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T O Neild

Publications and source records attributed to T O Neild.

56 records · Page 4Linked to original sources
PubMedDate not supplied

Electrophysiological basis of arteriolar vasomotion in vivo.

We tested the hypothesis that cyclic changes in membrane potential (E(m)) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters. Diameter oscillations (approximately 3 min(-1)) were preceded (approximately 3 s) by oscillations in E(m) of smooth muscle cells (SMC) and endothelial cells (EC). Oscillations in E(m) were resolved into six phases: (1) a period (6 +/- 2 s) at the most negative E(m) observed during vasomotion (-46 +/- 2 mV) correlating (r = 0.87, p < 0.01) with time (8 +/- 2 s) at the largest diameter observed during vasomotion (41 +/- 2 microm); (2) a slow depolarization (1.8 +/- 0.2 mV s(-1)) with no diameter change; (3) a fast (9.1 +/- 0.8 mV s(-1)) depolarization (to -28 +/- 2 mV) and constriction; (4) a transient partial repolarization (3-4 mV); (5) a sustained (5 +/- 1 s) depolarization (-28 +/- 2 mV) correlating (r = 0.78, p < 0.01) with time (3 +/- 1 s) at the smallest diameter (27 +/- 2 microm) during vasomotion; (6) a slow repolarization (2.5 +/- 0.2 mV s(-1)) and relaxation. The absolute change in E(m) correlated (r = 0.60, p < 0.01) with the most negative E(m). Sodium nitroprusside or nifedipine caused sustained hyperpolarization and dilation, whereas tetraethylammonium or elevated PO(2) caused sustained depolarization and constriction. We suggest that vasomotion in vivo reflects spontaneous, cyclic changes in E(m) of SMC and EC corresponding with cation fluxes across plasma membranes.

Action Potentials↗
PubMedDate not supplied

Inhibition of vasoconstriction and Ca2+ currents mediated by neuropeptide Y Y2 receptors.

The effects of neuropeptide Y (NPY) and agonists selective for NPY Y1 and Y2 receptors were studied on contraction and Ca2+ currents in arterial smooth muscle. In isolated arterioles from the guinea pig small intestine, small brief constrictions were evoked by depolarising the arteriolar smooth muscle using high K+ solution applied from a micropipette. The constrictions were reduced in amplitude by the Y2-selective agonists PYY(13-36) and N-acetyl[Leu28, Leu31]NPY-(24-36) in concentrations from 20-100 nM. NPY or the Y1 selective agonist [Leu31 Pro34]NPY in concentrations from 50 pM to 100 nM increased the amplitude of the constrictions, with a maximum effect at 10 nM. Smooth muscle cells were isolated from rat small mesenteric arteries, and voltage-activated Ca2+ currents measured by whole cell patch clamping. The peak amplitude of the Ca2+ currents was decreased by N-acetyl[Leu28, Leu31]NPY-(24-36), and by NPY (100 nM). [Leu31, Pro34]NPY either had no effect or slightly increased the Ca2+ currents. We conclude that Y2 receptors on vascular smooth muscle can reduce Ca2+ currents induced by depolarisation, and thus oppose constriction caused by smooth muscle depolarisation.

Animals↗