6c produced negligible contractions in arteries from both groups. ET-1 concentration-responses curves in arteries measured using video microscopy or a myograph were similar. ET-1 and S6c caused veins to contract, and there were no differences between responses to these agonists in tissues from DOCA-salt hypertensive rats or normotensive control rats. Studies using ET(A) and ET(B) receptor antagonists indicated that ET-1-induced venoconstriction was mediated by ET(A) receptors. Potassium chloride concentration-response curves were similar in arteries and veins from normotensive control rats and DOCA-salt hypertensive rats. ET-1 mRNA levels in DOCA-salt hypertensive rat arteries or veins were not different from those in normotensive control rat arteries and veins. CONCLUSIONS: These data indicate that ET-1 reactivity is maintained in mesenteric veins, but not arteries, in DOCA-salt hypertension. Therefore, the sustained increase in venomotor tone mediated by ET(A) receptors that is known to occur in vivo in DOCA-salt hypertensive rats is not caused by direct venoconstriction.

Animals↗
PubMed2005

Impact of nitric oxide synthase inhibitor and chloride channel antagonist on mesenteric vascular conductance in anesthetized Dahl normotensive and hypertensive rats.

The effects of nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) and chloride channel antagonist niflumic acid on vascular responsiveness to the effect of alpha1-adrenoceptor stimulation in the mesenteric bed of Dahl salt-resistant normotensive (SRN) and salt-sensitive hypertensive (SSH) rats were examined. Dahl salt-resistant and salt-sensitive rats were fed a high-salt diet (4% NaCl) for 7 weeks, and blood pressure, heart rate, and mesenteric blood flow were measured before and after treatment with L-NAME (0.3 mg/kg, IV) and/or niflumic acid (10 mg/kg, IV). Morphometry of the primary mesenteric blood vessel was also assessed. Administration of alpha1-adrenoceptor agonist cirazoline produced a dose-dependent increase in blood pressure, decrease in heart rate, mesenteric blood flow, and mesenteric vascular conductance in SRN and SSH rats. L-NAME significantly increased basal blood pressure and decreased basal mesenteric blood flow and vascular conductance in SRN but not in SSH rats. Niflumic acid attenuation of cirazoline-mediated decreases in mesenteric blood flow and vascular conductance was more pronounced in the SRN than SSH rats. This difference in the inhibitory actions of niflumic acid was absent following its concomitant administration with L-NAME. It seems that tonic release of nitric oxide modulates niflumic acid-sensitive chloride channels in vascular muscle. Blood vessels from SSH rats had significantly larger smooth muscle thickness and lumen diameter, but the ratio of the 2 were not different between the SRN and SSH. Our findings support the view that alterations in receptor-mediated signal transduction, rather than just changes in blood vessel architecture, are responsible for differences in behavior of blood vessels in salt-induced hypertensive rats.

Animals↗
PubMed1996

Endothelium-dependent modulation of pacemaking in lymphatic vessels of the guinea-pig mesentery.

1. Endothelial control of the rate of constrictions and the underlying pacemaker potentials has been studied in vitro in guinea-pig mesenteric lymphatic vessels. 2. ACh stimulated 60% of intraluminally perfused vessels to slow or abolish lymphatic constrictions. This action was inhibited by atropine and was likely to be due to the release of endothelium-derived nitric oxide (EDNO) as the effect was absent after endothelial lysis, mimicked by sodium nitroprusside (SNP), blocked by N omega-nitro L-arginine (NOLA) and partially inhibited by Methylene Blue (MB). 3. The remaining 40% of perfused vessels did not mechanically respond to ACh or SNP. In four of seven such vessels this appeared to be due to excessive perfusion-associated release of EDNO, as incubation with NOLA restored the response to SNP. 4. Application of NOLA or MB in perfused vessels significantly increased constriction frequency, further indicating perfusion-associated release of EDNO. 5. ACh induced a marked increase in endothelial [Ca2+]i of both mechanically responding and non-responding vessels. This ACh-induced increase could be repetitively induced when Ca2+ was present in the perfusate, but rapidly ran down when a Ca(2+)-free EGTA perfusate was used. 6. Intracellular recordings from the smooth muscle of non-perfused vessel segments demonstrated an ACh-induced hyperpolarization and decrease in membrane resistance, changes which were prevented by atropine, NOLA, MB and endothelial lysis and mimicked by SNP. 7. ACh directly reduced the size of the underlying pacemaker potentials termed spontaneous transient depolarizations (STDs). 8. NOLA and MB enhanced STDs in non-perfused vessel segments indicating an endogenous release of EDNO. 9. It is concluded that the lymphatic endothelium produces and releases EDNO endogenously, during perfusion or after stimulation with ACh, to decrease the efficacy of STDs to generate action potentials and resultant constrictions.

