Effects of aortic nerve stimulation on discharges of sympathetic neurons innervating rat tail artery and vein

1998 ◽  
Vol 275 (4) ◽  
pp. R942-R949 ◽  
Author(s):  
Christopher D. Johnson ◽  
Michael P. Gilbey
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Activity ◽  
Volume Expansion ◽  
Sympathetic Neurons ◽  
Data Set ◽  
Tail Artery ◽  
Aortic Nerve ◽  
Blood Volume Expansion ◽  
Rat Tail ◽  
Stimulation Of

Activity was recorded from postganglionic sympathetic neurons (PSNs) innervating either the caudal ventral artery (CVA) or a lateral vein (LV) of the tail circulation of anesthetized rats. The study sought to determine whether sympathetic activity directed at the CVA and LV was influenced by cardiovascular mechanoreceptor afferents and whether this effect was differential. Cardiac rhythmicity was not a robust component of either CVA PSN activity or LV PSN activity. Stimulation of an aortic nerve with short trains was followed by a decreased probability of discharge in both CVA and LV PSNs that was followed by a series of peaks that showed a constant periodicity that was not significantly different from that revealed by autocorrelogram analysis over the same data set. The latter dominant periodicity is referred to in this and related previous publications as the T rhythm. Furthermore, blood volume expansion and long-train aortic nerve stimulation produced a significant decrease in the frequency of the T rhythm. It is concluded that the CVA and LV sympathetic activity can be influenced by inputs from cardiovascular mechanoreceptors and that this effect is mediated in part by a modulation of the T rhythm.

Acute resetting of baroreceptor reflex in rabbits: a central component

1986 ◽  
Vol 250 (5) ◽  
pp. H866-H870 ◽  
Author(s):  
D. L. Kunze
Keyword(s):  
Arterial Pressure ◽  
Test Stimulus ◽  
Nerve Stimulation ◽  
Sympathetic Activity ◽  
Constant Stimulus ◽  
Baroreceptor Reflex ◽  
Pressure Response ◽  
Stimulus Period ◽  
Aortic Nerve ◽  
Stimulation Of

Electrical stimulation of the aortic nerve of the anesthetized rabbit was used to determine whether there is a central nervous system component to acute resetting of the baroreceptor reflex. After stimulation of the aortic nerve for 5 min at 10 Hz, a ramp test stimulus to the nerve produced a reflex arterial pressure response that was attenuated as compared with that produced by the same ramp prior to the five-min stimulation period. Renal sympathetic nerve activity was recorded simultaneously to determine whether a reduction in the magnitude of the reflex inhibition of sympathetic activity produced by the depressor nerve stimulation could account for the attenuated arterial pressure response. Renal activity during the test ramp was reduced to the same value both before and after the constant stimulus period and thus did not correlate with the attenuated pressure response. There was, however, prolonged inhibition of tonic sympathetic activity after the 5-min stimulus period such that during the test stimulus there was less sympathetic activity to inhibit. The results were similar when sympathetic activity was recorded from branches of the sciatic nerve and from thoracic postganglionic nerves. In these nerves the period of prolonged inhibition after aortic nerve stimulation was up to 5 min. The attenuated pressure response to baroreceptor nerve stimulation after a constant stimulus appears to reflect the reduced change in sympathetic activity rather than the value to which the sympathetic activity falls.

Aortic nerve-activated cardioinhibitory neurons and interneurons

1975 ◽  
Vol 229 (3) ◽  
pp. 783-789 ◽  
Author(s):  
J Schwaber ◽  
N Schneiderman
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Baroreceptor Reflex ◽  
Motor Nucleus ◽  
Vagus Nerves ◽  
Antidromic Activation ◽  
Medial Nucleus ◽  
Aortic Nerve ◽  
Dorsal Motor Nucleus ◽  
Stimulation Of

Unit activity evoked by electrical stimulation of the aortic and vagus nerves was recorded in the dorsal motor nucleus and nucleus solitarius of unanesthetized rabbits. Cardioinhibitory cells which showed antidromic activation to stimulation of the vagus nerve and synaptic activation to stimulation of the aortic nerve were localized in lateral dorsal motor nucleus 0.5-0.8 mm anterior of the obex. Additionally, units were found that appeared to be interneurons in the medullary pathway subserving baroreceptor reflex effects on cardioinhibitory neurons. These cells were activated by aortic, and usually vagus, nerve stimulation, appeared to be polysynaptically activated, and were located in medial nucleus solitarius rostral to the obex. Neurons reflecting a cardiac rhythm but not activated by aortic nerve stimulation were also observed.

