Actions of neurotransmitters and other messengers on Ca2+ channels and K+ channels in smooth muscle cells

doi:10.1016/S0163-7258(97)87271-3

Pharmacology & Therapeutics

Volume 73, Issue 2, 1997, Pages 91-119

https://doi.org/10.1016/S0163-7258(97)87271-3 Get rights and content

Abstract

Ion channels play key roles in determining smooth muscle tone by setting the membrane potential and allowing Ca²⁺ influx. Perhaps not surprisingly, therefore, they also provide targets for neurotransmitters and other messengers that act on smooth muscle. Application of patch-clamp and molecular biology techniques and the use of selective pharmacology has started to provide a wealth of information on the ion channel systems of smooth muscle cells, revealing complexity and functional significance. Reviewed are the actions of messengers (e.g., noradrenaline, acetylcholine, endothelin, angiotensin II, neuropeptide Y, 5-hydroxytryptamine, histamine, adenosine, calcitonin gene-related peptide, substance P, prostacyclin, nitric oxide and oxygen) on specific types of ion channel in smooth muscle, the L-type calcium channel, and the large conductance Ca²⁺-activated, ATP-sensitive, delayed rectifier and apamin-sensitive K⁺ channels.

References (354)

J.A. Bellan et al.
Selective and complete blockade of acetylcholine-induced relaxation in rabbit aortic rings by N^ω-nitro-L-arginine but not by glybenclamide
Eur. J. Pharmacol.
(1993)
L.A. Blatter et al.
Nitric oxide decreases [Ca²⁺]_i in vascular smooth muscle by inhibition of the calcium current
Cell Calcium
(1994)
G.E. Boeckxstaens et al.
Involvement of nitric oxide in the inhibitory innervation of the human isolated colon
Gastroenterology
(1993)
C. Delaey et al.
Prostanoid-induced contractions are blocked by sulfonylureas
Eur. J. Pharmacol.
(1995)
S. England et al.
Inhibition of voltage-dependent Ca²⁺-current by α-adrenoceptor agonists in smooth muscle cells
Pflügers Arch.
(1995)
A. Galvez et al.
Purification and characterization of a unique, potent, peptidyl probe for the high conductance calcium-activated potassium channel from venom of the scorpion Buthus tamalus
J. Biol. Chem.
(1990)
A.S.O. Adeagbo et al.
Endothelium and BRL 34915-induced vasodilatation in rat isolated perfused mesenteric arteries: role of G-proteins, K⁺ and calcium channels
Br. J. Pharmacol.
(1990)
A.S.O. Adeagbo et al.
Varying extracellular [K⁺]: a functional approach to separating EDHF- and EDNO-related mechanisms in perfused rat mesenteric arterial bed
J. Cardiovasc. Pharmacol.
(1993)
L. Aguilar-Bryan et al.
Cloning of the β cell high affinity sulfonylurea receptor: a regulator of insulin secretion
Science
(1995)
E.A. Aiello et al.
Phosphorylation by protein kinase A enhances delayed rectifier K⁺ current in rabbit vascular smooth muscle cells
Am. J. Physiol.
(1995)

H.I. Akbarali et al.

Effect of sodium nitroprusside on Ca²⁺ currents in opossum esophageal circular muscle cells

Am. J. Physiol.

(1994)

Q. Al-Awqati

Regulation of ion channels by ABC transporters that secrete ATP

Science

(1995)

H.D. Allescher et al.

Mechanisms of neurotensin-induced inhibition in rat ileal smooth muscle

Am. J. Physiol.

(1992)

C.M. Angrave et al.

Inhibition by bradykinin of ATP-sensitive K⁺-current in smooth muscle cells isolated from guinea-pig ileum

J. Physiol.

(1995)

S.L. Archer et al.

Nitric oxide and cGMP cause vasorelaxation by activation of a charybdotoxin-sensitive K channel by cGMP-dependent protein kinase

T. Aversano et al.

Blockade of the ATP-sensitive potassium channel modulates reactive hyperemia in the cainine coronary circulation

Circ. Res.

