Sympathetic denervation facilitates L-type Ca2+ channel activation in renal but not in mesenteric resistance arteries

Abstract

Sympathetic denervation enhances L-type Ca channel-dependent signaling in renal but not in mesenteric arteries. This effect may be partly explained by the decreased VSMC membrane potential in denervated renal arteries.

Trophic sympathetic influence weakens pro-contractile role of Cl− channels in rat arteries during postnatal maturation

“…Chronic sympathetic denervation increased smooth muscle sensitivity of agonist-induced contraction. This is in accordance with previous findings showing the increase in arterial sensitivity to contractile stimuli 21,44 .…”

“…As such a mechanism, we propose here that postnatal reduction in the contribution of Cl − conductance to arterial contraction is associated with trophic influence of sympathetic nerves. This suggestion is based on several findings: (1) the development of sympathetic vasomotor innervation occurs during the first postnatal month in rats 8,16 ; (2) sympathetic nerves are known to have trophic influence on arterial structure and function 8,17,18 ; (3) sympathetic nerves modulate the expression and activity of several ion channels and pumps [19][20][21][22] ; (4) TMEM16A protein and sympathetic nerves exhibit opposite expression gradients along the vascular tree 23,24 . However, experimental evidence for the trophic influences of vascular sympathetic innervation on Cl − channel expression and/or function is not available yet.…”

Pro‐contractile role of chloride in arterial smooth muscle: Postnatal decline potentially governed by sympathetic nerves

“…It has been known for decades that sympathetic nerves exert a trophic influence on vascular structure and function (Adeoye, Silpanisong, Williams, & Pearce, 2015;Bevan, 1984). Importantly, the sympathetic nerves determine smooth muscle cell resting membrane potential and excitability by modulating the expression/activity of ion channels, pumps and cell-to-cell electrical coupling (Abel & Hermsmeyer, 1981;Fleming, 1999;Heumann et al, 2016;Slovut et al, 2004). After surgical denervation or neonatal sympathectomy, arteries of adult animals show supersensitivity to contractile stimuli that could not be explained by the changes in a specific population of receptors but is associated with membrane depolarization of the smooth muscle cells (Bentzer et al, 1997;Fleming, 1999;Heumann et al, 2016).…”

“…Importantly, the sympathetic nerves determine smooth muscle cell resting membrane potential and excitability by modulating the expression/activity of ion channels, pumps and cell-to-cell electrical coupling (Abel & Hermsmeyer, 1981;Fleming, 1999;Heumann et al, 2016;Slovut et al, 2004). After surgical denervation or neonatal sympathectomy, arteries of adult animals show supersensitivity to contractile stimuli that could not be explained by the changes in a specific population of receptors but is associated with membrane depolarization of the smooth muscle cells (Bentzer et al, 1997;Fleming, 1999;Heumann et al, 2016). This depolarization facilitates activation of the voltage-dependent L-type Ca 2+ channels in sympathectomized arterial smooth muscle exposed to contractile agents (Heumann et al, 2016).…”

“…After surgical denervation or neonatal sympathectomy, arteries of adult animals show supersensitivity to contractile stimuli that could not be explained by the changes in a specific population of receptors but is associated with membrane depolarization of the smooth muscle cells (Bentzer et al., ; Fleming, ; Heumann et al., ). This depolarization facilitates activation of the voltage‐dependent L‐type Ca 2+ channels in sympathectomized arterial smooth muscle exposed to contractile agents (Heumann et al., ). However, the mechanism of ion transport responsible for this positive shift in the membrane potential is poorly understood.…”