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S N Wu

Publications and source records attributed to S N Wu.

At least 19 recordsLinked to original sources
PubMed1997

Influence of beta-adrenergic and vagal activity on the effect of exogenous adenosine on supraventricular tachycardia termination.

Adenosine, which binds to cell surface receptors and couples with guanosine triphosphate-binding inhibitory proteins (G(i)), is potent in terminating supraventricular tachycardia (SVT). However, whether the differences in autonomic tone will influence this effect remains unknown. This study was designed to investigate the role of beta-adrenergic and vagal activity on the action of adenosine. Forty patients with clinically documented SVT (22 with atrioventricular node reentrant tachycardia and 18 with atrioventricular reciprocating tachycardia) were divided into 4 groups with 10 patients in each group. In groups 1 and 2, adenosine was intravenously injected during the baseline state and during infusion of isoproterenol (2 and 4 microg/min, respectively). Group 2 patients received atropine (0.04 mg/kg) injection before isoproterenol infusion. In groups 3 and 4, intravenous injection of adenosine was given during the baseline state and after injection of atropine (0.02 and 0.04 mg/kg, respectively). Group 4 patients received propranolol (0.2 mg/kg) before atropine injection. The minimal dose of adenosine to terminate tachycardia during isoproterenol infusion of 2 microg/min was greater than that during the baseline state in both groups 1 and 2. The minimal dose of adenosine during isoproterenol infusion with 4 microg/min was higher than that with 2 microg/min in group 2, but not in group 1 patients. In both groups 3 and 4, the minimal dose of adenosine required to terminate tachycardia during atropine injection with 0.02 mg/kg was greater than that during the baseline state. The minimal effective dose of adenosine during atropine injection with 0.04 mg/kg was higher than that with 0.02 mg/kg in group 4, but not in group 3 patients. In conclusion, either limb of the autonomic nervous system may modulate the adenosine dosage required for termination of SVT. Patients taking drugs such as beta blockers or vagolytic agents may need alterations in the dose of adenosine for therapy.

Adenosine↗
PubMed1997

Ionic mechanisms of tetrandrine in cultured rat aortic smooth muscle cells.

The ionic mechanism of tetrandrine, an alkaloid extracted from the Chinese medicinal herb Radix stephania tetrandrae, was investigated in A7r5 vascular smooth muscle cells. The nystatin-perforated whole-cell voltage-clamp technique was performed to examine the effects of tetrandrine on ionic currents. Tetrandrine (1-100 microM) reversibly caused an inhibition of L-type voltage-dependent Ca2+ current (I(Ca,L)) in a concentration-dependent manner. Tetrandrine did not cause any change in the overall shape of the current-voltage relationship of I(Ca,L). The IC50 value of tetrandrine-induced inhibition of I(Ca,L) was 5 microM. In the presence of Bay K 8644 (3 microM) or cyclopiazonic acid (30 microM), tetrandrine still produced a significant inhibition of I(Ca,L). The inhibitory effects of tetrandrine on I(Ca,L) exhibited tonic and use-dependent characteristics. Moreover. tetrandrine (3 microM) shifted the steady-state inactivation curve of I(Ca,L) to more negative membrane potentials by approximately -15 mV. These results indicate that tetrandrine directly inhibits the voltage-dependent L-type Ca2+ current in vascular smooth muscle cells, which may predominantly contribute to the vasodilatory actions of tetrandrine.

Alkaloids↗
PubMed1997

Differential effects of adenosine on antegrade and retrograde fast pathway conduction in atrioventricular nodal reentry.

