Adenosine modulation of vasoconstrictor responses to stimulation of sympathetic nerves and norepinephrine infusion in the superior mesenteric artery of the cat

1988 ◽  
Vol 66 (7) ◽  
pp. 937-941 ◽  
Author(s):  
W. Wayne Lautt ◽  
Leslie K. Lockhart ◽  
Dallas J. Legare
Keyword(s):  
Superior Mesenteric Artery ◽  
Nerve Stimulation ◽  
Adenosine Receptors ◽  
Mesenteric Artery ◽  
Sympathetic Nerves ◽  
Sympathetic Nerve Stimulation ◽  
Vascular Bed ◽  
Norepinephrine Infusion ◽  
Resistance Vessels ◽  
Stimulation Of

Vasoconstriction induced by sympathetic nerve stimulation and by norepinephrine infusion in the superior mesenteric artery of cats anesthetized with pentobarbital was inhibited by adenosine infusions in a dose-related way. The responses to nerve stimulation were not inhibited to a greater extent than the responses to norepinephrine, thus suggesting no presynaptic modulation of sympathetic nerves supplying the resistance vessels of the feline intestinal vascular bed. Blockade of adenosine receptors using 8-phenyltheophylline did not alter the degree of constriction induced by nerve stimulation or norepinephrine infusion, indicating that in the fasted cat, endogenous adenosine co-released or released subsequent to constriction does not affect the peak vasoconstriction reached. Isoproterenol caused similar degrees of vasodilation as adenosine but did not show significant antagonism of the pooled responses to nerve stimulation or norepinephrine infusion; there was no tendency for the degree of dilation induced by isoproterenol to correlate with the inhibition of constrictor responses. Thus, the effect of adenosine on nerve- and norepinephrine-induced constriction is not secondary to nonspecific vasodilation.

Responses of isolated perfused arteries to catecholamines and nerve stimulation

1965 ◽  
Vol 209 (2) ◽  
pp. 376-382 ◽  
Author(s):  
Larry A. Rogers ◽  
Richard A. Atkinson ◽  
John P. Long
Keyword(s):  
Nerve Stimulation ◽  
Mesenteric Artery ◽  
Muscle Tone ◽  
Low Frequency ◽  
Sympathetic Nerves ◽  
Gas Mixture ◽  
Constant Flow ◽  
Pressor Responses ◽  
Resistance Vessels ◽  
Small Resistance

An isolated preparation of the dog's mesenteric artery with branching small resistance vessels and sympathetic nerves attached has been devised. The branching arterial segments were perfused by a constant-flow technique; the pressor responses to intra-arterially injected catecholamine and to nerve stimulation were recorded. The preparation gave reproducible pressor responses to injected catecholamine and to nerve stimulation for periods of several hours. Decreasing the temperature or increasing the pH (by decreasing CO2 in the gas mixture) of the vessel bath increased arterial smooth muscle tone and potentiated the pressor responses to injected catecholamine and to nerve stimulation. Increasing the temperature of the bath decreased the tone and reactivity of this preparation. Low-frequency continuous nerve stimulation potentiated the responses of this preparation to intra-arterially injected catecholamines.

Vascular escape from vasoconstriction and post-stimulatory hyperemia in the superior mesenteric artery of the cat

1988 ◽  
Vol 66 (9) ◽  
pp. 1174-1180 ◽  
Author(s):  
W. Wayne Lautt ◽  
Dallas J. Legare ◽  
Leslie K. Lockhart
Keyword(s):  
Superior Mesenteric Artery ◽  
Adenosine Receptors ◽  
Mesenteric Artery ◽  
Vascular Tone ◽  
Low Dose ◽  
Data Interpretation ◽  
High Dose ◽  
Partial Recovery ◽  
Sympathetic Nerve Stimulation

