Functional Evidence for Inward-Rectifier Potassium Channels in Rat Cremaster Muscle Arterioles

Loeb, Alex L.; Gődény, Ildikó; Longnecker, David E.

doi:10.1006/mvre.1999.2187

Cited by 26 publications

(31 citation statements)

References 11 publications

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“…An influence of K Ca channel activity on the resting tone of gracilis muscle arterioles has also been reported by this laboratory and others (5,44), but these findings do not extend to arterioles in all skeletal muscles or in some other vascular beds. For example, arteriolar smooth muscle K Ca channel activity appears to be silent under resting conditions in rat and hamster cremaster muscle (23,31) and rat cerebral cortex (39). These vessel-tovessel differences in the steady-state activity of K Ca channels at normal vascular tone could be due to differences in the Ca 2ϩ set point of these channels, as suggested by Jackson and Blair (23).…”

Section: Discussionmentioning

confidence: 85%

High dietary salt reduces the contribution of 20-HETE to arteriolar oxygen responsiveness in skeletal muscle

Marvar

Falck²,

Boegehold

2007

American Journal of Physiology-Heart and Circulatory Physiology

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coupling of tissue blood flow to cellular metabolic demand involves oxygen-dependent adjustments in arteriolar tone, and arteriolar responses to oxygen can be mediated, in part, by changes in local production of 20-HETE. In this study, we examined the long-term effect of dietary salt on arteriolar oxygen responsiveness in the exteriorized, superfused rat spinotrapezius muscle and the role of 20-HETE in this responsiveness. Rats were fed either a normal-salt (NS, 0.45%) or high-salt (HS, 4%) diet for 4 -5 wk. There was no difference in steady-state tissue PO 2 between NS and HS rats, and elevation of superfusate oxygen content from 0% to 10% caused tissue PO 2 to increase by the same amount in both groups. However, the resulting reductions in arteriolar diameter and blood flow were less in HS rats than NS rats. Inhibition of 20-HETE formation with or 17-octadecynoic acid (17-ODYA) attenuated oxygen-induced constriction in NS rats but not HS rats. Exogenous 20-HETE elicited arteriolar constriction that was greatly reduced by the large-conductance Ca 2ϩ -activated potassium (K Ca) channel inhibitors tetraethylammonium chloride (TEA) and iberiotoxin (IbTx) in NS rats and a smaller constriction that was less sensitive to TEA or IbTx in HS rats. Arteriolar responses to exogenous angiotensin II were similar in both groups but more sensitive to inhibition with DDMS in NS rats. Norepinephrine-induced arteriolar constriction was similar and insensitive to DDMS in both groups. We conclude that 20-HETE contributes to oxygen-induced constriction of skeletal muscle arterioles via inhibition of K Ca channels and that a high-salt diet impairs arteriolar responses to increased oxygen availability due to a reduction in vascular smooth muscle responsiveness to 20-HETE. 20-hydroxyeicosatetraenoic acid; vascular control; blood flow; NaCl LOCAL OXYGEN AVAILABILITY is an important determinant of microvascular resistance and tissue blood flow (10,17,22,41), and consumption of a high-salt diet can lead to changes in resistance vessel function that alter the relationship between oxygen and vascular tone. For example, small gracilis muscle feed arteries from rats fed high salt for as little as 3 days consistently show an impaired dilator response to reduced oxygen levels (47, 48). However, the effect of oxygen on the tone of smaller arterioles in rat cremaster muscle is unchanged after 3 days on a high-salt diet (13). This suggests that either a longer period of high-salt intake is required to alter the oxygen responsiveness of these more distal resistance vessels or that there is a fundamental difference between extraparenchymal arteries and intramuscular arterioles in the susceptibility of oxygen-sensitive tone to dietary salt. The first aim of this study was to distinguish between these possibilities by determining whether a prolonged period of high-salt intake can change the relationship between oxygen and vascular tone in the arteriolar network of skeletal muscle.The mechanisms through which oxygen can influence resistance vessel to...

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Section: Discussionmentioning

confidence: 85%

High dietary salt reduces the contribution of 20-HETE to arteriolar oxygen responsiveness in skeletal muscle

Marvar

Falck²,

Boegehold

2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…7,31,79,81-83 Preliminary data support a role for K IR channels in K + -induced dilation of arterioles in cremaster muscle. 55 However, previous studies in this preparation have shown that K + induced dilation can be inhibited by millimolar concentrations of ouabain. 84 Thus, the role played by K IR channels in K + -induced vasodilation of skeletal muscle arterioles remains unclear.…”

Section: K Ir Channels and Vascular Tonementioning

confidence: 80%

“…79 Preliminary studies suggest that 50 μmol/L Ba 2+ causes constriction of rat arterioles in cremaster muscle in vivo. 55 In contrast, studies of hamster cremasteric arteriolar muscle cells have found no effect of Ba 2+ on currents around the resting membrane potential. 26 These data are inconsistent with the hypothesis that K IR channels are active under resting conditions.…”