Although adenosine depresses antegrade atrioventricular (AV) nodal conduction, the effects of adenosine on antegrade and retrograde fast pathway conduction in AV nodal reentry have not been determined. In 17 patients (five men, 12 women, mean age 49 +/- 12 years) with common slow-fast AV nodal reentrant tachycardia, the antegrade slow pathway conduction was selectively and completely ablated by radiofrequency catheter ablation while the antegrade and retrograde fast pathway conduction remained intact. During high right atrial pacing at a mean pacing cycle length of 474 +/- 36 msec, adenosine was rapidly injected intravenously at an initial dose of 0.5 mg followed by stepwise increases of 0.5 mg or 1.0 mg given at 5-minute intervals until second-degree AV block developed. During right ventricular apical pacing at the same pacing cycle lengths (mean 474 +/- 36 msec) as those in the study of antegrade conduction, intravenous injection of incremental doses of adenosine was repeated until ventriculoatrial (VA) block occurred. The adenosine-induced prolongation of VA conduction was also determined in the presence of verapamil (loading dose 0.15 mg/kg, maintenance dose 0.005 mg/kg/min) in seven of 17 patients. The dose of adenosine required to produce AV block, the increase in the atrio-His interval by 50% and the maximal response were 3.4 +/- 1.4 mg, 1.8 +/- 0.6 mg, and 58% +/- 5%, respectively. On the other hand, the dose of adenosine required to produce VA block, the increase in the VA interval by 50%, and the maximal response were 8.2 +/- 2.9 mg, 3.4 +/- 0.6 mg, and 20% +/- 5%, respectively, in the control and 3.7 +/- 0.5 mg, 3.5 +/- 0.7 mg, and 23% +/- 5%, respectively, in the presence of verapamil. In conclusion, adenosine has a differential potency to depress AV and VA conduction in patients with AV nodal reentry, with greater potency for slowing antegrade fast than retrograde fast pathway conduction. Verapamil had an additive effect to adenosine on slowing retrograde VA conduction, which further supports the evidence that the retrograde fast pathway in part involves an AV nodal-like structure.

Adenosine↗
PubMed1997

Glyceryl nonivamide: a capsaicin derivative with cardiac calcitonin gene-related peptide releasing, K+ channel opening and vasorelaxant properties.

In this study, the aorta vasorelaxant, coronary calcitonin gene-related peptide (CGRP) releasing, and atrial contractility effects of glyceryl nonivamide (GLNVA) were investigated in guinea pigs. In the isolated thoracic aorta, although GLNVA (0.01-50 microM) concentration dependently induced endothelium-independent relaxations and relaxed phenylephrine-(1.0 microM) induced contractions, it failed to relax 80 mM KCI-induced contractions. The GLNVA (1.0 microM) relaxation response in the aorta was significantly inhibited by tetraethylammonium (2.5-10 mM) or ouabain (5.0 microM) and was attenuated by increased extracellular potassium gradient (10-30 mM). Glibenclamide (0.01-10 microM) dose dependently antagonized the GLNVA relaxant effect. In the isolated perfused guinea pig heart, GLNVA (0.1-10 microM) increased CGRP-like immunoreactivity outflow from coronary circulation in a concentration-dependent manner. In the isolated right and left guinea pig atria, GLNVA (0.01-10 microM) produced concentration-dependent positive inotropic and chronotropic effects, but these effects were inhibited by pretreatments with ruthenium red (1.0 microM), capsazepine (10 microM), human calcitonin-gene-related peptide (CGRP(8-37)) (1.0 microM) and sensory neuron denervation, respectively. Based on these findings, we suggest that CGRP may be released by GLNVA from cardiovascular sensory neuron, and it then activates CGRP receptors on the coronary artery and atrium. The GLNVA-induced vasorelaxant effect in the vascular smooth muscle of the aorta is due to CGRP release associated K+ channel opening, and this effect eliminates capsaicin-derived excitability-associated K+ channel blocking activities.

Animals↗
PubMed1996

Volume-sensitive chloride channels in the primary culture cells of human cervical carcinoma.

