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PubMed1990

Effects of pinacidil on isolated human corpus cavernosum penis.

Intracavernous injection of vasoactive agents causing vasodilatation is widely recognized in the diagnosis and treatment of erectile dysfunction. However, papaverine, the drug most commonly used for this purpose, may produce priapism and fibrotic lesions, and alternatives without these disadvantages are desirable. In this study we investigated the effects of pinacidil, a vasodilator drug supposed to act through the opening of K+ channels, on isolated human corpus cavernosum penis. Besides abolishing spontaneous contractile activity, pinacidil effectively relaxed preparations precontracted by noradrenaline 10(-6) M and inhibited contractions induced by electrical field stimulation of nerves. Furthermore, pinacidil depressed contractions induced by low-K+ solutions (less than or equal to 20 mM) and concentration-dependently increased the efflux of 86Rb from preloaded tissue. The results suggest that pinacidil is effective in relaxing isolated human erectile tissue, probably by way of increased K+ permeability and subsequent hyperpolarization. Clinical testing seems justified in order to find out if K(+)-channel openers can be used in the pharmacological treatment of impotence.

Aged↗

PubMed1989

Age-dependence of the effects of pinacidil on rat aorta.

The effect of the K+ channel opening drug, pinacidil, has been examined on aortic ring preparations from young (2 months) and aged (greater than 24 months) rats. The potency (neg log IC50) values for pinacidil in relaxing K+ (20 mM)-contracted preparations were in the range expected for its K+ channel opening (hyperpolarizing) effects but were not significantly different between young (6.34) and aged (6.31) rats. Thus, ageing does not affect the drug's potency as a K+ channel opening drug. The more marked depression of the maximum response to noradrenaline by pinacidil (10 microM) in aged rats (85% reduction) compared with young rats (43% reduction), reflected a reduced alpha-adrenoceptor reserve for noradrenaline in preparations from aged rats. Pinacidil, in concentrations greater than 10 microM, was able to relax preparations contracted with 80 mM K+ suggesting that it may have a second mechanism which does not involve hyperpolarization. It was more potent in producing this effect on the preparations from aged rats.

1-Methyl-3-isobutylxanthine↗

PubMed1993

Negative inotropic effect of pinacidil on the rat left atria.

Cromakalim at 50 microM and pinacidil at 0.1-10 microM had no effect, but pinacidil at 0.1 mM had a negative inotropic effect on the rat electrically-driven left atria without altering the positive inotropic responses to isoprenaline or phenylephrine alone. Glibenclamide had no effect but 4-aminopyridine, procaine (30 microM) and tetraethylammonium (3 mM) augmented the cardiac stimulation response. The ability of pinacidil to attenuate the cardiac stimulation response was not altered by glibenclamide, 4-aminopyridine or procaine but was prevented by pretreatment with tetraethylammonium. Thus, on the rat left atria, pinacidil has a negative inotropic effect which is unrelated to the opening of ATP-sensitive potassium channels, but may be due to opening the inward rectifying potassium channels.

Animals↗

PubMed2000

Differential response of K(ATP) channels containing SUR2A or SUR2B subunits to nucleotides and pinacidil.

ATP-sensitive K-channels (K(ATP) channels) are the target for K(ATP)-channel openers (KCOs), such as pinacidil and P1075. These channels are formed from pore-forming Kir6.2 and regulatory sulfonylurea receptors (SUR2A in heart and skeletal muscle; SUR2B in smooth muscle). The two isoforms of SUR2 differ only in their final 42 amino acids, a region that includes neither the Walker A and B nucleotide binding motifs nor the proposed KCO binding site, yet channels containing SUR2A or SUR2B respond differently to both nucleotides and KCOs. We explored the basis for this difference by expressing Kir6.2/SUR2A and Kir6.2/SUR2B currents in Xenopus laevis oocytes. Kir6.2/SUR2B but not Kir6.2/SUR2A currents were activated by the Mg-nucleoside triphosphates MgATP and MgGTP, whereas both channel types responded to the diphosphates MgADP and MgGDP. This activation of Kir6.2/SUR2B currents by MgATP explains how the ATP concentration-response curve is shifted to the right in the presence of Mg(2+). In the absence of nucleotide, pinacidil and P1075 activated Kir6.2/SUR2B and Kir6.2/SUR2A currents, but the presence of nucleotide slowed the drug off-rates. In the presence of MgATP, the response to pinacidil reversed approximately 14 times more slowly with SUR2B than SUR2A. The EC(50) for ATP, measured by its ability to slow the pinacidil off-rate, was also approximately 20 times higher for channels containing SUR2A than SUR2B. Our findings suggest that nucleotide binding and/or hydrolysis is enhanced in SUR2B compared with SUR2A, and that the greater KCO-affinities of SUR2B compared with SUR2A may be a consequence of this altered nucleotide handling.

