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PubMed1989

A functional study of the development of the cardiac sympathetic neuroeffector junction in the SHR.

We studied the function of the cardiac sympathetic nerve varicosity in isolated right atrial preparations of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats at 4, 9, 14, 20 and 50 weeks of age. Cumulative concentration-atrial period response (C-R) curves to isoprenaline showed similar maximum response and sensitivity (EC50) at all ages but there was an age-related fall in resting atrial rate. Similar results were found for methoxamine (alpha 1-adrenoceptor agonist) although the maximum response was significantly less than for isoprenaline. The time-dependent recovery (T 1/2) of the fall in atrial period in response to sympathetic nerve stimulation from electrical field pulses (1-32 at 1 Hz) was enhanced by neuronal uptake inhibition by desipramine (0.1-1 mumol/l), to a similar degree at all ages. Pre-junctional alpha 2-adrenoceptor stimulation by clonidine caused progressively more inhibition of the number of field pulses-fall in period relationship with age. SHR atria were similar to WKY rat atria at all ages except for a further impairment of the development of pre-junctional alpha 2-adrenoceptors. These studies indicate that the function of the cardiac sympathetic varicosity matures early (by 4 weeks) and overall there is very little impairment in SHR versus WKY rat atria.

Aging↗
PubMed1986

Effects of aging at the adrenergic cardiac neuroeffector junction.

Adrenergic neural degeneration was seen to increase with age. This is thought to contribute to the decreased cardiac content of the transmitter. Pharmacologically, it was found with the use of tyramine that virtually all of the norepinephrine (NE) pool is available for release, and that there is no difference in the amount of NE released in relation to age. Cardiac responsiveness to adrenergic agonists decreases with age. Our results suggest that this is caused in great measure by increased activity of the prejunctional, neuronal uptake mechanism in the older animal.

Aging↗
PubMed1987

Post-tetanic contractile events further support the interaction of multiple neurotransmitters in the neuroeffector junction of the rat vas deferens.

Post-tetanic events were recorded in isolated, superfused, epididymal and prostatic halves of the rat vas deferens. Increasing the frequency of nerve stimulation from 0.15 to 15 Hz (1-30 s) and then back to 0.15 Hz produced a post-tetanic potentiation (PTP) of the muscular responses in the epididymal end but a post-tetanic inhibitory response (PTI) in the prostatic half. Both effects were abolished by tetrodotoxin or animal pretreatment with 6-hydroxy dopamine (6-OHDA). PTP was markedly reduced by reserpine treatment or tissue incubation with prazosin. PTI was not altered by adrenergic drugs but partially reduced by tissue application of bicuculline or strychnine, revealing that gamma-aminobutyric acid (GABA) may modulate the motor transmission towards the prostatic half of the rat ductus.

Animals↗
PubMed1981

Effects of 5-hydroxytryptamine on neuroeffector junction in human pulmonary artery.

The effects of 5-hydroxytryptamine on release of norepinephrine and on contraction of smooth muscle in human pulmonary artery were studied. Helical strips were prepared from intra-parenchymal arteries removed 3-18 h after death. The strips were labeled with L-[7-3H]norepinephrine and mounted for superfusion and isometric tension recording. Electrical stimulation (10 V, 2 ms, 2 Hz) of the strips increased the release of total radioactivity; this release was blocked by tetrodotoxin. 5-Hydroxytryptamine (10(-5) M) exerted a cocaine-sensitive, indirect sympathomimetic effect on the overflow of norepinephrine from resting strips. This action was not blocked by methysergide. No effect of 5-hydroxytryptamine on release of norepinephrine from electrically stimulated tissue could be demonstrated. 5-Hydroxytryptamine (10(-5) M) also caused contractions of pulmonary smooth muscle, not blocked by phentolamine (10(-5) M) but mediated in part through methysergide-sensitive 5-hydroxytryptamine receptors.

Adolescent↗
PubMed1984

Evidence for prejunctional and postjunctional antagonism of the sympathetic neuroeffector junction by acetylcholine in canine cardiac Purkinje fibers.