(1991)

J.M. Baraban et al.

Phorbol ester effects on neurotransmission: interactions with neurotransmitters and calcium in smooth muscle

A. Baron et al.

Dual effect of thrombin on voltage-dependent Ca²⁺ channels of portal vein smooth muscle cells

Circ. Res.

(1993)

V. Bauer et al.

The nature of non-cholinergic, non-adrenergic transmission in longitudinal and circular muscles of the guinea-pig ileum

J. Physiol.

(1982)

O. Bayguinov et al.

Role of nitric oxide as an inhibitory neurotransmitter in the canine pyloric sphincter

Am. J. Physiol.

(1993)

O. Bayguinov et al.

Patterns of electrical activity and neural responses in canine proximal duodenum

Am. J. Physiol.

(1992)

D.J. Beech

Inhibitory effects of histamine and bradykinin on calcium current in smooth muscle cells isolated from guinea-pig ileum

J. Physiol.

(1993)

D.J. Beech

Inhibition by D609 of histamine receptor coupling to Ca channels in smooth muscle cells isolated from guinea-pig ileum

Br. J. Pharmacol.

(1995)

D.J. Beech et al.

Properties of the cromakalim-induced potassium conductance in smooth muscle cells isolated from the rabbit portal vein

Br. J. Pharmacol.

(1989)

D.J. Beech et al.

Voltage-dependent outward current with fast kinetics in single smooth muscle cells isolated from the rabbit portal vein

J. Physiol.

(1989)

D.J. Beech et al.

Two components of potassium current activated by depolarization of single smooth muscle cells from the rabbit portal vein

J. Physiol.

(1989)

D.J. Beech et al.

K channel activation by nucleotide diphosphates and its inhibition by glibenclamide in vascular smooth muscle cells

Br. J. Pharmacol.

(1993)

C.D. Benham et al.

Spontaneous transient outward currents in single visceral and vascular smooth muscle cells of the rabbit

J. Physiol.

(1986)

C.D. Benham et al.

Noradrenaline modulation of calcium in single smooth muscle cells from rabbit ear artery

J. Physiol.

(1988)

R.A. Bialecki et al.

K_Ca channel antagonists reduce NO donor-mediated relaxation of vascular and tracheal smooth muscle

Am. J. Physiol.

(1995)

K. Bian et al.

Glyburide actions on the dihydropyridine-sensitive Ca²⁺ channel in rat vascular muscle

J. Vasc. Res.

(1994)

G. Bkaily et al.

Angiotensin II increases Isi and blocks IK in single aortic cells of rabbit

Pflügers Arch.

(1988)

A.L. Blatz et al.

Single apamin-blocked Ca-activated K⁺ channels of small conductance in cultured rat skeletal muscle

Nature

(1986)

V.M. Bolotina et al.

Nitric oxide directly activates calcium-dependent potassium channels in vascular smooth muscle

Nature

(1994)

T.B. Bolton et al.

Smooth muscle potassium channels: their electrophysiology and function

T.B. Bolton et al.

Properties of calcium stores and transient outward currents in single smooth muscle cells of rabbit intestine

J. Physiol.

(1989)

T.B. Bolton et al.

Evidence that histamine and carbachol may open the same ion channels in longitudinal smooth muscle of the guinea-pig ileum

J. Physiol.

(1981)

A. Bonev et al.

Arginine-vasopressin induces mode-2 gating in L-type Ca²⁺ channels (smooth muscle cells of the urinary bladder of the guinea-pig)

Pflügers Arch.

(1992)

A.D. Bonev et al.

ATP-sensitive potassium channels in smooth muscle cells from guinea-pig urinary bladder

Am. J. Physiol.

(1993)

A.D. Bonev et al.

Muscarinic inhibition of ATP-sensitive K⁺ channels by protein kinase C in urinary bladder smooth muscle

Am. J. Physiol.

(1993)

A.D. Bonev et al.