Adenosine Triphosphate↗

PubMed2000

Pinacidil suppresses contractility and preserves energy but glibenclamide has no effect during muscle fatigue.

The effects of 10 microM glibenclamide, an ATP-sensitive K(+) (K(ATP)) channel blocker, and 100 microM pinacidil, a channel opener, were studied to determine how the K(ATP) channel affects mouse extensor digitorum longus (EDL) and soleus muscle during fatigue. Fatigue was elicited with 200-ms-long tetanic contractions every second. Glibenclamide did not affect rate and extent of fatigue, force recovery, or (86)Rb(+) fractional loss. The only effects of glibenclamide during fatigue were: an increase in resting tension (EDL and soleus), a depolarization of the cell membrane, a prolongation of the repolarization phase of action potential, and a greater ATP depletion in soleus. Pinacidil, on the other hand, increased the rate but not the extent of fatigue, abolished the normal increase in resting tension during fatigue, enhanced force recovery, and increased (86)Rb(+) fractional loss in both the EDL and soleus. During fatigue, the decreases in ATP and phosphocreatine of soleus muscle were less in the presence of pinacidil. The glibenclamide effects suggest that fatigue, elicited with intermittent contractions, activates few K(ATP) channels that affect resting tension and membrane potentials but not tetanic force, whereas opening the channel with pinacidil causes a faster decrease in tetanic force, improves force recovery, and helps in preserving energy.

Action Potentials↗

PubMed1990

Hypoglycemic sulfonylureas antagonize the effects of cromakalim and pinacidil on 86Rb fluxes and contractile activity in the rat aorta.

Cromakalim, pinacidil and nitroprusside provoked concentration-dependent relaxations of K(+)-depolarized rat aortae. Glibenclamide, tolbutamide and to a lesser extent tetraethylammonium antagonized the vasorelaxant action of cromakalim and pinacidil. Cromakalim, pinacidil but not nitroprusside elicited a marked increase in 86Rb outflow from preloaded and perifused aortic rings. These increases in 86Rb outflow were inhibited in a concentration-dependent manner by glibenclamide and tetraethylammonium. Our data extend previous observations indicating the involvement of K+ channels in the vasorelaxant properties of cromakalim and pinacidil. Moreover, the present findings suggest that both compounds could interfere with a vascular type of ATP-sensitive K+ channels.

Animals↗

PubMed2002

Effects of pinacidil on electrophysiological properties of epicardial border zone of healing canine infarcts: possible effects of K(ATP) channel activation.

BACKGROUND: K(ATP) channels, activated by ischemia, participate in the arrhythmogenic response to acute coronary occlusion. The function of these channels in border zones of healing infarcts, where arrhythmias also arise, has not been investigated. Do these channels remain maximally activated during infarct healing, or do they downregulate after a period of time? Both might preclude further activation. METHODS AND RESULTS: Myocardial infarction was produced in dogs by ligation of the left anterior descending coronary artery. Impulse propagation in the epicardial border zone (EBZ) of 4-day-old healing infarcts was mapped during administration of pinacidil, a K(ATP) channel activator, directly into the EBZ coronary blood supply. Pinacidil restored conduction and excitability when the EBZ was initially inexcitable and had large regions of block (6 of 8 experiments). This allowed reentrant circuits to form in the EBZ, causing tachycardia (4 of 8 experiments). In hearts with an initially excitable EBZ, pinacidil shortened the effective refractory period and abolished conduction block at short cycle lengths (7 experiments). This effect prevented initiation of reentry (1 of 2 experiments). CONCLUSIONS: The response to pinacidil indicates that K(ATP) channels in the EBZ remain functional and can be activated to influence electrophysiological properties and arrhythmogenesis.