Previous study shows volume-sensitive chloride currents are induced by hypotonicity in human cervical cancer cell lines, but not in normal cervical epithelium. To ascertain whether the preferential activation of these channels in cancer cell lines could be similarly and directly detected in cervical cancer tissues, we studied volume-sensitive chloride channels on the primary culture cells of invasive cervical carcinoma using the whole-cell patch-clamp technique. The process of regulatory volume decrease (RVD) was also studied using electronic cell sizing to measure cell volume. Results demonstrate that, in these cultured cells, RVD was mediated in part by chloride loss through the volume-sensitive Cl- channels. A small background current with a slope conductance of 0.32 +/- 0.07 nS/pF at +30 mV (n=60 cells from 10 different samples) was observed. Hypotonicity induced a fast activating and outward rectifying current which was reversed at about 0 mV, and the slope conductance at +30 mV was increased by 10-fold to 3.62 +/- 0.62 nS/pF. These effects were readily reversed by returning the cells to isotonic medium. Moreover, DIDS, NPPB, and 1,9-dideoxyforskolin, reversibly abolished the volume-sensitive Cl- currents. The EC50 required for the inhibitory effect of DIDS, NPPB and 1,9-dideoxyforskolin was 150, 120, and 50 microM, respectively. Volume-sensitive Cl- channels were ubiquitously expressed in cultured cells from 10 samples of different cancer stages, histopathologic types, and state of HPV DNA positivity. Interestingly, similar outward rectifying chloride currents were activated by intracellular 300 microM GTP gamma S. It is proposed that this Cl- conductance may play an important role leading to RVD in human cervical cancer.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1996

Endothelin-1 and vasopressin activate Ca(2+)-permeable non-selective cation channels in aortic smooth muscle cells: mechanism of receptor-mediated Ca2+ influx.

The effects of vasopressin and endothelin-1 on cultured aortic smooth muscle cell lines (A7r5) were investigated by measurements of intracellular calcium [Ca2+]i and the patch-clamp techniques. Vasopressin and endothelin-1 (100 nM) evoked an initial peak followed by a smaller sustained rise of [Ca2+]i in the presence of extracellular calcium [Ca2+]o. In the absence of [Ca2+]o, only the initial peak of [Ca2+]i was observed. Therefore, the initial peak of [Ca2+]i was mainly due to calcium release from the storage sites, whereas the later sustained rise of [Ca2+]i was due to the calcium entry from outside. The sustained rise of [Ca2+]i was unaffected by nifedipine (10 microM) significantly, but was completely abolished by La3+ (1 mM). Under current clamp conditions with K(+)-internal solution, vasopressin and endothelin-1 (100 nM) produced hyperpolarization, then followed by depolarization. Under voltage clamp conditions at a holding potential of -40 mV, both vasopressin and endothelin-1 first activated the outward current, then followed by a long-lasting inward current with a high noise level. The first outward current was abolished by charybdotoxin (100 nM), Cs+ in the patch pipette and high EGTA (10 mM) in the pipette, suggesting that it was a Ca(2+)-sensitive K+ current (IK.Ca). The inward current was still elicited with the patch pipette containing Cs(+)-internal solution, and reversed at about 0 mV. The reversal potential was not significantly altered by the replacement of [Cl-]i or [Cl-]o, proposing that the inward current is a cation selective channel (IN.S.). The inward current was also observed even when extracellular cations are Ca2+. La3+ (1 mM), Cd2+ (1 mM) completely abolished the vasopressin-induced (IN.S.), however, nifedipine (10 microM) failed to inhibit it significantly. Single channel activities were recorded in the cell-attached configurations when vasopressin or endothelin-1 was applied to the bathing solution. The unitary conductance of the channels was approximately 20 pS with 140 mM Na+, Cs+, or K+ in the pipette, but was 15 pS with 110 mM Ca2+ in the pipette. Permeabilities sequence calculated from the reversal potentials was Na+ not equal to Cs+ not equal to K+ > Ca+. These results provide evidence that calcium entry and membrane depolarization elicited by vasopressin or endothelin-1 are mediated by a receptor-mediated Ca(2+)-permeable non-selective cation channel in aortic smooth muscle cells.