This study determined whether acetylcholine inhibited changes in action potential duration and developed tension in canine Purkinje fibers produced by norepinephrine released during field stimulation more than it inhibited changes produced by superfusion with norepinephrine. Field stimulation increased action potential duration measured at 75% of repolarization by 9.6 ms and increased active tension by 35.5%. Acetylcholine (10(-6) M) almost completely inhibited changes in action potential duration and developed tension during field stimulation. Norepinephrine (10(-8) M to 5 X 10(-8) M) superfusion during normal pacing increased developed tension by 40.6%. Acetylcholine (10(-6) M) reduced this increase to 19.7%. Thus, acetylcholine inhibited the increase in tension during field stimulation by 90.7%, whereas it inhibited equivalent increases in tension produced by superfusion with norepinephrine by only 51.4% (p less than 0.01). These data suggest that acetylcholine antagonizes the effects of adrenergic stimulation by pre- and postjunctional inhibitory actions in canine cardiac Purkinje fibers.

Acetylcholine↗
PubMed1984

Alpha-adrenoceptors and facilitation at a sympathetic neuroeffector junction.

Excitatory junction potentials were recorded from the mouse vas deferens following 5 stimuli at 1Hz and a single stimulus at times from 100 msec to 9 sec later. E.j.ps facilitate and facilitation decayed over a biexponential time course, with time constants of 120 msec and 4.3 sec. Clonidine (10(-8)-10(-7) M) depressed e.j.p. amplitude, and also accelerated both phases of the decay of facilitation. Yohimbine (10(-7) M) and piperoxan (10(-7)-10(-6) M) increased the amplitude of all but the first e.j.p. in a train, and slowed both phases of the decay of facilitation. One way in which prejunctional modulation by alpha-adrenoceptors may occur is therefore by modifying the carry-over of facilitation from one stimulus to the next.

Animals↗
PubMed1976

Effects of amide-linked local anesthetics on adrenergic neuroeffector junction in cutaneous veins of dog.

When changes in isometric tension of helical strips of dog saphenous veins were recorded, etidocaine caused a dose-dependent depression of the contractile responses to nerve stimulation, norepinephrine and K+. The response to nerve stimulation was significantly more depressed than that to exogenous norepinephrine. Similar results were obtained with lidocaine. In preparations incubated in solutions containing 3H-norepinephrine and mounted for superfusion and isometric tension recording, etidocaine depressed the contractions and diminished the release of 3H-norepinephrine evoked by nerve stimulation. Thus, in addition to an inhibitory effect on the responses of smooth muscle cells, amide-linked local anesthetic agents such as etidocaine depress adrenergic neurotransmission in the blood vessel wall, which helps explain their vasodilator properties in the intact organism. In unstimulated preparations and during contractions caused by K+, etidocaine increased the efflux of 3H-norepinephrine and deaminated metabolites. After incubation with the monamine oxidase inhibitor, pargyline, etidocaine augmented markedly the efflux of 3H-norepinephrine. During responses to tyramine, it augmented the release of 3H-norepinephrine more than the efflux of deaminated compounds. This suggests that etidocaine augments the leakage of norepinephrine out of the storage vesicles, making more catecholamines available for intraneuronal deamination.

Amides↗
PubMed1990

Presynaptic alpha 2-autoinhibition in a vascular neuroeffector junction where ATP and noradrenaline act as co-transmitters.

1. alpha 2-Autoinhibition of transmitter release was investigated in the largest rami caecales of the rabbit ileocolic artery. Vasoconstriction, elicited by electrical field stimulation or by exogenous agonists, was measured as an increase in perfusion pressure. 2. Short periods of electrical stimulation elicited monophasic vasoconstriction, whereas longer periods (greater than 10 s) produced biphasic vasoconstriction. Prazosin had no significant effect on the first component of the biphasic vasoconstriction elicited by electrical stimulation, but did reduce the second component at higher frequencies. alpha, beta-Methylene ATP significantly attenuated the first component whilst the second component was relatively resistant. 3. The alpha 2-adrenoceptor antagonist yohimbine did not change responses evoked by very short pulse trains (less than 2 s) but enhanced responses to longer pulse trains. When vasoconstriction was biphasic, both phases were potentiated by yohimbine. 4. The results indicate that the vasoconstriction elicited by brief trains of sympathetic nerve impulses is mainly or exclusively mediated by ATP, whereas at longer pulse trains a noradrenergic component comes into play. The potentiation produced by yohimbine is due to interruption of presynaptic alpha 2-adrenoceptor-mediated autoinhibition of transmitter release. The autoinhibition affects both purinergic and adrenergic components of sympathetic neurotransmission.