Neuropeptide Y, phenylephrine, serotonin, and histamine inhibit ATP-sensitive K⁺ channel currents by protein kinase C in smooth muscle cells from rabbit mesenteric artery

Biophys. J.

(1995)

J.E. Brayden

Membrane hyperpolarisation is a mechanism of endothelium-dependant cerebral vasodilation

Am. J. Physiol.

(1990)

J.E. Brayden

Hyperpolarization and relaxation of resistance arteries in response to adenosine diphosphate

Circ. Res.

(1991)

J.E. Brayden et al.

Regulation of arterial tone by activation of calcium-dependent potassium channels

Science

(1992)

M. Bridgewater et al.

Characteristic features of inhibitory junction potentials evoked by single stimuli in the guinea-pig isolated taenia caeci

J. Physiol.

(1995)

M.R. Briejer et al.

5-HT-induced neurogenic relaxations of the guinea-pig proximal colon: investigation into the role of ATP and VIP in addition to nitric oxide

Naunyn Schmiedebergs Arch. Pharmacol.

(1995)

E.P. Burke et al.

Acetylcholine increases intracellular [Ca²⁺] and decreases inward Ca²⁺ current in isolated smooth muscle cells of the canine gastric antrum

Gastroenterology

(1994)

N.G. Byrne et al.

Action of noradrenaline on single smooth muscle cells freshly dispersed from the rat anococcygeus muscle

J. Physiol.

(1987)

F. Cabell et al.

Inhibition of adenosine-induced coronary vasodilation by block of large-conductance Ca²⁺-activated K⁺ channels

Am. J. Physiol.

(1994)

A. Carl

Multiple components of delayed rectifier K⁺ current in canine colonic smooth muscle

J. Physiol.

(1995)

Cited by (82)