Section: K Ir Channels and Vascular Tonementioning

confidence: 95%

Ion Channels and Vascular Tone

2000

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Ion channels in the plasma membrane of vascular muscle cells that form the walls of resistance arteries and arterioles play a central role in the regulation of vascular tone. Current evidence indicates that vascular smooth muscle cells express at least 4 different types of K + channels, 1 to 2 types of voltage-gated Ca 2+ channels, ≥2 types of Cl − channels, store-operated Ca + (SOC) channels, and stretch-activated cation (SAC) channels in their plasma membranes, all of which may be involved in the regulation of vascular tone. Calcium influx through voltage-gated Ca 2+, SOC, and SAC channels provides a major source of activator Ca 2+ used by resistance arteries and arterioles. In addition, K + and Cl − channels and the Ca 2+ channels mentioned previously all are involved in the determination of the membrane potential of these cells. Membrane potential is a key variable that not only regulates Ca +2 influx through voltage-gated Ca 2+ channels, but also influences release of Ca 2+ from internal stores and Ca 2+ -sensitivity of the contractile apparatus. By controlling Ca 2+ delivery and membrane potential, ion channels are involved in all aspects of the generation and regulation of vascular tone. Keywords muscle; smooth; vascular; arterioles; potassium channels; calcium channels; vascular resistance; vasoconstriction Vascular tone, the contractile activity of vascular smooth muscle cells in the walls of small arteries and arterioles, is the major determinant of the resistance to blood flow through the circulation. Thus, vascular tone plays an important role in the regulation of blood pressure and the distribution of blood flow between and within the tissues and organs of the body. Regulation of the contractile activity of vascular smooth muscle cells in the systemic circulation is dependent on a complex interplay of vasodilator and vasoconstrictor stimuli from circulating hormones, neurotransmitters, endothelium-derived factors, and blood pressure. All of these signals are integrated by vascular muscle cells to determine the activity of the contractile apparatus of the muscle cells and hence the diameter and hydraulic resistance of a blood vessel. Ion channels play a central role in this process. Like all muscle cells, vascular smooth muscle uses Ca 2+ as the trigger for contraction. Calcium influx through channels in the plasma membrane and Ca 2+ release from intracellular stores are the major source of activator Ca 2+ . In addition, the movement of ions through ion channels determines, to a large extent, membrane potential. Membrane potential, along with cytosolic Ca 2+ concentration, regulates and modulates the influx 1,2 and release 3-5 of Ca 2+ through ion channels and the sensitivity of the contractile machinery to Ca 2+.6 Vascular smooth muscle cells express ≥4 different types of K + channels, 7,8 1 to 2 types of voltage-gated Ca 2+ channels, 1,2 ≥2 types of Cl − channels, 9-11 store-operated Ca + channels, 12,13 and stretch-activated cation channels 14-16 in their plasma membranes, all of which may...

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“…In cardiovascular disease, K + channels functionally change [22][23][24] . Hypertension develops, with functional downregulation of K V channels but up-regulation of BK Ca in smooth muscle [25] .…”

Section: Discussionmentioning

confidence: 99%

Magnesium lithospermate B dilates mesenteric arteries by activating BKCa currents and contracts arteries by inhibiting KV currents

Zhang

Chen

et al. 2010

Acta Pharmacol Sin

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Aim: To examine the involvement of K + channels and endothelium in the vascular effects of magnesium lithospermate B (MLB), a hydrophilic active component of Salviae miltiorrhiza Radix. Methods: Isolated rat mesenteric artery rings were employed to investigate the effects of MLB on KCl-or norepinephrine-induced contractions. Conventional whole-cell patch-clamp technique was used to study the effects of MLB on K + currents in single isolated mesenteric artery myocytes. Results: MLB produced a concentration-dependent relaxation in mesenteric artery rings precontracted by norepinephrine (1 μmol/L) with an EC 50 of 111.3 μmol/L. MLB-induced relaxation was reduced in denuded artery rings with an EC 50 of 224.4 μmol/L. MLB caused contractions in KCl-precontracted artery rings in the presence of N-nitro-L-arginine methyl ester (L-NAME) with a maximal value of 130.3%. The vasodilatory effect of MLB was inhibited by tetraethylammonium (TEA) in both intact and denuded artery rings. In single smooth muscle cells, MLB activated BK Ca currents (EC 50 156.3 μmol/L) but inhibited K V currents (IC 50 26.1 μmol/L) in a voltageand concentration-dependent manner. Conclusion: MLB dilated arteries by activating BK Ca channels in smooth muscle cells and increasing NO release from endothelium, but it also contracted arteries precontracted with KCl in the presence of L-NAME.

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Functional Evidence for Inward-Rectifier Potassium Channels in Rat Cremaster Muscle Arterioles

Cited by 26 publications

References 11 publications

High dietary salt reduces the contribution of 20-HETE to arteriolar oxygen responsiveness in skeletal muscle

High dietary salt reduces the contribution of 20-HETE to arteriolar oxygen responsiveness in skeletal muscle

Ion Channels and Vascular Tone

Magnesium lithospermate B dilates mesenteric arteries by activating BKCa currents and contracts arteries by inhibiting KV currents

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