Adenosine Triphosphate↗
PubMed1991

Pharmacological characterization of the inhibitory activity of beta h-endorphin (beta h-EP), [Arg9,19,24,28,29]-beta h-EP, [Gln8,Gly31]-beta h-EP-Gly-Gly-NH2, in the neuroeffector junction of the mouse vas deferens.

The inhibitory opioid activities of beta h-endorphin (beta h-EP), its structurally related peptide analogues [Gln8,Gly31]-beta h-EP-Gly-Gly-NH2 (Gly-Gly-beta h-EP), [Arg9,19,24,28,29]-beta h-EP (Arg-beta h-EP) and methionine enkephalin have been examined in the electrically stimulated mouse vas deferens bioassay. All four peptides behaved as full agonists; methionine enkephalin was the most potent followed by Arg-beta h-EP, beta h-EP and Gly-Gly-beta h-EP. Neither Gly-Gly-beta h-EP nor Arg-beta h-EP antagonized the inhibitory action of beta h-EP or methionine enkephalin. An hour of tissue exposure to 30 nM beta-funaltrexamine followed by thorough washing, displaced to the right, in a parallel fashion, the concentration-response curves of beta h-EP and analogues. Whereas the displacement of the concentration response curves was 8 to 10-fold for beta h-EP and Arg-beta h-EP, it was only about 3-fold for Gly-Gly-beta h-EP and methionine enkephalin. Naltrindole was the most potent antagonist of methionine enkephalin with an apparent pA2 of 9.4; its potency as an antagonist of beta h-EP and related analogues was approximately one-tenth of this with pA2 values approximately 8.5. Norbinaltorphimine also antagonized the action of the opioid peptides with pA2 values close to 7.8.

Animals↗
PubMed1993

Inhibitory effects of bupivacaine and lidocaine on adrenergic neuroeffector junctions in rat tail artery.

BACKGROUND: Various local anesthetic agents have been shown to cause relaxation of isolated vascular segments contracted by catecholamines and other constrictor drugs. This report describes the actions of the amide-linked local anesthetic, bupivacaine, on adrenergic responsiveness of isolated arterial smooth muscle, and compares bupivacaine effects with those of lidocaine. METHODS: Helical strips of rat tail artery mounted in a muscle bath for measurement of isometric force generation were contracted in response to adrenergic nerve stimulation, increased potassium concentration, tyramine, or exogenous norepinephrine. RESULTS: Treatment with bupivacaine or lidocaine caused depression of contraction to all four stimuli. Contraction to adrenergic nerve stimulation was more sensitive to the inhibitory effects of local anesthetics than was contraction to elevated potassium, tyramine, or exogenous norepinephrine. Furthermore, bupivacaine was more effective in reducing contraction to adrenergic nerve stimulation than was lidocaine (EC50: bupivacaine = 4 x 10(-6) M; lidocaine = 61 x 10(-6) M). In arteries incubated in solutions containing [3H]-norepinephrine and mounted for superfusion and isometric force recording, both bupivacaine and lidocaine (10(-5) M) depressed the contractions and diminished the release of radioactivity evoked by nerve stimulation. At the concentration tested, bupivacaine was more effective than lidocaine in reducing both contraction and the efflux of radioactivity as indicated by the magnitude of depression compared with control activities. CONCLUSIONS: These findings suggest that lidocaine and bupivacaine depress adrenergic neurotransmission and inhibit smooth muscle contraction. Bupivacaine is a more potent inhibitor of adrenergic neurotransmission in the blood vessel wall than is lidocaine.

Animals↗
PubMed1988

Electrical activity at the sympathetic neuroeffector junction in the guinea-pig vas deferens.