Rat venular pressure-diameter relationships are regulated by sympathetic activity

1990 ◽  
Vol 259 (3) ◽  
pp. H674-H680 ◽  
Author(s):  
A. A. Shoukas ◽  
H. G. Bohlen
Keyword(s):  
Blood Volume ◽  
Sympathetic Activity ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Nervous System Activity ◽  
Blood Volume Expansion ◽  
Capacitance Characteristics ◽  
Sympathetic Nervous ◽  
Relationship Of ◽  
The Relationship

The hypothesis that the pressure-diameter relationship of intestinal venules in rats is primarily determined by sympathetic nervous system activity was tested. The pressure-diameter relationship of the smallest to largest diameter (20-100 microns) intestinal venules of the rat was measured at rest, during hemorrhage to increase sympathetic neural activity, and during saline volume expansion to decrease sympathetic activity. During hemorrhage, the diameter of all venules decreased approximately 10% at 10 mmHg venous pressure, and the slope of the pressure-diameter relationship increased approximately 50% above control. Blood volume expansion led to an approximately 10% increase in venule diameter at 10 mmHg and a 25% decrease in slope. Denervation of the vessels causes concomitant vasodilation, which was greater than the vasodilation caused by blood volume expansion. Hemorrhage after denervation caused no significant changes in the relationship when compared with denervated control. Nitroprusside caused an even greater vasodilation when compared with the pressure-diameter relationship after denervation. The results suggest that the slope and 10-mmHg intercept of the pressure-diameter relationship for the largest through smallest intestinal venules and, therefore, their vascular compliance and capacitance characteristics are primarily determined by sympathetic activity.

Phospholipase D is activated by G protein and not by calcium ions in vascular smooth muscle

1996 ◽  
Vol 270 (3) ◽  
pp. H1031-H1037
Author(s):  
E. F. LaBelle ◽  
R. M. Fulbright ◽  
R. J. Barsotti ◽  
H. Gu ◽  
E. Polyak
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
G Protein ◽  
Phospholipase D ◽  
Pertussis Toxin ◽  
Alpha Toxin ◽  
Tail Artery ◽  
Agonist Stimulation ◽  
Rat Tail ◽  
Stimulation Of

We assessed the sensitivity of phospholipase D (PLD) activity in vascular smooth muscle to cytosolic Ca2+ by increasing cytosolic Ca2+ levels independently of agonist stimulation. When rat tail artery was preloaded with the Ca2+ indicator fluo 3 pentaacetoxymethyl ester, the addition of high extracellular K+, caffeine, or norepinephrine rapidly enhanced cytosolic Ca2+ levels. Neither increased extracellular K+ nor caffeine addition increased phosphatidylethanol production, indicating that cytosolic Ca2+ elevation alone did not stimulate PLD. In contrast, norepinephrine stimulated phosphatidylethanol production in this tissue. In strips of tail artery permeabilized with alpha-toxin and incubated in solutions containing free Ca2+ concentrations observed during physiological stimulation (pCa 6.4), PLD was not stimulated, whereas incubation with guanosine 5'-O-(3-thiotriphosphate) at pCa 7.0 activated this enzyme. Aluminum fluoride (AlF4-) stimulated PLD, and this activity was insensitive to pertussis toxin after stimulation by either norepinephrine or AlF4-. These results indicate that PLD in vascular smooth muscle is activated by norepinephrine via stimulation of a pertussis toxin-insensitive G protein and not via an increase in intracellular Ca2+ levels.

Some effects of the ionophore X-537A on the isolated rat tail artery

1978 ◽  
Vol 56 (3) ◽  
pp. 474-482 ◽  
Author(s):  
Vladimír Palatý ◽  
Mary E. Todd
Keyword(s):  
Smooth Muscle ◽  
Contractile Response ◽  
Rat Tail Artery ◽  
Concentration Gradients ◽  
Irreversible Loss ◽  
Tail Artery ◽  
Endogenous Catecholamines ◽  
Rat Tail ◽  
Isolated Rat ◽  
Stimulation Of

The effects of micromolar concentrations of the ionophore X-537A (RO 2-2985) were studied using isolated preparations of the rat tail artery. The ionophore causes complete release of catecholamines from adrenergic nerves, which is the sole cause of the transient contractile response. The amines are released by a nonexocytotic process which seems to be related to the ability of X-537A to act as an efficient transmembrane carrier of Na+, K+, and H+ The ionophore also causes an almost complete and irreversible loss of the cocaine-sensitive component of metaraminol uptake by the tissue. X-537A dissipates the transmembrane concentration gradients of Na and K in the smooth muscle component of the preparation. This effect is unrelated to the release of endogenous catecholamines, and it can also be observed after the Na pump has been inhibited with ouabain. It is fully reversible, though not readily, and it can be induced repeatedly. In catecholamine-depleted strips, X-537A dissipates the transmembrane Na+ and K+ gradients without causing any change in tension. Stimulation of the rate of O2 consumption by X-537A in catecholamine-depleted tissue is reversible, and it is unaffected by ouabain and (or) removal of external Ca2+.

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