Animals↗

PubMed2002

Alpha1-adrenoceptor-mediated breakdown of phosphatidylinositol 4,5-bisphosphate inhibits pinacidil-activated ATP-sensitive K+ currents in rat ventricular myocytes.

Phosphatidylinositol 4,5-bisphosphate (PIP2) stimulates ATP-sensitive K+ (K(ATP)) channel activity. Because phospholipase C (PLC) hydrolyzes membrane-bound PIP2, which in turn may potentially decrease K(ATP) channel activity, we investigated the effects of the alpha1-adrenoceptor-G(q)-PLC signal transduction axis on pinacidil-activated K(ATP) channel activity in adult rat and neonatal mouse ventricular myocytes. The alpha1-adrenoceptor agonist methoxamine (MTX) reversibly inhibited the pinacidil-activated K(ATP) current in a concentration-dependent manner (IC50 20.9+/-6.6 micromol/L). This inhibition did not occur when the specific alpha1-adrenoceptor antagonist, prazosin, was present. An involvement of G proteins is suggested by the ability of GDPbetaS to prevent this response. Blockade of PLC by U-73122 (2 micromol/L) or neomycin (2 mmol/L) attenuated the MTX-induced inhibition of K(ATP) channel activity. In contrast, the MTX response was unaffected by protein kinase C inhibition or stimulation by H-7 (100 micro mol/L) or phorbol 12,13-didecanoate. The MTX-induced inhibition became irreversible in the presence of wortmannin (20 micro mol/L), an inhibitor of phosphatidylinositol-4 kinase, which is expected to prevent membrane PIP2 replenishment. In excised inside-out patch membranes, pinacidil induced a significantly rightward shift of ATP sensitivity of the channel. This phenomenon was reversed by pretreatment of myocytes with MTX. Direct visualization of PIP2 subcellular distribution using a PLCdelta pleckstrin homology domain-green fluorescent protein fusion constructs revealed reversible translocation of green fluorescent protein fluorescence from the membrane to the cytosol after alpha1-adrenoceptor stimulation. Our data demonstrate that alpha1-adrenoceptor stimulation reduces the membrane PIP2 level, which in turn inhibits pinacidil-activated K(ATP) channels.

Adenosine Triphosphate↗

PubMed1991

Essential role of nucleotide diphosphates in nicorandil-mediated activation of cardiac ATP-sensitive K+ channel. A comparison with pinacidil and lemakalim.

Vasorelaxant agents such as pinacidil, lemakalim, and nicorandil, known as K+ channel openers, can activate the ATP-sensitive K+ channel (KATP channel) in cardiac myocytes. The aim of this study was to elucidate the molecular mechanisms underlying the K+ channel opener-mediated cardiac KATP channel activation by using the inside-out patch-clamp technique in guinea pig ventricular myocytes. Effects of pinacidil, lemakalim, and nicorandil on the KATP channel were examined both before and after channel "run-down". Since nucleotide diphosphates (NDPs) could activate the channel after complete run-down, effects of the drugs on the NDP-induced channel openings were also examined. We made the following observations: 1) Pinacidil (10-100 microM) and lemakalim (300 microM) activated the KATP channel before run-down and after run-down when NDPs were present. 2) Nicorandil (30 microM-1 mM) activated the KATP channel only in the presence of NDPs regardless of the condition of the channel with respect to run-down. 3) None of these K+ channel openers activated the channel after run-down in the absence of NDPs. These observations suggest that NDP binding is essential for nicorandil-mediated activation of the KATP channel and indicate that the molecular mechanisms underlying nicorandil activation are distinct from those of pinacidil and lemakalim activation of the KATP channel. We discuss the possible interactions between the drugs and the KATP channel based on a functional channel model.

Adenosine Diphosphate↗

PubMed1988

Ion channel effects of pinacidil in vascular muscle.

Cellular investigation of the vasodilator, pinacidil, was carried out to determine the membrane mechanisms leading to vascular muscle relaxation. Patch clamp recording of whole cell currents from isolated vascular muscle cells of rat azygos vein demonstrated a significant increase in K+ currents when 1 to 50 mumol/L pinacidil was added. The increases of K+ current by pinacidil were small (number of openings increased by 2%) when the recording pipette (and intracellular solution) contained 10 mmol/L EGTA, but were relatively large (50-300% increase in number of openings) when calcium in the intracellular solution was greater than 300 mumol/L. These observations suggest that pinacidil causes vasodilatation by increasing potassium conductance, primarily or completely via the large (200pS), calcium-dependent K+ channel.