1. The relationship between the nerve terminal action potential and transmitter release from sympathetic postganglionic nerve terminals has been studied in vitro by focal extracellular recording. 2. In the absence of stimulation, 'spontaneous excitatory junction currents' (SEJCs) were recorded with amplitudes up to 500 microV, durations of 50-80 ms and frequencies of occurrence of 0.3-0.05 Hz; SEJCs of unusually long time course were also observed. The SEJCs were not recorded in tissues pre-treated with 6-hydroxydopamine to destroy sympathetic nerves, were unaffected by tetrodotoxin (TTX), the competitive alpha-adrenoceptor antagonists, prazosin and phentolamine, the irreversible alpha-adrenoceptor antagonist benextramine but were blocked by alpha,beta-methylene ATP which desensitizes P2-purinoceptors. 3. During trains of supramaximal stimuli at 0.1-4 Hz stimulus locked 'excitatory junction currents' (EJCs) were evoked intermittently from the population of varicosities located under the suction electrode with a probability of occurrence of 0.005-0.8. Although EJCs occurred intermittently, they were always preceded by an associated, non-intermittent, nerve impulse (delay less than or equal to 3 ms). 4. The EJCs reflect transmitter release from nerves because they were abolished by TTX, removal of calcium from the bathing medium, exposure to alpha-beta-methylene ATP and exhibited frequency-dependent facilitation. 5. Amplitude distributions of SEJCs and EJCs recorded in the same attachment were similar and skewed towards low-amplitude events. Individual SEJCs and EJCs could be found which were identical in amplitude and time course. 6. Locally applied TTX blocked impulse propagation and transmitter release in the terminal region; electrotonic invasion of the terminals from the point of block did not activate the transmitter release process. 7. These studies indicate that (1) intermittence of transmitter release is caused by a low probability of release in the invaded varicosity and is not caused by conduction failure in the terminal regions, (2) only a single quantum is normally secreted when the release mechanism of a varicosity is activated by the nerve impulse and (3) active invasion of the terminals is necessary for transmitter release to occur.

Action Potentials↗
PubMed1993

Calcium channels at the adrenergic neuroeffector junction in the rabbit ear artery.

Neurotransmitter release is dependent on influx of Ca2+ through voltage-operated calcium channels (VOCCs). These channels may be divided into L, N, T and P subtypes. To investigate the subtypes of VOCC involved in transmitter release from adrenergic nerves in the isolated rabbit ear artery, the effects of some subtype selective VOCC antagonists were examined on contractile responses induced by electrical field stimulation (EFS), and exposure to an isosmolar (low Na+, normal Cl- content) or a hyperosmolar (normal Na+, high Cl- content) 60 mM K+ solution. Tetrodotoxin (TTX) and the L channel blocker nimodipine were present in the latter experiments to inhibit sodium-dependent action potential discharge and the direct contractile effect of K+ depolarization on the smooth muscle cells. Prazosin abolished the contractile effect of EFS, indicating that the response was elicited by activation of adrenergic nerves. The EFS-induced contractions were concentration-dependently inhibited by the N channel blocker omega-conotoxin (pIC50 = 9.0) and the proposed L channel blocker T-cadinol (pIC50 = 4.5), while nimodipine and the T channel blocker tetramethrin had no effect. The isosmolar and hyperosmolar K+ solutions induced a prazosin-sensitive contraction, amounting to 46% and 10% of the response to 10(-5) M noradrenaline (NA), respectively. omega-Conotoxin inhibited the contractile response to the hyperosmolar K+ solution, but not that to the isosmolar K+ solution. T-cadinol preferentially inhibited the response to the hyperosmolar K+ solution. Tetramethrin had no effect on contractions induced by either type of K+ solution.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Prejunctional and postjunctional effects of neuropeptide Y at the noradrenergic neuroeffector junction of the perfused mesenteric arterial bed of the rat.

The effect of neuropeptide Y (NPY) on periarterial nerve stimulation-induced release of norepinephrine (NE) and increase in perfusion pressure in the perfused mesenteric arterial bed of the rat was examined. Perfusate effluents were continuously collected and assayed for endogenous NE by high-pressure liquid chromatography (HPLC) coupled to electrochemical detection. Perfusion pressure was continuously monitored by means of a pressure transducer. Periarterial nerve stimulation (8 or 16 Hz, 60 V, 2-ms duration for 30 s) resulted in a readily detectable increase in NE release and perfusion pressure that was attenuated by the prior administration of tetrodotoxin (TTX) (10(-5) M) or guanethidine (5 X 10(-5) M). NPY exerted both prejunctional and postjunctional effects on noradrenergic neurotransmission in this preparation. The peptide produced a concentration-dependent reduction in the release of NE over a concentration range of 10(-10) - 10(-7) M. A similar inhibition effect occurred at 8, 10, and 16 Hz. In contrast, low concentrations (10(-10) and 10(-9) M) decreased the effect of nerve stimulation on perfusion pressure, whereas higher concentrations (10(-7) M) produced a marked potentiation. The alpha 2-adrenoceptor antagonist, yohimbine, did not alter the inhibitory effect of NPY on evoked NE release or the effect on perfusion pressure. Prazosin similarly did not alter the inhibitory effect of NPY on NE release but prevented the increase in perfusion pressure. We conclude that NPY modulates noradrenergic neurotransmission in the mesenteric arterial bed by decreasing the evoked release of NE and producing a concentration-dependent biphasic response on vascular smooth muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effects of age on neurotransmission at the cardiac sympathetic neuroeffector junction.