Aorta, Thoracic↗
PubMed1996

Effects of verapamil, propranolol, and procainamide on adenosine-induced negative dromotropism in human beings.

Adenosine, verapamil, propranolol, and procainamide are widely used antiarrhythmic drugs. The interactions among them are still not known in human beings. Adenosine-induced negative dromotropic effects were assessed by rapid bolus injection of adenosine during constant high right atrial pacing in each patient. The initial dose of adenosine was 0.5 mg and was followed by a stepwise increment of 0.5 mg until atrioventricular (AV) nodal block occurred. The negative dromotropic actions of adenosine were examined in the control state and in the following three protocols in three groups of patients: (1) In 12 patients (group 1), intravenous verapamil, 0.15 mg/kg, was given; (2) In 12 patients (group 2), intravenous propranolol, 0.1 mg/kg, was given; and (3) in 10 patients (group 3), intravenous procainamide, 15 mg/kg, was given. The dose-response curves of adenosine on AV nodal conduction were almost identical in the control state and after verapamil, propranolol, or procainamide injection. However, verapamil, in contrast to propranolol, significantly reduced the dose of adenosine required to produce AV nodal block, from 4.4 +/- 0.7 mg to 2.7 +/- 0.3 mg (p < 0.01). Of note, procainamide exerted no significant effects on adenosine-induced negative dromotropism on AV nodal conduction or AV nodal block. In conclusion, the negative dromotropic effects of adenosine are preserved and independent even in the presence of verapamil, propranolol, or procainamide. Both verapamil and propranolol can exhibit additive effects with adenosine in prolonging AV nodal conduction time; however, only verapamil can reduce the dose of adenosine required to produce AV nodal block. This finding indicates that the dose of adenosine may be reduced for patients who have already been treated with verapamil.

Adenosine↗
PubMed1996

Analytical studies of spontaneous and vasopressin-induced calcium oscillations in cultured vascular smooth muscle cells.

Spontaneous and vasopressin-induced Ca2+ oscillations in cultured vascular smooth muscle (A7r5) cells were further examined and characterized. Intracellular Ca2+ concentrations ([Ca2+]i) were measured by use of a high-performance laser cytometer. When the oscillatory patterns in [Ca2+]i were analyzed with a power spectrum method, about 80% of cells exhibited spontaneous Ca2+ oscillations with the frequency of 0.02-0.5 Hz. Nifedipine abolished these repetitive spikes, whereas pinacidil partially attenuated their amplitude and frequency. When vasopressin (100 nM) was applied to A7r5 cells, there was an initial rise in [Ca2+]i, followed by a delayed sustained increase in [Ca2+]i. The one-pool, nonoscillatory model was employed to fit this biphasic change, and the difference between the observed response and the simulated response was then analyzed with a power spectral method. About 50% of cells were noted to display oscillatory patterns in [Ca2+]i after sustained increase in [Ca2+]i. The present study indicates that spontaneous Ca2+ oscillations in A7r5 cells are modulated by the activity of ATP-sensitive K+ channels and are not related to pertussis toxin-sensitive GTP-binding protein(s). On the basis of the one-pool, nonoscillatory model, it is suggested that the buffering capacity of internal stores appears to be stronger in the cells with spontaneous Ca2+ oscillations than in those in a quiescent state, and the vasopressin-mediated inhibition of accumulation by internal stores was attenuated when the cells exhibited spontaneous Ca2+ oscillations. The implementation of this minimum kinetic model integrated with a power spectrum method would be an alternative to understand the oscillating behavior in [Ca2+]i.

Adenosine Triphosphate↗
PubMed1996

Analysis of mechanical restitution and post-rest potentiation in isolated rat atrium.