Acetylcholine↗
PubMed1992

[Biological cycle of Paralibyostrongylus hebrenicutus (Nematoda: Trichostrongylidae)].

Paralibyostrongylus hebrenicutus accomplishes its life cycle spontaneously in captive Atherurus africanus, its natural host, and in experimentally infected guinea pigs and rabbits. Morphogenesis and larval morphology were studied in the guinea pig and described herein. Host infection were achieved either by subcutaneous or by oral inoculation. The entsheathed infective larvae moult soon after penetration in the vertebrate host. Following subcutaneous inoculation, they reach the lungs very probably through the lymphatic vessels and the right heart at H8, and the stomach as soon as D2. However, a possible direct migration by the mesenteric lymphatic vessels and crossing of the digestive wall cannot be excluded as a few larvae were found in the peristomachal mesentery. Following ingestion, L3 larvae reached the stomach directly. 24 hours post-ingestion, they were localized deep inside the gastric mucosa crypts lumen. The same larval localization was observed at D3 after a subcutaneous inoculation. At D5, regardless of the inoculation route, larvae reached their definitive position, embedded in the gastric mucosa mucus lining, where they underwent the 3rd moulting (L3-L4) followed by the 4th moulting (L4-Ad) at D19. Eggs appeared at D28. Except for the inflammatory granuloma seen in the lungs and the mesentery from H24 to D3, the nematode induced no tissue lesion. The genus Paralibyostrongylus is one of the most primitive in the Libyostrongylinae-Cooperiinae line. The double transmission route, may have made possible the transition from primitive cycles by cutaneous penetration to more specialized cycles by the oral route, the latter being responsible for the evolutionary success of the group in large herbivores.

Animals↗
PubMedDate not supplied

Mast cell degranulation alters lymphatic contractile activity through action of histamine.

OBJECTIVE: Mast cells reside in most tissues and in close association with blood vessels and nerves, areas where lymphatic vessels are also present. Mast cells and lymphatic vessels are two important players in the development of the inflammatory process. This study was designed to examine the effects of mast cell degranulation on the contractile activity of mesenteric lymphatic vessels. METHODS: Lymphatic vessel contractile activity was assessed in vitro by video microscopy of the mesentery of cow's milk-sensitized guinea pigs upon application of beta-lactoglobulin and compared to the response measured in sham animals. RESULTS: Application of 5-10 microM beta-lactoglobulin increased lymphatic vessel constriction frequency and decreased constriction amplitude (n = 12). This effect was not seen in sham-treated animals (n = 16) and was not due to an increased number of mast cells in the mesentery of the milk-sensitized animals, as revealed by histological examination. Two known mast cell-derived mediators, histamine and thromboxane A2, via stable mimetic U46619 also altered lymphatic pumping in a similar manner, but only pretreatment with the histamine H1 receptor antagonist pyrilamine (1 microM) could reduce the beta-lactoglobulin-induced response. The thromboxane A2 receptor antagonist, SQ 29548, and the 5-lipoxygenase inhibitor, caffeic acid, were without significant effect. CONCLUSION: In the in vitro mesenteric preparation, mast cell degranulation altered lymphatic contractile activity via the release of a mediator suggested to be histamine and the subsequent activation of H1 receptors. This action could potentially interfere with the expected ability of lymphatic vessels to reduce edema during inflammation.

Animals↗
PubMed2000

Resveratrol induces vasorelaxation of mesenteric and uterine arteries from female guinea-pigs.

Naturally occurring hydroxystilbenes have been shown to induce vasorelaxation. Here, we studied the mechanism of resveratrol-induced vasorelaxation in different types of blood vessels, namely mesenteric (resistance) and main uterine (conductance) arteries, from female guinea-pigs on day 7 and day 15 of the oestrous cycle. Resveratrol (5-70 micromol/l) induced concentration-dependent relaxation of both mesenteric and uterine arteries preconstricted with either noradrenaline (NA; 10 micromol/l) or KCl (125 mmol/l). Resveratrol was 2-fold more potent in inducing relaxation of mesenteric arteries than of uterine arteries. Its effects on uterine arteries from both day-7 and day-15 guinea-pigs were similar, irrespective of the constrictor used, but it was significantly (P<0.01) more potent in inducing relaxation of mesenteric arteries contracted with NA compared with those constricted with KCl. In day-7 arteries precontracted with NA, N(G)-nitro-L-arginine methyl ester (L-NAME; 10 micromol/l) had no effects on the time course of resveratrol-induced vasorelaxation in either mesenteric or uterine arteries. However, indomethacin (50 micromol/l) significantly (P<0.05) potentiated resveratrol's effect on mesenteric, but not uterine, arteries. Indomethacin had no effect on resveratrol-induced vasorelaxation of arteries contracted with KCl, whereas L-NAME significantly (P<0.05) reduced the effects of resveratrol on uterine, but not on mesenteric, arteries. In day-15 arteries, L-NAME significantly (P<0.01) attenuated the effects of resveratrol on mesenteric arteries contracted with NA. Indomethacin had no effect on resveratrol activity. This study indicates that: (a) the effect of resveratrol on resistance arteries is greater than that on conductance arteries; (b) the effects of resveratrol are not mediated via prostanoids, but NO may play a role; and (c) the stage of the oestrous cycle has no influence on resveratrol-induced vasorelaxation.

