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J J Reid

Publications and source records attributed to J J Reid.

At least 37 records · Page 2Linked to original sources
PubMed1995

Sexual dimorphism in copackaging of luteinizing hormone-releasing hormone and galanin into neurosecretory vesicles of hypophysiotrophic neurons: estrogen dependency.

Hypophysiotrophic neurons projecting to hypophyseal portal vessels in the median eminence of the hypothalamus maintain the operation of the master gland, the pituitary, by secreting releasing and release-inhibiting hormones into the bloodstream. LHRH, synthesized in neurons of the rat prosencephalon, is one of the key substances that governs the anterior pituitary-gonadal axis. Recently, it has been shown that the peptide galanin (GAL) is coproduced in a subpopulation of LHRH neurons and is a potent modulator of central processes regulating reproduction. A better understanding of the secretory mechanisms involved in pulsatile hormone release from LHRH axons of the median eminence requires exploration of the organelle domain that displays the cosynthesized peptides in terminal boutons. This study shows that LHRH- and GAL-immunoreactive axons overlap heavily in the lateral part of the median eminence. Double fluorescent labeling revealed colocalization of the peptides at the level of single axon terminals. By means of dual colloidal gold immunolabeling, LHRH and GAL were detected in the same secretory vesicles at the ultrastructural level. The incidence of colocalizing vesicles was high in the female (45%) and low in the male (3%) rat. Ovariectomy resulted in a dramatic decline in the number of LHRH/GAL-coexpressing vesicles (23%), which was reversed (55%) by the administration of estradiol. The observations indicate a sex-related difference in the packaging of LHRH and GAL and suggest that the events are estrogen dependent. Furthermore, the simultaneous release of GAL and LHRH from the colocalizing vesicles provides a mechanism that might ensure the potentiating effect of GAL on LHRH by synchronizing events at the receptor sites in the anterior pituitary.

Animals↗
PubMed1994

Changes in the responsiveness to endothelin-1 in isolated atria from diabetic rats.

This study investigates the influence of diabetes on the cardiac responsiveness to endothelin-1. The effects of endothelin-1 on rate and force of contraction were examined in isolated right and left atria, respectively, obtained from either streptozotocin (65 mg/kg)-treated rats (diabetic) or vehicle (0.02 M citric acid)-treated rats (control). The positive chronotropic and inotropic effects of endothelin-1 did not change in atria from diabetic rats at 2 and 4 weeks, but were reduced at 8 and 12 weeks. The positive chronotropic response to noradrenaline, but not to sympathetic nerve stimulation, was also reduced in 12-week diabetic rats. Endothelin-1 caused a decrease in the positive chronotropic and inotropic responses to sympathetic nerve stimulation and to noradrenaline; these inhibitory effects of endothelin-1 were not altered in 2-, 4-, 8- or 12-week diabetic rats. The study demonstrates that atrial responses to endothelin-1 and to noradrenaline are reduced by streptozotocin-induced diabetes, but the alteration depends on the duration of diabetes.

Animals↗
PubMed1994

Nitric oxide-mediated neurotransmission is attenuated in the anococcygeus muscle from diabetic rats.

The effect of STZ-induced diabetes of 8-weeks duration was examined on nitric oxide-mediated neurotransmission in the rat anococcygeus muscle. In the presence of noradrenergic blockade and raised tissue tone, relaxant response to nerve stimulation (0.5-5 Hz, for 10 s), sodium nitroprusside (5 and 10 nmol/l) and nitric oxide (1 and 3 mumol/l) were significantly reduced in anococcygeus muscles from diabetic rats compared to responses from control rats (p < 0.05). In contrast, relaxations to papaverine (3 and 10 mumol/l) were not reduced in tissues from diabetic rats. The nitric oxide synthesis inhibitor NOLA (100 mumol/l) abolished relaxant responses to nerve stimulation but had no effect on responses to any of the relaxant agents used. Exposure to NOLA at 10 mumol/l reduced stimulation-induced relaxations; this reduction was significantly greater in tissues from the diabetic group than from the control group (p < 0.05), probably as a consequence of the smaller relaxant responses in muscles from diabetic rats. Contractile responses to nerve stimulation (1-10 Hz, for 10 s), but not noradrenaline (0.03-30 mumol/l), were significantly greater in anococcygeus muscles from diabetic rats than from control rats (p < 0.05). NOLA (100 mumol/l) significantly enhanced stimulation-induced contractions (p < 0.05), however the enhancement was significantly less in tissues from diabetic rats (p < 0.05). The results suggest that STZ-induced diabetes impairs smooth muscle reactivity to nitric oxide in the rat anococcygeus muscle.