Animals↗

PubMed1993

Urinary metabolites of pinacidil: I. Isolation and identification of the metabolites in rat urine.

1. The urinary metabolites of pinacidil administered orally to rats, were analysed by h.p.l.c. Seven metabolites were isolated from rat urine following fractionation on an HP-20 column and purified by t.l.c. 2. The major metabolite was pinacidil-pyridine-N-oxide (M-1). omega-Hydroxypinacidil (M-2) and dealkylpinacidil (M-3) were less abundant metabolites, and minor metabolites were the M-2-aldehyde, in which an intramolecular ring had formed (M-4), M-2-pyridine-N-oxide (M-5), carbamoyl-pinacidil (M-7) and M-7-pyridine-N-oxide (M-6). 3. Metabolic pathways of pinacidil in rats were postulated from the isolated metabolites.

Animals↗

PubMed2001

Pinacidil prevents membrane depolarisation and intracellular Ca2+ loading in single cardiomyocytes exposed to severe metabolic stress.

Recently, it has been proposed that, besides sarcolemmal K(ATP) channels, the activation of mitochondrial K(ATP) channels may also contribute to the cardioprotective action of potassium channel openers. In this respect, use of drugs that target both mitochondrial and sarcolemmal K(ATP) channels, such as pinacidil, may be a promising therapeutic strategy against metabolic injury of the heart. Therefore, the main objective of the present study was to determine whether pinacidil could maintain the value of resting membrane potential and intracellular Ca2+ homeostasis in cardiac cells exposed to metabolic stress. Experiments were performed on isolated ventricular cardiomyocytes. The membrane potential was monitored during experiments using whole cell patch clamp electrophysiology and the intracellular Ca2+ concentration was measured by a digital epifluorescence imaging. Chemical hypoxia-reoxygenation was induced by application and removal of the mitochondrial poison 2,4 dinitrophenol (DNP). Under hypoxia-reoxygenation, membrane depolarisation and intracellular Ca2+ loading was induced by Ca2+ influx during hypoxia and release of Ca2+ from intracellular stores during reoxygenation. The K(ATP) channel activator, pinacidil, prevented intracellular Ca2+ loading and membrane depolarisation, irrespective of whether the channel opener was applied throughout the duration of hypoxia-reoxygenation or transiently during the hypoxic or reoxygenation stage. Thus, the present study provides evidence that pinacidil, a non-selective K(ATP) channel opener, can handle membrane potential and intracellular Ca2+ homeostasis in cardiomyocytes under hypoxia-reoxygenation irrespective of the stage of the metabolic insult. This provides further evidence, at the single cell level, that targeting K(ATP) channels may be a valuable approach to protect the myocardium against metabolic challenge.

Animals↗

PubMed1999

Effect of pinacidil on the contractile response of cyclophosphamide-treated rat vas deferens.

Effect of pinacidil, a K+ channel opener, was studied on contractility of cyclophosphamide-treated rat vas deferens. The mean IC50 value of pinacidil against 1 mmol barium chloride induced rhythmic contractions and 40 mmol potassium chloride induced tonic contractions was significantly (P < 0.01 and P < 0.001, respectively) increased in the cyclophosphamide treated group as compared to the control. The mean EC50 value of norepinephrine (NE) in the presence of pinacidil (10(-6) mol) was significantly (P < 0.001) increased in the cyclophosphamide treated group. These findings indicate that the responsiveness of rat vas deferens smooth muscle to pinacidil is reduced following cyclophosphamide treatment.

Animals↗

PubMed2001

Myocardial protection of immature rabbits with an ATP-sensitive K+ channel opener pinacidil.