Acetylcholine↗
PubMed1986

Effects of calcium entry blockers on Ca2+-induced contraction of depolarized and noradrenaline-exposed rat resistance vessels.

The effects of four calcium entry blockers (CEBs), diltiazem (D), verapamil (V), nifedipine (NF) and nicardipine (NC), were investigated on Ca2+ concentration-effect curves of rat depolarized (K+, 40 mM) or noradrenaline (NA, 3 microM)-exposed mesenteric resistance vessels. Under control conditions, NA-exposed vessels were more sensitive to Ca2+ (pD2: 4.12 +/- 0.11) than depolarized vessels (pD2: 3.16 +/- 0.02, P less than 0.01) whereas the maximal active wall tensions were not significantly different (2.86 +/- 0.11 mN/mm and 2.11 +/- 0.34 mN/mm respectively). In depolarized vessels, D, V, NF and NC induced a concentration-dependent shift to the right and a depression of the maximal effect of the Ca2+ curves, which suggested a non-competitive antagonism. The IC50 (concentration of CEB producing a 50% inhibition of the maximal contractile response from control curve) values were: D: 3 X 10(-7), V: 1.3 X 10(-7), NF: 4.5 X 10(-9), NC: 3 X 10(-9) M. In NA-exposed vessels, the CEBs produced a concentration-dependent shift to the right of the Ca2+ curves before depressing their maximal effect. This suggested that the antagonism was different from that observed in depolarized arteries. In this case, the IC50 values were: D: 4.5 X 10(-7), V: 2 X 10(-7), NF: 9 X 10(-9), NC: 7 X 10(-9) M. Although the gating mechanisms activated in this study were differently affected by CEBs, since there were marked qualitative differences in their antagonistic effects on Ca2+ concentration-effect curves, depolarization and NA promoted the entry of Ca2+ into smooth muscle cells of rat resistance vessels by mechanisms with the same sensitivity to CEBs as expressed by IC50 values.

Animals↗
PubMed1988

Spontaneous and ouabain-induced efflux of catecholamines and dihydroxyphenylglycol in two canine blood vessels.

The spontaneous efflux of endogenous noradrenaline, dopamine, dihydroxyphenylglycol (DOPEG) from adrenergic nerve endings of 2 canine blood vessels (the mesenteric artery and the saphenous vein) were studied during 8 successive incubation periods of 15 min each. Extraneuronal uptake and O-methylation were minimized by the presence of adequate concentrations of tropolone and hydrocortisone. Both vessels had an efflux characterized by a decline in the 3 catechols, which was most marked for noradrenaline; the mesenteric artery lost larger amounts than the saphenous vein. Ouabain caused a large increase in the efflux of noradrenaline and dopamine and a reduction of DOPEG efflux. Cocaine had only a modest effect, more evident in the case of the mesenteric artery, increasing noradrenaline and reducing DOPEG effluxes. The combination of ouabain and cocaine had no additive effects, and the effects of ouabain were even reduced (on some parameters) by cocaine. Accordingly, the noradrenaline:DOPEG ratio was markedly increased by ouabain, but not by cocaine; cocaine significantly reduced the effects of ouabain. The ratio dopamine:noradrenaline was decreased by cocaine and by ouabain. Comparison of tissue content and efflux allowed us to conclude that apparently no significant de novo synthesis of noradrenaline occurred during the incubation period. We conclude that a fast and early component of spontaneous efflux is due to loss from the neurons and that its greater magnitude in the mesenteric artery may be due to differences in neuronal [Na+] and/or to differences in neuronal membrane adenosine triphosphatase activity. The results also suggest that neuronal reuptake plays only a minor role in the handling of spontaneously released noradrenaline.

Animals↗