Vasodilatation and smooth muscle membrane potential changes in arterioles from the guinea‐pig small intestine.

Abstract

to the dilatation. 6. In 48 % of arterioles tested the dilatation appeared to be mediated solely by acetylcholine. In 31 % there was a cholinergic component, but no evidence for the involvement of acetylcholine in the remaining 21 %. When the non-cholinergic dilatation occurred without a hyperpolarization we conclude that it was due to vasoactive intestinal peptide; otherwise it may have been due to either galanin or dynorphin.

The Enteric Nervous System and Its Extrinsic Connections

“…The primary transmitter of the noncholinergic secretomotor effect is VIP. Stimulation of single neurons and measurement of the resulting changes in the diameter of submucosal blood vessels provide direct evidence for the presence of both cholinergic and noncholinergic vasodilator neurons [104][105][106]. Immunohistochemical studies, combined with denervation, confirm that both intrinsic cholinergic and noncholinergic neurons innervate submucosal arterioles [107].…”

Sympathetic Control of Arterial Membrane Potential by ATP-Sensitive K + -Channels

“…[7][8][9][10][11][12][13] Hashitani et al 13 have demonstrated that in guinea pig choroidal arterioles, perivascular nerve stimulation evokes biphasic hyperpolarization consisting of inhibitory junction potentials (IJPs) and slow hyperpolarization along with some depolarization and have suggested that IJPs may result from the activation of muscarinic receptors, whereas slow hyperpolarization appears to involve NO, derived either from nitrergic nerve terminals or from the endothelium. In guinea pig small intestinal arterioles 11 and in rabbit lingual artery, 7 nerve stimulation also elicits hyperpolarization that is blocked by muscarinic receptor blockers and is mimicked by exogenous ACh. ACh is thought to act on the vascular endothelium to release endothelium-derived hyperpolarizing factor 5,6 or to exert a direct action on muscarinic receptors located on the vascular smooth muscle to induce hyperpolarization.…”

“…However, considering the importance of membrane potential as a determinant of smooth muscle tone, even a subtle change in membrane potential might be expected to influence muscle tone, 25,26 especially in the presence of contractile agonists, 25 and several studies have demonstrated that neurogenic vasodilatation is correlated with hyperpolarization. 7,8,11,12 Furthermore, several recent studies including those on rat mesenteric artery 35 have demonstrated the involvement of K ATP channels in ␤-agonistinduced vasorelaxation. 35,36 It is thus conceivable that the membrane hyperpolarization produced by neurally released catecholamines through activation of K ATP may play some sort of modulatory role in the regulation of arterial tone in rat mesenteric circulation.…”

“…[5][6][7] In accord with these observations, neurogenic hyperpolarization has been demonstrated in certain vascular beds. [7][8][9][10][11][12][13] However, the underlying mechanisms of such hyperpolarization appear to differ considerably, depending on the vascular bed studied or species, [7][8][9][10][11][12][13] and the evaluation of such responses in resistance arteries has been hampered by depolarizing responses and contractions during repetitive nerve stimulation, which result in difficulty in maintaining microelectrode impalements. Furthermore, little is known regarding the ionic mechanisms of neurogenic hyperpolarization.…”

Calcium responses induced by acetylcholine in submucosal arterioles of the guinea‐pig small intestine

“…Although this is assumed to also be the case in arterioles, it has not been experimentally confirmed, since the removal of endothelial cells causes damage to the arteriolar smooth muscle (Neild et al 1990;Kotecha & Neild, 1995;Hashitani & Suzuki, 1997). The present experiments used fura_2 fluorescence to examine changes in [Ca¥]é induced by ACh in submucosal arterioles.…”