Intravascular pressure-evoked changes in intracellular calcium [Ca2+]i and tone in rat mesenteric and rabbit cerebral arteries in vitro

Coombes, JE; Hughes, Alun D.; Thom, Simon

doi:10.1038/sj.jhh.1000902

Cited by 7 publications

(3 citation statements)

References 16 publications

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“…This indicates that although they do not display a decrease in diameter, they do show active tone development and maintenance of diameter rather than passive dilation. 41,42 Consistent with previous reports, 43 2nd order conduit RMAs did not exhibit active constriction and only dilated passively in response to elevated pressure. However, in the presence of 4-AP or correolide, these vessels maintained a stable diameter with increasing transmural pressure.…”

Section: Plane Et Al Kv1 Channels and Myogenic Contraction 221supporting

confidence: 80%

“…For example, cerebral and skeletal muscle arteries show a pronounced decrease in diameter with increasing pressure, 5,41 whereas RMAs of similar diameter do not. 41,42 However, smaller resistance RMAs do show a pressure-induced increase in [Ca 2ϩ ] i similar to that of cerebral vessels 41 and their pressure-diameter curve is flattened at higher pressures (ie, Ն60 mm Hg). This indicates that although they do not display a decrease in diameter, they do show active tone development and maintenance of diameter rather than passive dilation.…”

Section: Plane Et Al Kv1 Channels and Myogenic Contraction 221mentioning

confidence: 99%

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Heteromultimeric Kv1 Channels Contribute to Myogenic Control of Arterial Diameter

Plane

Johnson

Kerr

et al. 2005

Circulation Research

117

109

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Abstract-Inhibition of vascular smooth muscle (VSM) delayed rectifier K ϩ channels (K DR ) by 4-aminopyridine (4-AP; 200 mol/L) or correolide (1 mol/L), a selective inhibitor of Kv1 channels, enhanced myogenic contraction of rat mesenteric arteries (RMAs) in response to increases in intraluminal pressure. The molecular identity of K DR of RMA myocytes was characterized using RT-PCR, real-time PCR, and immunocytochemistry. Transcripts encoding the pore-forming Kv␣ subunits, Kv1.2, Kv1.4, Kv1.5, and Kv1.6, were identified and confirmed at the protein level with subunit-specific antibodies. Kv␤ transcript (␤1.1, ␤1.2, ␤1.3, and ␤2.1) expression was also identified. Kv1.5 message was Ϸ2-fold more abundant than that for Kv1.2 and Kv1.6. Transcripts encoding these three Kv1␣ subunits were Ϸ2-fold more abundant in 1st/2nd order conduit compared with 4th order resistance RMAs, and Kv␤1 was 8-fold higher than Kv␤2 message. RMA K DR activated positive to Ϫ50 mV, exhibited incomplete inactivation, and were inhibited by 4-AP and correolide. However, neither ␣-dendrotoxin or -dendrotoxin affected RMA K DR , implicating the presence of Kv1.5 in all channels and the absence of Kv1.1, respectively. Currents mediated by channels because of coexpression of Kv1.2, Kv1.5, Kv1.6, and Kv␤1.2 in human embryonic kidney 293 cells had biophysical and pharmacological properties similar to those of RMA K DR . It is concluded that K DR channels composed of heteromultimers of Kv1 subunits play a critical role in myogenic control of arterial diameter. Key Words: delayed rectifier potassium channel Ⅲ KCNA Ⅲ vascular smooth muscle Ⅲ myogenic contraction Ⅲ arterial diameter T he ability of small resistance arteries to develop myogenic tone in response to elevations in intraluminal (or transmural) pressure is an essential autoregulatory mechanism and an important determinant of peripheral vascular resistance, regional blood flow, and blood pressure. Pressureinduced depolarization of vascular smooth muscle (VSM) leading to increased intracellular Ca 2ϩ ([Ca 2ϩ ] i ) via voltagedependent activation of Ca 2ϩ channels is required for myogenic tone development. 1,2 However, the depolarization does not evoke regenerative action potentials, rather incremental changes in diameter are achieved by graded, steady-state depolarizations. 3 Our understanding of the ionic basis of this precise control of myogenic depolarization is incomplete.Increased intraluminal pressure is thought to activate nonselective cation or Cl Ϫ channels of VSM cells, 2 with the level of depolarization attributable to these channels precisely controlled by an activation of VSM K ϩ channels. 3 Compelling evidence for a contribution of large Ca 2ϩ -activated K ϩ channels (BK Ca ) to this feedback control comes from studies using specific inhibitors (eg, iberiotoxin) and transgenic mice lacking the BK Ca modulatory ␤1 subunit. 4 However, whether other channels are also involved in controlling myogenic depolarization in VSM is not clear.Voltage-gated delayed rectifier channels (K DR ) ...