Animals↗
PubMed1994

Effect of aminoguanidine on the impaired nitric oxide-mediated neurotransmission in anococcygeus muscle from diabetic rats.

The contribution of advanced glycation end-product (AGE) formation to alterations in nitrergic neurotransmission caused by 8-week streptozotocin-induced diabetes has been examined in the rat anococcygeus muscle. Relaxant responses to nitrergic nerve stimulation (0.5-5 Hz, 10-sec train), to nitric oxide (NO; 0.1-3 microM), to the NO donor, sodium nitroprusside (SNP; 5-500 nM), and to the cell-permeable analogue of cyclic guanosine monophosphate (cGMP), 8-bromo-cGMP (15 and 30 microM), were significantly smaller in muscles from diabetic rats than from control rats. Pretreatment with aminoguanidine hemisulphate (1 milligram drinking water) to inhibit AGE formation, did not alter the relaxant responses to nitrergic nerve stimulation, NO or SNP in tissues from control rats, or responses to NO or SNP in tissues from diabetic rats, however relaxations to nitrergic nerve stimulation were further reduced in tissues from diabetic rats. In anococcygeus muscles from untreated animals, a 20-min exposure to aminoguanidine (1 mM) in vitro had no effect on relaxations to nitrergic nerve stimulation. The results suggest that diabetes impairs nitrergic transmission in the rat anococcygeus at least partly through alterations in the cGMP-relaxation pathway. The impaired neurotransmission does not appear to be related to the formation of AGEs.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1994

Sympathomimetic actions of methylenedioxymethamphetamine in rat and rabbit isolated cardiovascular tissues.

The aim of this study was to investigate the actions of methylenedioxymethamphetamine (MDMA) in several isolated cardiovascular tissues. In spontaneously beating rat atria, concentration-dependent positive chronotropic responses to MDMA and amphetamine were blocked by the neuronal-uptake inhibitor desipramine (1 microM) and the beta-adrenoceptor antagonist propranolol (1 microM). In atria incubated with [3H]noradrenaline to label transmitter stores, 10 microM MDMA and 1 microM amphetamine increased the resting outflow of radioactivity, while 1 microM desipramine had no effect on resting outflow. The MDMA- and amphetamine-induced release of radioactivity were blocked by 1 microM desipramine. MDMA, amphetamine and desipramine each enhanced the electrical stimulation-induced (2 Hz, 30-s train) release of radioactivity; the enhancing effects of MDMA and amphetamine were blocked by 1 microM desipramine. In rat isolated perfused hearts, MDMA (1 and 10 microM) increased heart rate by a similar amount to the increase caused by noradrenaline (10 and 50 nM). MDMA also induced dysrhythmias in 7 out of 11 rat isolated perfused heart preparations. In rabbit isolated perfused and superfused ear arteries preloaded with [3H]noradrenaline, MDMA increased the resting release of radioactivity by 230 +/- 18% (n = 6) of control resting release; the increase was accompanied by a rise in perfusion pressure of 17 +/- 7 mmHg (n = 6). MDMA also facilitated the vasoconstrictor responses to noradrenaline (3-9 ng) and perivascular nerve stimulation (1-5 Hz, 10-s train). MDMA-induced vasoconstriction and the facilitation of vasoconstrictor responses to noradrenaline and electrical stimulation were blocked by 1 microM desipramine.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamine↗
PubMed1993

Light and electron microscopic immunocytochemical localization of PKC delta immunoreactivity in the rat central nervous system.