Pico145 inhibits TRPC4-mediated mI<inf>CAT</inf> and postprandial small intestinal motility
2023, Biomedicine and Pharmacotherapy
In intestinal smooth muscle cells, receptor-operated TRPC4 are responsible for the majority of muscarinic receptor cation current (mI_CAT), which initiates cholinergic excitation-contraction coupling. Our aim was to examine the effects of the TRPC4 inhibitor Pico145 on mI_CAT and Ca²⁺ signalling in mouse ileal myocytes, and on intestinal motility. Ileal myocytes freshly isolated from two month-old male BALB/c mice were used for patch-clamp recordings of whole-cell currents and for intracellular Ca²⁺ imaging using Fura-2. Functional assessment of Pico145’s effects was carried out by standard in vitro tensiometry, ex vivo video recordings and in vivo postprandial intestinal transit measurements using carmine red. Carbachol (50 µM)-induced mI_CAT was strongly inhibited by Pico145 starting from 1 pM. The IC₅₀ value for the inhibitory effect of Pico145 on this current evoked by intracellularly applied GTPγS (200 µM), and thus lacking desensitisation, was found to be 3.1 pM, while carbachol-induced intracellular Ca²⁺ rises were inhibited with IC₅₀ of 2.7 pM. In contrast, the current activated by direct TRPC4 agonist (-)-englerin A was less sensitive to the action of Pico145 that caused only ∼43 % current inhibition at 100 pM. The inhibitory effect developed rather slowly and it was potentiated by membrane depolarisation. In functional assays, Pico145 produced concentration-dependent suppression of both spontaneous and carbachol-evoked intestinal smooth muscle contractions and delayed postprandial intestinal transit. Thus, Pico145 is a potent GI-active small-molecule which completely inhibits mI_CAT at picomolar concentrations and which is as effective as trpc4 gene deficiency in in vivo intestinal motility tests.
A1-adenosine acute withdrawal response and cholecystokinin-8 induced contractures are regulated by Ca<sup>2+</sup>- and ATP-activated K<sup>+</sup> channels
2015, Pharmacological Research
Citation Excerpt :
We found that when the SKCa blocker apamin was used, the inhibition of the CCk-8 contracture induced by the acute A1 receptors stimulation was overcome in a dose related manner (Fig. 6b). This suggests that the activation of these channels might regulate the release of neurotransmitters responsible for the CCk-8-induced contracture in GPI [15,16,19,31,33,49,50]. On the other hand, in the presence of CCk-8, the A1-withdrawal precipitated contracture was not affected by apamin (Fig. 6c), likely because the neurones involved in the A1-withdrawal contracture, which are activated by the presence of CCk-8, are not sensitive to the activation of SKCa channels.
In isolated guinea-pig ileum (GPI), the A1-adenosine acute withdrawal response is under the control of several neuronal signalling systems, including the μ/κ-opioid and the cannabinoid CB₁ systems. It is now well established that after the stimulation of the A1-adenosine system, the indirect activation of both μ/κ-opioid and CB₁ systems is prevented by the peptide cholecystokinin-8 (CCk-8). In the present study, we have investigated the involvement of the Ca²⁺/ATP-activated K⁺ channels in the regulation of both acute A1-withdrawal and CCk-8-induced contractures in the GPI preparation. Interestingly, we found that: (a) the A1-withdrawal contracture is inhibited by voltage dependent Ca²⁺-activated K⁺ channels, K_v, while it is enhanced by the voltage independent Ca²⁺-activated K⁺ channels, SK_Ca; (b) in the presence of CCk-8, the inhibitory effect of the A1 agonist, CPA, on the peptide induced contracture is significantly enhanced by the voltage independent Ca²⁺-activated K⁺ channel, SK_Ca; and (c) the A1-withdrawal contracture precipitated in the presence of CCk-8 is controlled by the ATP-sensitive potassium channels, K_ATP. Our data suggest, for the first time, that both Ca²⁺- and ATP-activated K⁺ channels are involved in the regulation of both A1-withdrawal precipitated and CCk-8 induced contractures.
Nitric oxide signaling pathways involved in the inhibition of spontaneous activity in the guinea pig prostate
2012, Journal of Urology
We investigated nitric oxide mediated inhibition of spontaneous activity recorded in young and aging guinea pig prostates.
Conventional intracellular microelectrode and tension recording techniques were used.
The nitric oxide donor sodium nitroprusside (10 μM) abolished spontaneous contractions and slow wave activity in 5 young and 5 aging prostates. Upon adding the nitric oxide synthase inhibitor L-NAME (10 μM) the frequency of spontaneous contractile and electrical activity was significantly increased in each age group. This increase was significantly larger in 4 to 8 preparations of younger vs aging prostates (about 40% to 50% vs about 10% to 20%, 2-way ANOVA p <0.01). Other measured parameters, including the duration, amplitude and membrane potential of spontaneous electrical and contractile activity, were not altered from control values. The guanylate cyclase inhibitor ODQ (10 μM) significantly increased the frequency of spontaneous activity by 10% to 30% in 6 young guinea pig prostates (Student paired t test p <0.05). However, it had no effect on aging prostates. The cGMP analogue 8-Br-GMP (1 μM) and the PDE₅ inhibitor dipyridamole (1 μM) significantly decreased the frequency of contractile activity by about 70% in 4 to 9 young and older prostates (Student paired t test p <0.05).
The decrease in the response to L-NAME in spontaneous contractile and slow wave activity in aging prostate tissue compared to that in young prostates suggests that with age there is a decrease in nitric oxide production. This may further explain the increase in prostatic smooth muscle tone observed in age related prostate specific conditions, such as benign prostatic hyperplasia.
The mechanisms of the direct action of etomidate on vascular reactivity in rat mesenteric resistance arteries
2009, Anesthesia and Analgesia