The effect of age on the capacity of the right cardiac sympathetic nerve to release norepinephrine (NE) into perfusion effluent (NE overflow) was studied in hearts isolated from male Fischer 344 rats at 6, 12 and 24 months of age. The hearts were perfused through an aortic cannula with Krebs-Ringer solution and the cardiac sympathetic nerve was stimulated electrically with supra-maximal voltage at frequencies of stimulation that produced 20%, 50% or 80% of maximal NE overflow at each age. The content of NE in the perfusion effluent was measured by electro-chemical detection after alumina extraction and high-performance liquid chromatography separation. The NE overflow was significantly lower in hearts of 12- and 24-month-old animals compared to hearts from 6-month-old animals at each frequency of stimulation. In addition the frequency of stimulation necessary to produce 50% or 80% of maximal NE overflow was significantly greater in heart preparations from both 12- and 24-month-old animals compared to preparations from 6-month-old animals. Perfusion with cocaine (10(-6) M) significantly increased the quantity of NE in the effluent after nerve stimulation only in hearts from 12- and 24-month-old animals. Nevertheless, NE overflow remained significantly lower than that observed in hearts of 6-month-old animals. The results suggest that the capacity of the cardiac sympathetic nerve to release NE is diminished in 12- and 24-month-old animals. Furthermore, in these age groups an increase in neuronal uptake appears to reduce further the quantity of NE made available to the heart. These changes seem to occur by middle age and persist to senescence.

Aging↗
PubMed1983

Prejunctional and postjunctional actions of endogenous norepinephrine at the sympathetic neuroeffector junction in canine coronary arteries.

The effects of endogenous and of exogenous norepinephrine were studied in isolated rings of canine left circumflex coronary artery and its first ventricular branch. Norepinephrine was released from adrenergic nerve endings by transmural electrical stimulation and by tyramine. In rings contracted with prostaglandin F2 alpha, transmural electrical stimulation resulted in frequency-dependent relaxations which were blocked by propranolol or tetrodotoxin; tyramine and exogenous norepinephrine caused concentration-dependent relaxations which were blocked by propranolol. The tyramine-induced relaxations also were inhibited by cocaine. The left circumflex artery was less sensitive than its branch to beta-adrenergic activation; this difference was significant even between rings of the two vessels immediately adjacent to the branching point and was abolished by phentolamine. In the presence of propranolol, transmural electrical stimulation, tyramine and phenylephrine, produced contractions of the left circumflex artery, but not the branch; these contractions were prevented by phentolamine. Phentolamine, but not prazosin, augmented the beta-adrenergic response of left circumflex artery to low frequency stimulation; in arteries preincubated with 3H-norepinephrine, this was accompanied by an increased overflow of tritiated neurotransmitter. The prejunctional effect of phentolamine was also evident in branch coronary arteries which exhibit no postjunctional alpha-adrenergic responses. With high frequency stimulation, both alpha-adrenergic antagonists equally augmented the relaxation of left circumflex artery; the efflux of tritiated norepinephrine was not different from untreated arteries. These experiments demonstrate, in isolated coronary arteries, that the primary adrenergic response to released endogenous norepinephrine is beta-adrenergic relaxation. The prejunctional effects of nonspecific alpha-adrenergic antagonists preclude their use in determining the importance of postjunctional coronary alpha-adrenergic receptor activation caused by sympathetic nerve stimulation.

Adrenergic alpha-Antagonists↗
PubMed1989

Lack of mixed agonist-antagonist properties of [Gln8-Gly31]-beta h-EP-Gly-Gly-NH2 and [Arg9,19,24,28,29]-beta h-EP in the rat vas deferens neuroeffector junction: studies with naloxone, beta-funaltrexamine and ICI 174,864.