Protein kinase C (PKC) is one of the major cellular signal transduction systems. Since at least nine different PKC isoenzymes have been described, the purpose of the present studies was to identify the regional, cellular, and subcellular distributions of PKC delta in the rat central nervous system (CNS) by light and electron microscopic immunocytochemistry. We have found that PKC delta immunoreactivity is present in all major subdivisions of the rat CNS. Within each of the subdivisions, PKC delta immunoreactivity is localized to perikarya that monitor sensory and motor functions. More specifically, PKC delta is found in the olfactory bulb, cerebral cortex, lateral septum, thalamus, vestibular and cochlear nuclei, inferior olive, nucleus of the solitary tract, cerebellum, and superficial layers of the dorsal horn in the spinal cord. In most cases, the distribution of this isoenzyme is distinct from that of the conventional isoforms. Within the CNS, PKC delta is localized primarily in neurons; however, neurons of the same type are not uniformly labeled. This is most evident in the cerebellum, where alternating columns of Purkinje cells are immunostained. While PKC delta is prominent in perikarya, occasional immunostaining is seen in dendrites, fibers or axons, and nerve terminal. Electron microscopic analysis of the posterolateral nucleus of the thalamus reveals that the cell nucleus, the rough endoplasmic reticulum, and the plasma membrane are all immunopositive. Since each of the PKC subspecies may have different substrate, lipid, and other co-factor requirements, the regional, cellular, and subcellular distribution of each of these isoforms should help to define their functional environments.

Animals↗
PubMed1993

Interactions of methylenedioxymethamphetamine with monoamine transmitter release mechanisms in rat brain slices.

This study investigates the effects of methylenedioxymethamphetamine (MDMA) and amphetamine on monoamine release from rat superfused brain slices in both the presence and absence of vesicular stores of transmitter. MDMA caused the release of radioactivity from slices incubated with [3H]5-hydroxytryptamine, [3H]noradrenaline or [3H]dopamine with EC50 values of 1.9 mumol/l (95% confidence limits 1.5-2.3 mumol/l), 4.5 mumol/l (2.3-8.7 mumol/l), and greater than 30 mumol/l, respectively. In contrast, amphetamine (0.1-300 mumol/l) was more effective in releasing radioactivity from slices incubated with [3H]dopamine than [3H]noradrenaline or [3H]5-hydroxytryptamine. When Ca2+ was excluded from the superfusion fluid, the MDMA-induced release of radioactivity from slices incubated with [3H]dopamine was unaltered, but that from slices incubated with [3H]noradrenaline or [3H]5-hydroxytryptamine was enhanced. MDMA (10 mumol/l) facilitated the stimulation-induced (5 Hz, 1 min) outflow of radioactivity from slices incubated with [3H]noradrenaline or [3H]5-hydroxytryptamine to 7.5-fold and 2.1-fold of control values, respectively, but had no effect on that from slices incubated with [3H]dopamine. Amphetamine (1 mumol/l) increased the stimulation-induced outflow from slices incubated with [3H]noradrenaline, but not that from slices incubated with [3H]5-hydroxytryptamine or [3H]dopamine. Inhibition of monoamine oxidase by a 30-min incubation with pargyline (100 mumol/l) enhanced the releasing action of MDMA on all three monoamines. Pargyline (100 mumol/l) also enhanced the facilitation caused by MDMA, of the stimulation-induced outflow of radioactivity from slices incubated with [3H]noradrenaline, [3H]5-hydroxytryptamine or [3H]dopamine. In some experiments, slices were obtained from reserpinised rats (2.5 mg/kg s.c. 24 h prior) and pre-exposed for 30 min to the monoamine oxidase inhibitor parglyine (100 mumol/l). Under these conditions, electrical stimulation evoked a small residual stimulation-induced outflow of radioactivity from slices incubated with [3H]noradrenaline, and failed to evoke an outflow of radioactivity from slices incubated with [3H]5-hydroxytryptamine or [3H]dopamine. However, a Ca(2+)-dependent stimulation-induced outflow of radioactivity was evoked in the presence of either MDMA (10 mumol/l) or amphetamine (1 mumol/l) from slices incubated with either [3H]dopamine or [3H]noradrenaline, but not from slices incubated with [3H]5-hydroxytryptamine. The stimulation-induced outflow of radioactivity from slices incubated with [3H]noradrenaline was enhanced in the presence of desipramine (1 mumol/l), however this enhancement was less than that caused by 10 mumol/l MDMA or 1 mumol/l amphetamine. The Ca(2+)-dependent response to electrical stimulation in the presence of MDMA from slices incubated with [3H]noradrenaline was greatly reduced when rats were pretreated with a higher dose of reserpine (10 mg/kg s.c.).(ABSTRACT TRUNCATED AT 400 WORDS)

3,4-Methylenedioxyamphetamine↗
PubMed1993

Endothelin-1 may be a physiologic modulator of vasoconstriction in rat kidney.

