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Effects on potassium channels

In pituitary adenoma cells, dopamine was found to activate K+ currents through D2 type receptor, leading to cell hyperpolarization (Israel et al., 1985). Similar effects have been described in lactotroph and melanotroph cells in the anterior pituitary as well as in the mesencephalic neurons in the CNS (Israel et al., 1985 Lacey et al., 1988 Greif et al., 1995). The K+ current-induced hyperpolarization appears to underlie the inhibition of DA release mediated by D2 autoreceptors in dopamine neurons and of prolactin release in lactotroph cells. In particular, the blockade of K+ channel by 4-aminopyridine or tetramethylammonium abolished the inhibitory effect of D2 agonists on DA release (Bowyer and Weiner, 1989 Cass and Zahniser, 1991 Tang et al., 1994a). [Pg.125]

In striatal neurons, the effects of D2 receptor activation on K+ channels are more complex. Stimulation of the D2 receptor has been reported to open a K+ channel that displays a 85 pS conductance and a weak inward rectification, and this rectification seems to differ from that found in pituitary cells (Freedman and Weight, 1988 Einhorn et al., 1991 Greif et al., 1995). In contrast, D2 receptor activation was also reported to suppress K+ currents probably through Kir2 channels (Uchimura and North, 1990). However, the activation of K+ channels occurs in a membrane-delimited manner via Gpy mobilization, whereas inhibition of K+ channels could result from the D2 receptor mediated inhibition of adenylyl cyclase and the dephosphorylation of Kir2 subunit at its PKA sensitive site (Nicola et al., 2000). [Pg.125]


Carboxylic acids Valproic acid (Depakene, Depakote, others) Unclear may hyperpolarize membrane through an effect on potassium channels higher concentrations increase CNS GABA concentrations... [Pg.108]

The o-GTP complexes related to somatostatin receptors exert effects on potassium channels, thereby inhibiting GH secretion. [Pg.851]

D2R activation also increases outward potassium currents, leading to cell hyperpolarization in a number of preparations (Castelletti et al., 1989 Vallar et al., 1990 Einhorn et al., 1991 Lledo et al., 1992 Kitai and Surmeier, 1993). Although the effect on potassium channels has been established as G-protein-dependent, the a-subunit involved appears to differ with the tissue used, as in the pituitary Gai3 plays an essential role (Baertschi et al., 1992 Lledo et al., 1992), whereas Ga0 is involved in preparations from the rat mesencephalon (Liu et al., 1994a). [Pg.161]

Such severe generalized weakness and hypokalemia may be due to intracellular shift of potassium due to adrenergic stimulation by cocaine or a direct effect on potassium channels. [Pg.506]

Women appear to be at an increased risk of torsades de pointes because the baseline heart rate-corrected QT interval in women is, on average, longer than it is in men (103). The length of the QT interval is similar in males and females at birth, but shortens in males at puberty. The risk of this arrhythmia shows no sex difference before adolescence, and women have an increased incidence of torsades de pointes only after puberty. These observations are consistent with the fact that sex hormones affect potassium channel activity. Thus, estrogens have a down-regulating effect on potassium channel activity and androgens may be responsible for the QT interval shortening that is seen in postpubertal males (95, 96, 104). [Pg.331]

Antidysrhjhhmic drugs with class III activity prolong the total action potential duration. These drugs act by effects on potassium channels, altering the rate of repolarization. [Pg.268]

A schematic representation of how a decrease in oxygen tension (hypoxia) may affect carotid body glomus cell function. In the mitochondrial model, hypoxia affects either reactive oxygen species (ROS) production or ATP production of mitochondria. Both of these may affect the outward flux of potassium via the potassium channel with the downstream effects shown in the diagram. In the membrane model, the ROS production by membrane-bound molecules (cytochromes) is oxygen sensitive, and thereby affected by hypoxia. Thus, these membrane-bound molecules function as proximal oxygen sensors and cause effects on potassium channels with the downstream effects described in the figure and in the text... [Pg.286]

G protein effect on potassium channels. Adenosine release by CN must be considered a factor in CN-induced neural injury. [Pg.319]

Stein CM, Brown N, Carlson MG, Campbell P, Wood AJJ. Coadm inistration of glyburide and minoxidil, drugs with ojposing effects on potassium channels. Clin Pharmacol Ther (1997) 61,662-8. [Pg.898]

Dofetilide s mechanism of action involves blockade of the cardiac ion channel that carries the rapid component of the delayed rectifier potassium current, IKr. Dofetilide inhibits IKr with no significant effects on other repolarizing potassium currents (e.g., IKs, IKl) over a wide range of concentrations. At plasma concentrations within the therapeutic range, dofetilide has no effect on sodium channels or on either i- or p-adreno-ceptors. [Pg.189]

Mechanism of Action A selective potassium channel blocker that prolongs repolar-ization without affecting conduction velocity by blocking one or more time-dependent potassium currents. Dofetilide has no effect on sodium channels or adrenergic alpha or beta receptors. Therapeutic Effect Terminates reentrant tachyarrhythmias,... [Pg.389]