Citation Excerpt :
We also attempted to characterize norepinephrine (10 μM)-induced Ca2+ influx by evaluating the effects of nifedipine (0.01–10 μM, a selective blocker of the L-type voltage-gated Ca2+ channels [VGCCs]32) and niflumic acid (10–300 μM, a selective blocker of the Ca2+-activated Cl− [Cl−Ca] channels33) on norepinephrine (10 μM)-induced increases in [Ca2+]i and force in the ryanodine-treated strips. Because etomidate was recently reported to modulate the adenosine 5′-triphosphate-sensitive K+ (KATP) channel activity in vascular smooth muscle (VSM) cells,17 we also examined the effects of etomidate on the norepinephrine- induced increases in [Ca2+]i and force after treatment with glibenclamide (1 μM, a selective blocker of the KATP channels34). In preliminary experiments, 5 min were sufficient for all of these blockers to exert their maximal effects on the response to norepinephrine or KCl.
Etomidate minimally influences hemodynamics at a standard induction dose in young healthy patients, but can cause significant systemic hypotension at higher doses for induction or electroencephalographic burst suppression (i.e., cerebral protection) in patients with advanced age or heart disease, and during cardiopulmonary bypass. However, less is known about its action on systemic resistance arteries.
Using an isometric force recording method and fura-2-fluorometry, we investigated the action of etomidate on vascular reactivity in small mesenteric arteries from young (7–8 wk old, n = 179) and aged (96–98 wk old, n = 10) rats.
In the endothelium-intact strips from young rats, etomidate enhanced the contractile response to norepinephrine or KCl (40 mM) at 3 μM but inhibited it at higher concentrations (≥10 μM). The enhancement was still observed after treatment with N^G-nitro l-arginine, tetraethylammonium, diclofenac, nordihydroguaiaretic acid, losartan, ketanserin, BQ-123, or BQ-788, but was not observed in aged rats. In the endothelium-denuded strips from young rats, etomidate (≥10 μM) consistently inhibited the contractile response to norepinephrine or KCl without enhancement at 3 μM. In the fura-2-loaded, endothelium-denuded strips from young rats, etomidate inhibited norepinephrine- or KCl-induced increases in both intracellular Ca²⁺ concentration ([Ca²⁺]i) and force. Etomidate still inhibited the norepinephrine-induced increase in [Ca²⁺]i after depletion of the intracellular Ca²⁺ stores by ryanodine, which was sensitive to nifedipine. Etomidate had little effect on norepinephrine- or caffeine-induced Ca²⁺ release from the intracellular stores or Ca²⁺ uptake into the intracellular stores. During stimulation with norepinephrine or KCl, etomidate had little effect on the [Ca²⁺]i-force relation at low concentrations (≤30 μM) but caused its downward shift at 100 μM.
In small mesenteric arteries, etomidate influences the contractile response to norepinephrine or membrane depolarization through endothelium-dependent enhancing and endothelium-independent inhibitory actions. The enhancement is at least in part independent of nitric oxide, endothelium-derived hyperpolarizing factor, cyclooxygenase products, lipoxygenase products, angiotensin II, serotonin, or endothelin-1, but may involve some signaling pathway that is impaired by aging. The endothelium-independent inhibition is due to decreases in both the [Ca²⁺]i and myofilament Ca²⁺ sensitivity in vascular smooth muscle cells. The decrease in [Ca²⁺]i would be due mainly to inhibition of voltage-gated Ca²⁺ influx. The observed inability of lower concentrations (1–3 μM) of etomidate to cause significant vasodilation is consistent with minimal changes in hemodynamics during induction of anesthesia with etomidate in young subjects, whereas the observed vasodilator action of higher concentrations of etomidate might underlie systemic hypotension caused by higher doses of etomidate in the clinical setting.
Vasopressin: Mechanisms of action on the vasculature in health and in septic shock
2007, Critical Care Medicine
Vasopressin is essential for cardiovascular homeostasis, acting via the kidney to regulate water resorption, on the vasculature to regulate smooth muscle tone, and as a central neurotransmitter, modulating brainstem autonomic function. Although it is released in response to stress or shock states, a relative deficiency of vasopressin has been found in prolonged vasodilatory shock, such as is seen in severe sepsis. In this circumstance, exogenous vasopressin has marked vasopressor effects, even at doses that would not affect blood pressure in healthy individuals. These two findings provide the rationale for the use of vasopressin in the treatment of septic shock. However, despite considerable research attention, the mechanisms for vasopressin deficiency and hypersensitivity in vasodilatory shock remain unclear.
To summarize vasopressin's synthesis, physiologic roles, and regulation and then review the literature describing its vascular receptors and downstream signaling pathways. A discussion of potential mechanisms underlying vasopressin hypersensitivity in septic shock follows, with reference to relevant clinical, in vivo, and in vitro experimental evidence.
Search of the PubMed database (keywords: vasopressin and receptors and/or sepsis or septic shock) for articles published in English before May 2006 and manual review of article bibliographies.
The pathophysiologic mechanism underlying vasopressin hypersensitivity in septic shock is probably multifactorial. It is doubtful that this phenomenon is merely the consequence of replacing a deficiency. Changes in vascular receptors or their signaling and/or interactions between vasopressin, nitric oxide, and adenosine triphosphate-dependent potassium channels are likely to be relevant. Further translational research is required to improve our understanding and direct appropriate educated clinical use of vasopressin.
Direct modulation of TRPC ion channels by Gα proteins
2024, Frontiers in Physiology