The effect of endothelin-1 (ET-1), in concentrations well below threshold and near physiologic levels, has been examined on vasoconstrictor responses to perivascular nerve stimulation and norepinephrine in rat isolated kidney, perfused through the renal artery with physiologic salt solution. A 60-min exposure to ET-1 (1, 10, and 100 pM) had little or no effect on the basal perfusion pressure but enhanced responses to nerve stimulation (4 Hz, 10-s train) by 123 +/- 12% (n = 6), 125 +/- 8% (n = 6), and 226 +/- 49% (n = 7) of the control response, respectively. Responses to nerve stimulation were consistent in the absence of ET-1. Vasoconstrictor responses induced by norepinephrine (30-300 pmol) increased with time in control experiments, but the increase was markedly greater in the presence of 10 and 100 pM ET-1. The vasoconstrictor responses caused by nerve stimulation and norepinephrine were greatly increased by the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (NOLA, 100 microM). In the presence of NOLA, ET-1 (1 pM) enhanced the responses to nerve stimulation (1-8 Hz, 10-s trains) by a significantly greater amount than in the absence of NOLA, suggesting that the enhancement by ET-1 is suppressed by NO release. The responses to norepinephrine (3-100 pmol) were also enhanced by 1 pM ET-1 in the presence of NOLA. The data suggest that ET-1 in physiologically relevant concentrations may have a role in the modulation of vascular reactivity in the renal circulation.

Amino Acid Oxidoreductases↗
PubMed1993

Galanin-immunoreactive axons innervate somatostatin-synthesizing neurons in the anterior periventricular nucleus of the rat.

The anterior periventricular nucleus (PeN) regulates GH secretion by synthesizing and releasing somatotropin release-inhibiting factor (SRIF) into the portal circulation. This territory of the diencephalon is heavily innervated by axons of galanin (GAL)-immunoreactive (IR) neurons. The connections between GAL-IR fibers and hypophysiotropic SRIF neurons were studied by means of immunocytochemical double labeling at the light and electron microscopic levels. Retrograde axonal labeling with Fluoro-Gold revealed the anterior PeN as the main site of hypophysiotropic SRIF-synthesizing neurons. These cells were densely surrounded by GALergic axons that made contacts with their cell bodies and dendrites. At the ultrastructural level, diaminobenzidine-labeled SRIF neurons received synapsing GAL-IR axons marked with silver-gold particles. Both axo-somatic and axo-dendritic forms of connections were observed. These morphochemical data revealed an interaction between GAL- and SRIF-synthesizing neurons in the anterior PeN. Furthermore, the presence of synaptic connections between these neuronal systems suggests a role for GAL in the control of SRIF secretion and, in turn, in the regulation of GH release.

Animals↗
PubMed1992

Renal vasoconstriction is modulated by nitric oxide.

1. The effect of the nitric oxide synthesis inhibitor, NG-nitro-L-arginine (NOLA), has been examined on vascular reactivity in the rat isolated perfused kidney. 2. NOLA (10 mumol/L) had no effect on basal perfusion pressure, but significantly enhanced the vasoconstrictor responses to sympathetic nerve stimulation (1-16 Hz, 10 s) and noradrenaline (10-300 pmol). The enhancements were greater with the lower frequencies of stimulation and lower doses of noradrenaline. 3. The enhancing effect of 10 mumol/L NOLA on vasoconstrictor responses to nerve stimulation was partially prevented by 100 mumol/L L-arginine while 100 mumol/L D-arginine had no effect. 4. The results suggest that nitric oxide attenuates vasoconstrictor responses in the rat kidney, and provide evidence that nitric oxide has a physiological role in the modulation of vascular reactivity.

Animals↗
PubMed1992

Attenuation of vasoconstriction by endogenous nitric oxide in rat caudal artery.