Mechanical restitution and post-rest potentiation in isolated rat atria were studied in order to understand the intracellular Ca2+ handling during stimulation and interbeat interval. Various agents known to affect transmembrane Ca2+ inward current or Ca2+ accumulation of the sarcoplasmic reticulum were examined. The tissues were stimulated at 1 Hz and ectopic stimuli of different preceding intervals were driven by a programmable stimulator. The relationship between the force produced by the ectopic contraction and the duration of the preceding interval was plotted to construct mechanical restitution curves. Mechanical restitution curve was well fitted to two exponential processes, i.e., an early rapid phase followed by a slowly rising phase. It is suggested that the time constant in early phase (tau 1) of mechanical restitution curve is dependent on the reactivation of transmembrane Ca2+ inward currents as well as the translocation of Ca2+ within the sarcoplasmic reticulum. However, the time constant in late phase (tau 2) involves the rate of Ca2+ influx or efflux possibly via the Na+/Ca2+ exchange mechanism. The present studies suggest that in rat myocardium, verapamil enhances the buffering capacity of the sarcoplasmic reticulum inside the cell, while isoproterenol appears to short circuit the buffering barrier of the sarcoplasmic reticulum and enhance the flow of Ca2+ into the cytosol. Ryanodine, which accelerates the Ca2+ release from the sarcoplasmic reticulum, is believed to attenuate its buffering capacity. The present analytical methods to which the mechanical restitution and the post-rest potentiation are combined would represent a good model for the study of beat-to-beat intracellular Ca2+ handling in cardiac muscle.

Animals↗
PubMed1995

Volume-sensitive chloride channels associated with human cervical carcinogenesis.

Previous controversy has risen from the purported equivalence of the volume-sensitive chloride channels with P-glycoprotein. The aim of this study was to investigate the association between expression of volume-sensitive Cl- channels and the process of malignant transformation of cervical epithelial cells. We studied the activations of volume-sensitive and cAMP-mediated chloride currents in various human cervical squamous cells that were representative of different stages of cervical carcinogenesis, i.e., normal cervical epithelium, low-grade cervical intraepithelial neoplasia, carcinoma in situ, and invasive carcinoma using the whole-cell patch clamp technique. The volume-sensitive chloride channels, however, were significantly activated only in the four cervical cancer cell lines, primary culture cells of carcinoma in situ, and invasive cancer of the cervix. The expression of volume-sensitive chloride currents was independent of the state of human papillomavirus positivity. When these cells were exposed to hypotonic shock, the cells swelled, and outward rectified chloride currents were observed. These effects were readily reversed by returning the cells to isotonic medium. In addition, 4,4'-diisothiocyanatostilbene-2,2-disulfonic acid, 1,9-dideoxyforskolin, and verapamil reversibly abolished the volume-sensitive Cl- currents. In contrast, none of the cells from normal cervices and human papillomavirus-immortalized cell lines, the in vitro equivalent of low-grade cervical intraepithelial neoplasia, developed substantial chloride currents on exposure to hypotonicity. cAMP-mediated chloride currents were ubiquitously activated in all cervical squamous cells, regardless of the stages of carcinogenesis. This is the first report suggesting an in vivo association between the development of volume-sensitive chloride currents and human carcinogenesis.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1995

Effect of capsaicin on membrane currents in cultured vascular smooth muscle cells of rat aorta.

The application of capsaicin (1 microM) produced a minor relaxant effect in endothelium-denuded rat aortae. However, capsaicin caused a greater relaxation of blood vessels precontracted with high K+ or phenylephrine. The effects of capsaicin on the ionic currents were also examined in A7r5 vascular smooth muscle cells. The tight-seal whole-cell voltage clamp technique was used. Capsaicin inhibited the Ba2+ inward current (IBa) through the voltage-dependent L-type Ca2+ channel in a concentration-dependent fashion, whereas calcitonin gene-related peptide and phenylephrine produced a minor increase in IBa. Capsaicin did not alter the overall shape of current-voltage relationship of IBa. However, capsaicin (3 microM) shifted the quasi-steady-state inactivation curve of IBa to more negative membrane potential by about 5 mV. These effects of capsaicin on IBa were reversible. In addition, capsaicin had inhibitory effects on voltage dependent K+ currents. These results suggest that inhibition of the voltage-dependent L-type Ca2+ channel is involved in the capsaicin-induced relaxation of the vascular smooth muscle, whereas capsaicin-induced inhibition of voltage-dependent K+ channels might produce an increase in cell excitability.