View all citing articles on Scopus

View full text

Actions of neurotransmitters and other messengers on Ca2+ channels and K+ channels in smooth muscle cells

Abstract

Eur. J. Pharmacol.

Cell Calcium

Gastroenterology

Eur. J. Pharmacol.

Pflügers Arch.

J. Biol. Chem.

Endothelium and BRL 34915-induced vasodilatation in rat isolated perfused mesenteric arteries: role of G-proteins, K+ and calcium channels

Br. J. Pharmacol.

Varying extracellular [K+]: a functional approach to separating EDHF- and EDNO-related mechanisms in perfused rat mesenteric arterial bed

J. Cardiovasc. Pharmacol.

Cloning of the β cell high affinity sulfonylurea receptor: a regulator of insulin secretion

Science

Phosphorylation by protein kinase A enhances delayed rectifier K+ current in rabbit vascular smooth muscle cells

Am. J. Physiol.

Effect of sodium nitroprusside on Ca2+ currents in opossum esophageal circular muscle cells

Am. J. Physiol.

Regulation of ion channels by ABC transporters that secrete ATP

Science

Mechanisms of neurotensin-induced inhibition in rat ileal smooth muscle

Am. J. Physiol.

Inhibition by bradykinin of ATP-sensitive K+-current in smooth muscle cells isolated from guinea-pig ileum

J. Physiol.

Nitric oxide and cGMP cause vasorelaxation by activation of a charybdotoxin-sensitive K channel by cGMP-dependent protein kinase

Blockade of the ATP-sensitive potassium channel modulates reactive hyperemia in the cainine coronary circulation

Circ. Res.

Phorbol ester effects on neurotransmission: interactions with neurotransmitters and calcium in smooth muscle

Dual effect of thrombin on voltage-dependent Ca2+ channels of portal vein smooth muscle cells

Circ. Res.

The nature of non-cholinergic, non-adrenergic transmission in longitudinal and circular muscles of the guinea-pig ileum

J. Physiol.

Role of nitric oxide as an inhibitory neurotransmitter in the canine pyloric sphincter

Am. J. Physiol.

Patterns of electrical activity and neural responses in canine proximal duodenum

Am. J. Physiol.

Inhibitory effects of histamine and bradykinin on calcium current in smooth muscle cells isolated from guinea-pig ileum

J. Physiol.

Inhibition by D609 of histamine receptor coupling to Ca channels in smooth muscle cells isolated from guinea-pig ileum

Br. J. Pharmacol.

Properties of the cromakalim-induced potassium conductance in smooth muscle cells isolated from the rabbit portal vein

Br. J. Pharmacol.

Voltage-dependent outward current with fast kinetics in single smooth muscle cells isolated from the rabbit portal vein

J. Physiol.

Two components of potassium current activated by depolarization of single smooth muscle cells from the rabbit portal vein

J. Physiol.

K channel activation by nucleotide diphosphates and its inhibition by glibenclamide in vascular smooth muscle cells

Br. J. Pharmacol.