1. The effects of NG-nitro-L-arginine (L-NNA), NG-nitro-L-arginine methyl ester (L-NAME), haemoglobin and methylene blue have been examined on vascular reactivity in the rat isolated caudal artery. The effects of L-NNA and sodium nitroprusside were also investigated on the stimulation-induced (S-I) efflux of noradrenaline in the rat caudal artery. 2. L-NNA (10 microM) and L-NAME (10 microM) significantly attenuated the vasodilator responses to acetylcholine (1 nM-1 microM), but had no effect on vasodilator responses to papaverine (1-100 microM). 3. Vasoconstrictor responses to sympathetic nerve stimulation (3 Hz, 10 s), noradrenaline (0.01-1 microM), methoxamine (1-10 microM), 5-hydroxytryptamine (0.01-0.3 microM), phenylephrine (0.1-10 microM), endothelin-1 (10 nM) and KCl (40 mM) were significantly enhanced by 10 microM L-NNA. L-NAME (10 microM) caused a significant enhancement of vasoconstrictor responses to noradrenaline and sympathetic nerve stimulation in endothelium-intact, but not in endothelium-denuded tissues. 4. Haemoglobin and methylene blue (both 10 microM) enhanced the vasoconstrictor responses to sympathetic nerve stimulation and noradrenaline. The enhancements were absent in endothelium-denuded arterial segments. 5. In endothelium-denuded arterial segments precontracted with phenylephrine, the vasodilator responses to the nitric oxide donor, sodium nitroprusside (0.1-300 nM) were decreased by increasing the level of precontraction. 6. L-NNA (10 microM) had no effect on the S-I efflux of radioactivity from arteries in which transmitter stores had been labelled with [3H]-noradrenaline. 7. These results suggest that endothelial nitric oxide attenuates vasoconstrictor responses in the rat caudal artery through activation of soluble guanylate cyclase to decrease smooth muscle contractility. Therefore, the findings provide evidence that nitric oxide acts as a functional antagonist to oppose vasoconstriction.

Acetylcholine↗
PubMed1992

Measurement of capillary cholesterol as an aid to the management of hypertensive patients with hyperlipidaemia--an assessment of the Reflotron.

The Reflotron dry chemistry method of capillary cholesterol measurement has been widely adopted as a rapid means of population screening. We attempted to use it to monitor changes in cholesterol in a trial of intensive dietary intervention in hyperlipidaemic hypertensives. Four hundred and eighty-nine capillary cholesterol levels measured by the Reflotron were compared with levels for venous samples obtained simultaneously and assayed by the Biochemistry Department using conventional laboratory methods. The mean difference between them was 0.3 mmol/l +/- 0.8 (SD). Approximately one-third of the variability in the difference between the two methods was explained by the variables, Reflotron machine used and time (R2 = 54%, adjusted R2 = 34%). We conclude that the Reflotron is not suitable for accurate assessment of the modest changes in cholesterol which occur in individual patients during dietary intervention.

Blood Chemical Analysis↗
PubMed1991

Endothelial nitric oxide attenuates vasoconstrictor responses to nerve stimulation and noradrenaline in the rat tail artery.

The effects of the nitric oxide synthesis inhibitor, NG-nitro-L-arginine (NOLA), have been examined in perfused segments of rat tail artery. NOLA (1 and 10 microM) significantly enhanced the vasoconstrictor responses to perivascular nerve stimulation (5 Hz, 10 s) and noradrenaline (10 ng). The enhancing effects of NOLA were prevented by L-arginine, but not by D-arginine, and were absent in endothelium-denuded artery segments. The results suggest that nitric oxide derived from endothelial cells attenuates vasoconstrictor responses to both nerve stimulation and noradrenaline.

Acetylcholine↗
PubMed1991

Interactions between endothelin-1 and other chronotropic agents in rat isolated atria.

In isolated spontaneously beating right and left atria and in electrically driven left atrium from rat, endothelin-1 increased the rate and force of contraction, but significantly decreased the positive chronotropic and inotropic responses to sympathetic nerve stimulation. The decrease may be partly dependent on the positive cronotropic and inotropic effects of endothelin-1, since other agents with chronotropic activity (noradrenaline, isoprenaline, serotonin and Bay k 8644) also decreased stimulation-induced chronotropic responses. Endothelin-1 caused a significant rightward shift of the linear portion of the log concentration-response curve for the chronotropic actions of noradrenaline and isoprenaline. The changes in the log concentration-response curve were not a consequence of the direct chronotropic effect of endothelin-1, since they were still evident when the chronotropic action of endothelin-1 was offset by carbachol. Furthermore, the chronotropic agent, Bay k 8644, did not shift the linear portion of the log concentration-response curves for noradrenaline and isoprenaline. The mechanism of the effects of endothelin-1 in rat atria is not known, but they were not changed by blockade of alpha-adrenoceptors or of L-type voltage-sensitive Ca2+ channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Chronic cocaine treatment does not alter rat striatal D2 autoreceptor sensitivity to pergolide.