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Section: Plane Et Al Kv1 Channels and Myogenic Contraction 221supporting

confidence: 80%

Section: Plane Et Al Kv1 Channels and Myogenic Contraction 221mentioning

confidence: 99%

Heteromultimeric Kv1 Channels Contribute to Myogenic Control of Arterial Diameter

Plane

Johnson

Kerr

et al. 2005

Circulation Research

117

109

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“…5). Myogenic contractile responses to increased pressure were not recorded, but it has previously been reported that myogenic responses are less pronounced in mesenteric vessels than in other vascular beds such as cerebral vessels (Coombes et al 1999;Lagaud et al 1999).…”

Section: Mechanical Adequate Stimulusmentioning

confidence: 99%

Activation of intestinal spinal afferent endings by changes in intra‐mesenteric arterial pressure

Humenick

Chen

Wiklendt

et al. 2015

The Journal of Physiology

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Key pointsr A major class of mechano-nociceptors to the intestine have mechanotransduction sites on extramural and intramural arteries and arterioles ('vascular afferents').r These sensory neurons can be activated by compression or axial stretch of vessels. r Using isolated preparations we showed that increasing intra-arterial pressure, within the physiological range, activated mechano-nociceptors on vessels in intact mesenteric arcades, but not in isolated arteries. This suggests that distortion of the branching vascular tree is the mechanical adequate stimulus for these sensory neurons, rather than simple distension.r The same rises in pressure also activated intestinal peristalsis in a partially capsaicin-sensitive manner indicating that pressure-sensitive vascular afferents influence enteric circuits.r The results identify the mechanical adequate stimulus for a major class of mechano-nociceptors with endings on blood vessels supplying the gut wall; these afferents have similar endings to ones supplying other viscera, striated muscle and dural vessels.Abstract Spinal sensory neurons innervate many large blood vessels throughout the body. Their activation causes the hallmarks of neurogenic inflammation: vasodilatation through the release of the neuropeptide calcitonin gene-related peptide and plasma extravasation via tachykinins. The same vasodilator afferent neurons show mechanical sensitivity, responding to crushing, compression or axial stretch of blood vessels -responses which activate pain pathways and which can be modified by cell damage and inflammation. In the present study, we tested whether spinal afferent axons ending on branching mesenteric arteries ('vascular afferents') are sensitive to increased intravascular pressure. From a holding pressure of 5 mmHg, distension to 20, 40, 60 or 80 mmHg caused graded, slowly adapting increases in firing of vascular afferents. Many of the same afferent units showed responses to axial stretch, which summed with responses evoked by raised pressure. Many vascular afferents were also sensitive to raised temperature, capsaicin and/or local compression with von Frey hairs. However, responses to raised pressure in single, isolated vessels were negligible, suggesting that the adequate stimulus is distortion of the arterial arcade rather than distension per se. Increasing arterial pressure often triggered peristaltic contractions in the neighbouring segment of intestine, an effect that was mimicked by acute exposure to capsaicin (1 μM) and which was reduced after desensitisation to capsaicin. These results indicate that sensory fibres with perivascular endings are sensitive to pressure-induced distortion of branched arteries, in addition to compression and axial stretch, and that they contribute functional inputs to enteric motor circuits.

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Pharmacology of the mouse-isolated cerebral artery

Bai

Moien‐Afshari

Washio

et al. 2004

Vascular Pharmacology

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Intravascular pressure-evoked changes in intracellular calcium [Ca2+]i and tone in rat mesenteric and rabbit cerebral arteries in vitro

Cited by 7 publications

References 16 publications

Heteromultimeric Kv1 Channels Contribute to Myogenic Control of Arterial Diameter

Heteromultimeric Kv1 Channels Contribute to Myogenic Control of Arterial Diameter

Activation of intestinal spinal afferent endings by changes in intra‐mesenteric arterial pressure

Pharmacology of the mouse-isolated cerebral artery

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