The 1-27 truncated fragment of beta h-endorphin (beta h-EP) as well as [Gln8,Gly31]-beta h-EP-Gly-Gly-NH2 or [Arg9,19,24,28,29]-beta h-EP exhibited opiate agonist activity in the rat vas deferens bioassay; the potency of these peptides was 3 to 6 times less than that of beta h-EP. None of these compounds exhibited any degree of antagonism towards the inhibitory action of beta h-EP. Naloxone antagonized and reversed the inhibitory action of beta h-EP and its analogues though with varying potencies. The apparent naloxone-pA2 value for beta h-EP was 8.94; that for [Gln8-Gly31]-beta h-EP-Gly-Gly-NH2 was 8.08 and that for [Arg9,19,24,28,29]-beta h-EP was 8.38. beta-Funaltrexamine (beta-FNA) potently antagonized the inhibitory action of beta h-EP following non-equilibrium kinetics. Tissue preincubation with 10 nM beta-FNA for 60 min followed by extensive washing caused a 10-fold increase in the beta h-EP IC50. However, 10 nM beta-FNA caused only a 1.2 increase in the IC50 of [Gln8,Gly31]-beta h-EP-Gly-Gly-NH2 and a 4.1-fold increase in the IC50 of [Arg9,19,24,28,29]-beta h-EP. In contrast, preincubation of the tissue with 3 microM ICI 174,864 did not modify the potency of beta h-EP or its structural analogues. However, a 60 min pretreatment with 10 microM beta-FNA followed by the addition of 3 microM ICI 174,864 revealed a further decrease in the potency of the opiopeptins compared with tissues exposed to beta-FNA alone or ICI 174,864 alone. In conclusion, the inhibitory action of these peptides is remarkably sensitive to beta-FNA antagonism; in addition the peptides act as pure opiate agonists in marked contrast with the agonist-antagonist properties described in the CNS.

Animals↗
PubMed2001

Effects of a selective neuropeptide Y Y2 receptor antagonist, BIIE0246, on Y2 receptors at peripheral neuroeffector junctions.

1. This study investigated the effects of BIIE0246, a novel neuropeptide Y (NPY) Y2 receptor antagonist, on the inhibition of cholinergic neuroeffector transmission in rat heart and guinea-pig trachea and purinergic neuroeffector transmission in guinea-pig vas deferens produced by the NPY Y2 receptor agonist, N-acetyl [Leu28,31] NPY 24-36. 2. In pentobarbitone anaesthetized rats, supramaximal stimulation every 30 s, of the vagus nerve innervating the heart, increased pulse interval by approximately 100 ms. This response was attenuated by intravenous administration of N-acetyl [Leu28,31] NPY 24-36 (10 nmol x kg(-1)). 3. Transmural stimulation of segments of guinea-pig trachea at 1 min intervals with 5 s trains of stimuli at 0.5, 5, 10, 20 and 40 Hz evoked contractions which were reduced in force by N-acetyl [Leu28,31] NPY 24-36 (2 microM). 4. In guinea-pig vasa deferentia, the amplitude of excitatory junction potentials evoked by trains of 20 stimuli at 1 Hz was reduced in the presence of N-acetyl [Leu28,31] NPY 24-36 (1 microM). 5. In all preparations BIIE0246 attenuated the inhibitory effect of N-acetyl [Leu28,31] NPY 24-36 but had no effect when applied alone. 6. The findings support the view that the nerve terminals of postganglionic parasympathetic and sympathetic neurones possess neuropeptide Y Y2 receptors which, when activated, reduce neurotransmitter release.

Acetylcholine↗
PubMed1990

Action of potassium on neurochemical transmission at the cardiac adrenergic neuroeffector junction with aging.

The effect of age on potassium (K+)-induced norepinephrine release in the heart was studied in 6- and 24-month-old male Fischer-344 rats. Isolated hearts were perfused with Krebs-Ringer solution according to Langendorff method. K+ was employed as 2 ml bolus at the concentrations, of 70, 90, 100 and 120 microM. Norepinephrine content was measured by high pressure liquid-chromatography/electrochemical detection methodology. At each of the K- concentrations, the amount of norepinephrine released from preparations of 6-month-old animals was significantly greater than observed from preparations of 24-month-old animals. Since K(+)-induced release of norepinephrine is associated with calcium influx, the decrease in the capacity of K+ to cause norepinephrine release with age supports the hyothesis that diminution in transmitter release is due to altered calcium function.

Age Factors↗