OBJECTIVE: To investigate the effectiveness of pinacidil, an opener of ATP-sensitive K+ channels, in protecting the myocardium of immature rabbit hearts from ischemic reperfusion injury. METHODS: Rabbit hearts underwent 30 min of global normothermic ischemia followed by 30 min of reperfusion on the modified Langendorff apparatus. Fifty-two isolated hearts of 3-4 week-old immature rabbits were divided into 4 groups randomly. During ischemia, 3 different cardioplegic solutions were administered intermittently by infusion every 15 min (20-25 ml each time in all groups). Group 1: control group (n = 13); group 2: Krebs-Henseleit (K-H) solution with potassium (16 mmol/L) (n = 13); group 3: K-H solution with potassium (16 mmol/L) and pinacidil (50 mumol/L) (n = 13); group 4: K-H solution with potassium (16 mmol/L), pinacidil (50 mumol/L) and glibenclamide (10 mumol/L) (n = 13). The pre-ischemic and post-ischemic myocardial functions were assessed by the percentage recovery of the left ventricular developed pressure (LVDP); the left ventricular end-diastolic pressure (LVEDP); both the positive peak and negative peaks of the first derivative of the left ventricular pressures (+/- dp/dtmax); coronary flow; the level of creatine kinase (CK), lactic dehydrogenase (LDH) and aspartate transcarbamoylase (AST) in coronary sinus venous effluent; and by myocardial ultrastructural changes. RESULTS: Before myocardial ischemia, there were no significant differences among the four groups in any of the parameters mentioned above. Post-ischemic recovery of LVDP, LVEDP, +/- dp/dtmax, coronary flow, the level of CK, LDH and AST, and myocardial ultrastructural changes were better in group 3 than those in the three other groups. CONCLUSIONS: As a new and effective composition, pinacidil can significantly improve myocardial protection from cardioplegia for immature rabbit hearts.

Animals↗

PubMed2000

[Laboratory study on protective and therapeutic effects of pinacidil on pulmonary vascular remodeling in rats with hypoxia-induced pulmonary hypertension].

OBJECTIVE: To investigate the protective and therapeutic effects of pinacidil on hypoxia-induced pulmonary hypertension(HPH) and pulmonary vascular remodeling. METHODS: 46 male Wister rats were divided into control group, hypoxic group and treated group (hypoxic rat treated with pinacidil for 4 weeks). Rat models with chronic HPH were established by chronic hypobaric hypoxia [(10 +/- 0.5)% O2, 4 weeks)]. The mean pulmonary arterial pressure (mPAP) and right ventricle/left ventricle and septum [RV/(LV + S)] were measured and the small pulmonary arterial morphologic changes were observed with morphmetric analysis under microscopes in three groups. RESULTS: (1) The level of mPAP(28.4 +/- 2.8) mm Hg and RV/(LV + S) (0.30 +/- 0.03) were significantly higher in the hypoxic group than (16.2 +/- 1.8) mm Hg and (0.22 +/- 0.03) in control group respectively (P < 0.01). Morphometry investigation showed that the external diameter became smaller and that ratio of vascular wall thickness to external diameter (MT%) (25.7 +/- 2.6)% and ratio of vascular wall area to total area (MA%) (75.3 +/- 5.6)% significantly increased in the hypoxic group. (2) The mPAP(23.3 +/- 2.6) mm Hg, RV/(LV + S) (0.27 +/- 0.04) and pulmonary vascular pathologic changes MT%(22.1 +/- 2.5)% and MA% (67.0 +/- 6.1)% significantly decreased in the treated group, indicating that pinacidil inhibited HPH and hypoxia-induced thickening and muscularization of small pulmonary arteria. CONCLUSION: Pinacidil may partly prevent the development of HPH and pulmonary vascular remodeling.

Animals↗

PubMed2001

Myocardial protection with pinacidil induced hyperpolarized arrest during cardiopulmonary bypass.