Spontaneous transient outward currents in single visceral and vascular smooth muscle cells of the rabbit

J. Physiol.

Noradrenaline modulation of calcium in single smooth muscle cells from rabbit ear artery

J. Physiol.

KCa channel antagonists reduce NO donor-mediated relaxation of vascular and tracheal smooth muscle

Am. J. Physiol.

Glyburide actions on the dihydropyridine-sensitive Ca2+ channel in rat vascular muscle

J. Vasc. Res.

Angiotensin II increases Isi and blocks IK in single aortic cells of rabbit

Pflügers Arch.

Single apamin-blocked Ca-activated K+ channels of small conductance in cultured rat skeletal muscle

Nature

Nitric oxide directly activates calcium-dependent potassium channels in vascular smooth muscle

Nature

Smooth muscle potassium channels: their electrophysiology and function

Properties of calcium stores and transient outward currents in single smooth muscle cells of rabbit intestine

J. Physiol.

Evidence that histamine and carbachol may open the same ion channels in longitudinal smooth muscle of the guinea-pig ileum

J. Physiol.

Arginine-vasopressin induces mode-2 gating in L-type Ca2+ channels (smooth muscle cells of the urinary bladder of the guinea-pig)

Pflügers Arch.

ATP-sensitive potassium channels in smooth muscle cells from guinea-pig urinary bladder

Am. J. Physiol.

Muscarinic inhibition of ATP-sensitive K+ channels by protein kinase C in urinary bladder smooth muscle

Am. J. Physiol.

Neuropeptide Y, phenylephrine, serotonin, and histamine inhibit ATP-sensitive K+ channel currents by protein kinase C in smooth muscle cells from rabbit mesenteric artery

Biophys. J.

Membrane hyperpolarisation is a mechanism of endothelium-dependant cerebral vasodilation

Am. J. Physiol.

Hyperpolarization and relaxation of resistance arteries in response to adenosine diphosphate

Circ. Res.

Regulation of arterial tone by activation of calcium-dependent potassium channels

Actions of neurotransmitters and other messengers on Ca²⁺ channels and K⁺ channels in smooth muscle cells

Endothelium and BRL 34915-induced vasodilatation in rat isolated perfused mesenteric arteries: role of G-proteins, K⁺ and calcium channels

Varying extracellular [K⁺]: a functional approach to separating EDHF- and EDNO-related mechanisms in perfused rat mesenteric arterial bed

Phosphorylation by protein kinase A enhances delayed rectifier K⁺ current in rabbit vascular smooth muscle cells

Effect of sodium nitroprusside on Ca²⁺ currents in opossum esophageal circular muscle cells

Inhibition by bradykinin of ATP-sensitive K⁺-current in smooth muscle cells isolated from guinea-pig ileum

Dual effect of thrombin on voltage-dependent Ca²⁺ channels of portal vein smooth muscle cells

K_Ca channel antagonists reduce NO donor-mediated relaxation of vascular and tracheal smooth muscle

Glyburide actions on the dihydropyridine-sensitive Ca²⁺ channel in rat vascular muscle

Single apamin-blocked Ca-activated K⁺ channels of small conductance in cultured rat skeletal muscle

Arginine-vasopressin induces mode-2 gating in L-type Ca²⁺ channels (smooth muscle cells of the urinary bladder of the guinea-pig)

Muscarinic inhibition of ATP-sensitive K⁺ channels by protein kinase C in urinary bladder smooth muscle

Neuropeptide Y, phenylephrine, serotonin, and histamine inhibit ATP-sensitive K⁺ channel currents by protein kinase C in smooth muscle cells from rabbit mesenteric artery

Acetylcholine increases intracellular [Ca²⁺] and decreases inward Ca²⁺ current in isolated smooth muscle cells of the canine gastric antrum

Inhibition of adenosine-induced coronary vasodilation by block of large-conductance Ca²⁺-activated K⁺ channels

Multiple components of delayed rectifier K⁺ current in canine colonic smooth muscle