Animals↗
PubMed1995

Induction of Ca2+ oscillations by vasopressin in the presence of tetraethylammonium chloride in cultured vascular smooth muscle cells.

The change of cytosolic Ca2+ concentration ([Ca2+]i) caused by vasopressin was examined in indo-1-loaded A7r5 smooth muscle cells by use of the high-performance laser cytometer and ratiometric fluorescence method. Vasopressin (100 nM) caused an initial rapid rise and a delayed increase in [Ca2+]i (n = 6). However, in the presence of tetraethylammonium chloride (10 mM), vasopressin consistently triggered sustained Ca2+ oscillations which were preceded by a large peak of [Ca2+]i. The latency for the development of this huge increase in [Ca2+]i prior to the occurrence of sustained Ca2+ oscillations was always the same. The frequency and amplitude of this type of Ca2+ oscillation varied depending upon the extracellular Ca2+ concentration. Ca(2+)-free solution did not completely suppress the sustained Ca2+ oscillations, but caffeine (20 mM) effectively abolished them. The present findings indicate that in A7r5 smooth muscle cells, the sustained Ca2+ oscillations triggered by vasopressin in the presence of tetraethylammonium chloride were mainly due to Ca2+ release from IP3-sensitive Ca2+ stores and Ca2+ influx from extracellular space, and did not require the pacemaker activity derived from the surface membrane. Moreover, the vasopressin-induced change in [Ca2+]i appeared to be linked to pertussis toxin-insensitive GTP-binding protein(s).

Animals↗
PubMed1995

Inhibitory effect of ethanol on voltage-dependent potassium currents in single aortic smooth muscle cells.

The effect of ethanol on voltage-dependent K+ currents was examined in single aortic smooth muscle cells. The aortic smooth muscle cells were isolated from guinea pigs. The tight-seal patch clamp technique in whole cell configuration was employed. Ethanol (500 mM) reversibly inhibited voltage-dependent transient outward K+ current, the spontaneous transient oscillatory K+ current (STOC) and steady-state K+ current, whereas ethanol (50 mM) did not produce any change in these K+ currents. When the peak-height amplitudes of STOC were analyzed, the application of ethanol (50 mM) was noted to produce significant inhibition on both amplitude and frequency of STOC evoked at the holding potential of +10 mV. The results shown in the present study indicate that ethanol-induced inhibition of the voltage-dependent K+ channel, which is not required for the elicitation of either GTP-binding protein(s) or inositol triphosphate, may contribute to its vasoconstrictor effect because the inhibition of the voltage-dependent K+ channel may lead to the increase of cell excitability in vascular smooth muscle.

Animals↗
PubMed1994

Molecular mechanism of cibenzoline-induced anticholinergic action in single atrial myocytes: comparison with effect of disopyramide.

The anticholinergic effects of cibenzoline were examined and compared with those of disopyramide in atrial myocytes isolated from guinea pig heart. The tight-seal whole-cell voltage clamp technique was performed with a patch pipette filled with guanosine-5'-triphosphate (GTP) or guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S). In GTP-loaded cells, both acetylcholine (ACh) and adenosine (Ado) induced a specific K channel current through GTP-binding proteins by binding to the muscarinic and Ado receptors, respectively. Both cibenzoline and disopyramide suppressed the ACh-induced K current effectively in a concentration-dependent manner. The concentrations for half-maximal inhibition of the current (EC50) caused by cibenzoline and disopyramide were 8 and 3 microM, respectively. In GTP gamma S-loaded cells, the K current was irreversibly activated because GTP binding proteins were directly elicited by GTP gamma S. Cibenzoline effectively caused a decrease in the GTP gamma S-induced K current, whereas the extent of disopyramide action on the GTP gamma S-induced K current was much less. Cibenzoline also caused significant inhibition of Ado-induced K current in GTP-loaded cells. However, the action of disopyramide was less effective in inhibiting Ado-induced K current. These results indicate that cibenzoline has less potent anticholinergic effects than disopyramide in atrial myocytes. In addition, cibenzoline effectively inhibits the muscarinic K channel itself and/or GTP-binding proteins coupled to the channel, whereas the effect of disopyramide is attributed mainly to blockade of muscarinic receptors. These findings provide novel understanding of the molecular mechanism of anticholinergic action of cibenzoline.