OBJECTIVE: To investigate the myocardial protective effects of pinacidil-induced hyperpolarized arrest and compare with those afforded by conventional depolarized hyperkalemic arrest. METHODS: Eighteen dogs were equally divided into three groups: normothermic hyperpolarized group (Group A), hypothermic hyperpolarized group (Group B), and hyperkalemic group (Group C). Pinacidil (50 mumol/L) containing 37 degrees C St. Thomas solution (K+ 5 mmol/L, 10 ml/kg), pinacidil (50 mumol/L, Sigma, USA) containing 4 degrees C St. Thomas solution (K+ 5 mmol/L, 10 ml/kg) and 4 degrees C standard St. Thomas solution (K+ 16 mmol/L, 10 ml/kg) were infused respectively through the aortic root after aortic-clamping. Heart arrest and its recovery, ultrastructure of the myocardium, the level of serum myocardial enzymes, and lipid peroxide and adenine nucleotide of the myocardium were measured. Hemodynamics during ischemia and after reperfusion were observed. RESULTS: The percentages of normal mitochondria and glycogen did not change much during ischemia (except at 60 min) and after reperfusion in B Group, but declined markedly in Group C 30 min and 60 min after ischemia and 20 min after reperfusion (P < 0.01). In Group A, they were lower than those of Group B before ischemia, but higher than those of Group C. The recoveries of CO, SV, CI, LVSW, RVSW and MAP in Group B were significantly better than those in other two groups 15 min and 30 min after reperfusion (P < 0.05 and 0.01, respectively). However, they were still better in Group A than those in Group C (P < 0.05 and 0.01, respectively). The onset of heart arrest was faster in Groups C and B than that in Group A. Highly elevated serum myocardial enzymes were observed 60 min after ischemia and 20 min after reperfusion in Group C, while they were only mild in the hyperpolarized groups, especially in Group B, and their recoveries were rapid. Adenine nucleotides of the myocardium were better preserved in Group B than in other two groups 30 min, 60 min after ischemia, and 20 min after reperfusion (P < 0.05 and 0.01, respectively). They were also much better in Group A than in Group C (P < 0.05 and 0.01, respectively). Lipid peroxide of the myocardium were significantly lower in Group B than in other groups 20 min after reperfusion (P < 0.01), and they were lower in Group A than in Group C (P < 0.05). CONCLUSIONS: Myocardial protection for global ischemia during cardiopulmonary bypass (CPB) could be achieved with hyperpolarized heart arrest induced by pinacidil, an ATP-sensitive potassium channel opener, especially in the hypothermic state. The protection is weaker in normothermia but is still superior to that with traditional depolarized hyperkalemic arrest.

Adenine Nucleotides↗

PubMed1992

Differential effects of diazoxide, cromakalim and pinacidil on adrenergic neurotransmission and 86Rb+ efflux in rat brain cortical slices.

The effects of diazoxide, cromakalim and pinacidil on depolarization-evoked tritium overflow from the rat brain cortical slices preloaded with [3H]noradrenaline were studied. Diazoxide inhibited both transmural nerve stimulation (TNS)- and 25 mM K(+)-evoked tritium overflows more potently than cromakalim. Diazoxide effects were only partially antagonized and cromakalim ones were totally reversed by 1 microM glibenclamide. Diazoxide, but not cromakalim, reduced the 45 mM K(+)-evoked tritium overflow, which was not antagonized by glibenclamide. Both diazoxide and cromakalim stimulated 86Rb+ efflux to a similar extent, the effects being completely abolished by glibenclamide. Glibenclamide (> or = 3 microM) by itself enhanced the TNS-evoked tritium overflow. Pinacidil increased both TNS- and K+ (25 and 45 mM)-evoked tritium overflows with little effect on 86Rb+ efflux. Pinacidil-induced increase in the TNS-evoked tritium overflow was still observed in the presence of cocaine or hydrocortisone. Pinacidil failed to affect the inhibitory action of xylazine on the TNS-evoked tritium overflow, whereas phentolamine attenuated it. These results indicate that ATP-sensitive K+ channels are present in the adrenergic nerve endings of rat brain. These channels seem to be pharmacologically different from those reported for vascular smooth muscles and pancreatic beta-cells.

Animals↗

PubMed1992

Assessment of pinacidil in patients with primary Raynaud's phenomenon.

In fourteen patients with primary Raynaud's phenomenon we performed a double-blind, controlled study, comparing single doses of 12.5 and 25 mg of the potassium channel opener pinacidil with placebo and the active control nifedipine in randomised order. The main response criterium was the area under the curve (AUC) of the photoelectric plethysmography (PEP) during cooling and rewarming, performed 2-3 hours after administration of the study medication. Single doses of 12.5 and 25 mg pinacidil were shown not to be superior to placebo in respect of the AUC of PEP. Nifedipine, on the contrary, was significantly better than placebo. We conclude that no efficacy can be expected from the potassium channel opener pinacidil in the treatment of primary Raynaud's phenomenon. The efficacy of nifedipine cannot be explained from central rheological effects, as total blood viscosity was the same after pinacidil, nifedipine and placebo.

Adult↗