Rat superfused striatal slices, preloaded with [3H]dopamine, were electrically stimulated and the stimulation-induced outflow of radioactivity was taken as an index of dopamine release. In the presence of 10 microM nomifensine, exposure of striatal slices to unlabelled dopamine (0.3 microM) for 6 min prior to stimulation, significantly reduced stimulation-induced outflow. In contrast, a 21-min exposure to dopamine did not significantly alter stimulation-induced outflow. These results suggest that D2 receptors modulating dopamine release in the rat striatum may be rapidly desensitized in vitro. Rats were pretreated for 14 days with cocaine HCl (10 mg/kg/day i.p.) or saline. A progressive enhancement of locomotor activity in cocaine-treated rats over the pretreatment period compared to that in saline-treated rats indicated a behavioural sensitization to cocaine. The inhibitory effect of pergolide (1, 10 and 100 nM) on stimulation-induced outflow from striatal slices obtained from cocaine-pretreated rats was not different from that in slices obtained from saline-pretreated rats. Therefore no evidence was obtained for either a desensitization or a supersensitivity of striatal D2 autoreceptors by chronic cocaine administration.

Animals↗
PubMed1991

Differential sensitivities of avian and mammalian neuromuscular junctions to inhibition of cholinergic transmission by omega-conotoxin GVIA.

Nerve stimulation-induced contractions of the chick biventer cervicis muscle were slowly reduced by omega-conotoxin. However, omega-conotoxin had no effect on skeletal muscle function after i.v. injection in mice or on nerve stimulation-induced contractions of focally innervated muscle of the rat diaphragm or the rabbit proximal oesophagus, or the multiply innervated extra-ocular rectus muscle from rabbit. The lack of effect of omega-conotoxin on mammalian neuromuscular junctions was not due to the high safety factor in transmission or to a high local concentration of Ca2+ originating from the muscle, and could not be accounted for in terms of the operation of facilitatory or inhibitory feedback modulation of transmitter release from motoneurone terminals. It is concluded that the Ca2+ channels of mammalian motoneurone terminals differ from those of avian motoneurone terminals and other omega-conotoxin-sensitive nerve terminals.

Animals↗
PubMed1991

Modulation of norepinephrine-induced vasoconstriction by endothelin-1 and nitric oxide in rat tail artery.

The effects of endothelin-1 (ET-1) and an inhibitor of the synthesis of nitric oxide (NO) have been examined on vasoconstrictor responses to nerve stimulation and norepinephrine in the rat isolated perfused tail artery. In endothelium-denuded preparations, a 60-min exposure to 0.3 nM ET-1 had no effect on the basal perfusion pressure, but significantly enhanced responses to stimulation (1 Hz, 10 s) and norepinephrine (10 ng) to 124 +/- 9% (n = 6) and 139 +/- 14% (n = 8), respectively, of control responses. In endothelium-intact preparations, inhibition of NO synthesis by NG-nitro-L-arginine (NOLA, 10 microM) enhanced responses to stimulation (5 Hz, 10 s) and norepinephrine (10 ng) to 171 +/- 12% (n = 6) and 222 +/- 9% (n = 4), respectively, of control responses. The NOLA-induced enhancements were prevented by 100 microM L-arginine but not by 100 microM D-arginine, and did not occur in endothelium-denuded arteries. In other experiments, segments of rat tail artery were perfused in a low-volume (3.5 ml) recirculating system. The basal perfusion pressure was consistent for at least 60 min. In endothelium-denuded segments, vasoconstrictor responses to nerve stimulation (0.5 Hz, 10 s) or norepinephrine (10 ng) remained constant. However, in endothelium-intact segments, responses to stimulation and norepinephrine gradually increased to 158 +/- 13% (n = 6) and 152 +/- 8% (n = 5), respectively, of initial responses, after 45 min of recirculation. The increases were not related to NO, as they remained unchanged in the presence of 10 microM NOLA. Thus, it appears that a vasoconstriction-enhancing factor, possibly ET-1, is released from endothelial cells and accumulates in the perfusion fluid.

Animals↗