Animals↗
PubMed1994

Adenosine modulation of neurotransmission in penile erection.

1. Adenosine inhibited the noradrenaline-induced contraction of rabbit corpus cavernosum in a dose-dependent manner. The effect of adenosine was greater in intact corpus cavernosa than in endothelium-denuded preparations. This finding indicates that the relaxing effect of adenosine is partially endothelium-dependent and involved in the release of endothelium-derived relaxing factors. 2. Adenosine and its analogues relaxed the noradrenaline-induced contractile response as well as inhibited the transmural nerve induced contraction with the potency order: NECA > R-PIA > adenosine. These data indicate that adenosine can modulate both the non-adrenergic non-cholinergic and adrenergic neurotransmission. DMPX, an adenosine antagonist selective for the A2 receptors, abolished the electrically elicited relaxation. However, CGS 21680, selective for A2a receptor, had no effect on relaxation. Therefore, adenosine receptors involved in the modulation of neurotransmission in rabbit corpus cavernosum appear to be A2b subtype. 3. Adenosine also induced an increase in human cavernosal arterial velocity and resistive index measured by colour duplex sonography. The combination of adenosine and 10 micrograms prostaglandin E1 was more effective in resistive index and erection grade than 20 micrograms prostaglandin E1 alone. Our results suggest that adenosine seems to be an important neuromodulator for penile erection and can be an effective and alternative combination in the treatment of impotence.

Adenosine↗
PubMed1994

Rate-dependent properties of adenosine-induced negative dromotropism in humans.

BACKGROUND: The antiarrhythmic effects of sodium channel and calcium channel blockers are known to be rate dependent. Little is known about the rate-dependent effect of adenosine on human atrioventricular (AV) nodal conduction. The purpose of this study was to determine whether the negative dromotropic effect of adenosine is dependent on heart rate. METHODS AND RESULTS: Atrial pacing at 20-millisecond increments decreasing stepwise was performed, and the curves that relate the AH interval to the atrial pacing cycle length were analyzed. The change in AV nodal function was evaluated in three protocols: (1) In 8 group 1A and 6 group 1B patients, an intravenous infusion of adenosine at a dose of 140 and 320 micrograms.kg-1.min-1 was given, respectively; (2) a bolus injection of a fixed dose of adenosine was given to 12 group 2A patients without and 6 group 2B patients with propranolol (0.1 mg/kg) treatment; and (3) in 12 group 3 patients, the AV nodal function was evaluated after intravenous propranolol (0.05 mg/kg) and after subsequent intravenous aminophylline (loading dose, 5 mg/kg; maintenance dose, 0.9 mg.kg-1.h-1). No significant depression of AV nodal function could be demonstrated during intravenous infusion of adenosine. The bolus injection of adenosine could prolong the AH interval, which was dependent on heart rate and more significant at a shorter pacing cycle length. Intravenous propranolol significantly depressed the AV nodal conduction and shifted the curves of the AH interval versus the pacing cycle length to the right. Subsequent intravenous aminophylline shortened the AV nodal conduction time, however, in a rate-independent manner. CONCLUSIONS: The negative dromotropic effects induced by intravenous bolus injection of adenosine became more pronounced at fast atrial pacing rates. These results indicate that adenosine causes rate-dependent prolongation of AV nodal conduction in humans.

Adenosine↗