Local anesthetic action, also known as "membrane-stabilizing" action, is a prominent effect of several 3 blockers (Table 10-2). This action is the result of typical local anesthetic blockade of sodium channels (see Chapter 26) and can be demonstrated experimentally in isolated neurons, heart muscle, and skeletal muscle membrane. However, it is unlikely that this effect is important after systemic administration of these drugs, since the concentration in plasma usually achieved by these routes is too low for the anesthetic effects to be evident. These membrane-stabilizing 3 blockers are not used topically on the eye, where local anesthesia of the cornea would be highly undesirable. Sotalol is a nonselective 3-receptor antagonist that lacks local anesthetic action but has marked class III antiarrhythmic effects, reflecting potassium channel blockade (see Chapter 14). [Pg.210]

Rubidium exhibits a very high flux through potassium ion channels. Upon depolarization, this flux can be quantified as a measure of channel integrity (Tang et al. 2001 Chang et al. 2002). Fluorometric assays have been developed that can detect drug-induced effects on hERG channels. [Pg.73]

The Intent of these studies was to determine whether phosphorus and potassium/phosphorus chemistry would have a significant effect on MHD channel conductivity. Preliminary efforts are described below. [Pg.603]

Yamamoto T, Kakehata S, Yamada T, Saito T, Saito H, et al. 1997. Effects of potassium channel blockers on the acetylcholine-induced currents in dissociated outer hair cells of guinea pig cochlea. Neurosci Lett 236 79-82. [Pg.108]

Activated CBi receptors can also change fhe function of several types of potassium channels. In oocytes and AtT20 cells artificially expressing the CBi receptor, stimulation of inwardly rectifying potassium channels was repeatedly observed (Henry and Chavkin 1995 Mackie et al. 1995 Garcia et al. 1998 McAllister et al. 1999). Potassium A currents in cultured hippocampal neurons are stimulated by cannabinoids (Deadwyler et al. 1995 Mu et al. 2000). The effects of cannabinoids on potassium M currents in hippocampal brain slices have also been studied M currents were inhibited, which means an enhancement of neuronal excitability (Schweitzer 2000). The potassium K current is inhibited by cannabinoids in cultured hippocampal neurons (Hampson et al. 2000). As in the case of calcium channels, anandamide can elicit a CBi receptor-independent effect on potassium... [Pg.329]

Singer and colleagues studied the effect of non-esterified arachidonate on potassium channels by dissolving the fatty acid in the bathing medium and perfusing it on the inside of the smooth muscle membrane (in the inside-out configuration) or on its outside (in the outside-out configuration). In either case, they found that application of micromolar concentrations of the fatty acid would cause the activation of a potassium-selective channel (Fig. 3.6). This effect was not mediated by the formation of... [Pg.64]

Batrachotoxin has no effect on a calcium channel (18), or on potassium channels (795). However, batrachotoxin does appear to antagonize the increase in conductance elicited by nicotinic agonists in striated neuromuscular preparations (111) and adrenal glands (164, 165). The mechanism involved in inhibition of nicotinic receptor-controlled conductances by batrachotoxin remains unclear but actually might represent another site of action for the alkaloid. Batrachotoxin, however, has no effect on binding of a-bungarotoxin or histrionicotoxin to the acetylcholine receptor-channel... [Pg.229]

There ate many classes of anticonvulsant agent in use, many associated with side effect HabiUties of unknown etiology. Despite many years of clinical use, the mechanism of action of many anticonvulsant dmgs, with the exception of the BZs, remains unclear and may reflect multiple effects on different systems, the summation of which results in the anticonvulsant activity. The pharmacophore stmctures involved are diverse and as of this writing there is htde evidence for a common mechanism of action. Some consensus is evolving, however, in regard to effects on sodium and potassium channels (16) to reduce CNS excitation owing to convulsive episodes. [Pg.534]

Cromakalim (137) is a potassium channel activator commonly used as an antihypertensive agent (107). The rationale for the design of cromakalim is based on P-blockers such as propranolol (115) and atenolol (123). Conformational restriction of the propanolamine side chain as observed in the cromakalim chroman nucleus provides compounds with desired antihypertensive activity free of the side effects commonly associated with P-blockers. Enantiomerically pure cromakalim is produced by resolution of the diastereomeric (T)-a-meth5lben2ylcarbamate derivatives. X-ray crystallographic analysis of this diastereomer provides the absolute stereochemistry of cromakalim. Biological activity resides primarily in the (—)-(33, 4R)-enantiomer [94535-50-9] (137) (108). In spontaneously hypertensive rats, the (—)-(33, 4R)-enantiomer, at dosages of 0.3 mg/kg, lowers the systoHc pressure 47%, whereas the (+)-(3R,43)-enantiomer only decreases the systoHc pressure by 14% at a dose of 3.0 mg/kg. [Pg.253]


See other pages where Effects on potassium channels is mentioned: [Pg.125]    [Pg.65]    [Pg.45]    [Pg.125]    [Pg.65]    [Pg.45]    [Pg.370]    [Pg.45]    [Pg.137]    [Pg.400]    [Pg.45]    [Pg.34]    [Pg.58]    [Pg.77]    [Pg.220]    [Pg.134]    [Pg.328]    [Pg.74]    [Pg.35]    [Pg.986]    [Pg.143]    [Pg.201]    [Pg.184]    [Pg.145]    [Pg.442]    [Pg.532]    [Pg.449]    [Pg.143]    [Pg.171]    [Pg.96]    [Pg.117]   


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Channel effect

Channeling effects

Channelling effects

Potassium channels

Potassium effect

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