Vascular escape is seen as a partial recovery from initial vasoconstriction despite continued constrictor stimuli. Escape in the feline intestine (superior mesenteric artery) occurred for i.a. norepinephrine (NE) infusions (56% escape for low dose, 40% for high dose NE) and for sympathetic nerve stimulation (SNS) (65% for 1 Hz, 49% for 3 Hz, 44% for 9 Hz). Adenosine infusion or blockade of adenosine receptors (8-phenyltheophylline) did not alter the escape, showing that endogenous adenosine levels are unlikely to play any role in the mechanism of escape. Other aspects of escape were studied: equiconstrictor doses of NE given i.a. or i.v. lead to similar degrees of escape; propranolol and ouabain did not alter escape; the degree of escape was significantly greater for the low dose NE and the 1-Hz SNS than for higher intensities of stimulation, however, escape did not inversely correlate significantly with the initial degree of vasoconstriction when all data were pooled. Post-stimulatory hyperemia occurs upon cessation of vasoconstrictor stimuli, reaches a peak conductance within 1 min, and returns to baseline within about 3 min. Hyperemia was quantitated from the peak vasodilation and from the area under the flow–hyperemia curve. The hyperemias were not related to NE dose or SNS frequency nor did they correlate with initial vasoconstriction or extent of vascular escape. Contrary to the hypothesis that adenosine may mediate hyperemia, adenosine infusions reduced the response and adenosine receptor antagonism tended to elevate the response. Propranolol and ouabain did not produce significant effects on post-stimulatory hyperemia. A discussion of the merits of using vascular resistance or conductance to assess vascular tone and vascular escape concludes that in the in vivo systems in which changes in vascular tone result mainly in changes in blood flow, the use of resistance is unacceptable and may lead to serious error in data interpretation.

Adenosine modulation of hepatic arterial but not portal venous constriction induced by sympathetic nerves, norepinephrine, angiotensin, and vasopressin in the cat

1986 ◽  
Vol 64 (4) ◽  
pp. 449-454 ◽  
Author(s):  
W. Wayne Lautt ◽  
Dallas J. Legare
Keyword(s):  
Smooth Muscle ◽  
Hepatic Artery ◽  
Nerve Stimulation ◽  
Adenosine Receptors ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Resistance Vessels ◽  
Basal Tone ◽  
Intrinsic Regulation

Intrinsic regulation of hepatic arterial blood flow depends upon local concentrations of adenosine. The present data show that i.a. infusions of adenosine cause dilation of the hepatic artery and inhibition of arterial vasoconstriction induced by norepinephrine, vasopressin, angiotensin, and hepatic nerve stimulation. Vasoconstriction induced by submaximal nerve stimulation (2 Hz) and norepinephrine infusions (0.25 and 0.5 μg∙kg−1∙min−1, i.p.v.) were equally inhibited by adenosine. Supramaximal nerve stimulation (8 Hz) was inhibited to a lesser extent. The data are consistent with the hypotheses that (a) adenosine causes nonselective inhibition of vasoconstrictor influences on the hepatic artery; and (b) adenosine antagonizes neurally induced vasoconstriction by a purely postsynaptic effect and does not decrease norepinephrine release. In contrast with the hepatic artery, the intrahepatic portal resistance vessels are not affected by even large doses of adenosine; neither responses in basal tone nor antagonism of vasoconstrictor effects of nerve stimulation, norepinephrine, or angiotensin could be demonstrated. The data are consistent with the hypothesis that the smooth muscle of the portal resistance vessels does not contain adenosine receptors, whereas adenosine receptors on the smooth muscle of the hepatic arterial resistance vessels are of major regulatory importance. Whether endogenous levels of adenosine can reach sufficient concentration to modulate endogenous constrictors remains to be determined.

Mechanism of enhanced myogenic response in arterioles during sympathetic nerve stimulation

1992 ◽  
Vol 263 (4) ◽  
pp. H1185-H1189 ◽  
Author(s):  
P. Ping ◽  
P. C. Johnson
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Similar Degree ◽  
Sartorius Muscle ◽  
Myogenic Response ◽  
Pressure Reduction ◽  
Sympathetic Nerve Stimulation ◽  
Norepinephrine Infusion ◽  
Cell Velocity ◽  
Significant Mechanism

In a previous study we found that the arteriolar myogenic response was enhanced during sympathetic nerve stimulation in the cat sartorius muscle. In this study we determined whether the enhancement was unique to sympathetic nerve stimulation. Changes of arteriolar diameter and red cell velocity during femoral arterial pressure reduction from 110 to 60 mmHg were examined. Arterioles of 40 microns diameter were constricted by norepinephrine infusion to a similar degree as sympathetic nerve stimulation. Arteriolar dilation to pressure reduction was significantly enhanced during norepinephrine infusion and was not significantly different from that during sympathetic nerve stimulation. This indicates that junctional release of transmitters is not essential and rules out prejunctional inhibition of neurotransmitter release during pressure reduction as a significant mechanism in the enhanced dilation. Arteriolar dilation to pressure reduction was also enhanced during vasopressin or BAY K 8644 (a calcium channel agonist) infusion. In all instances, autoregulation of flow was significantly enhanced. These results demonstrate that modulation of the myogenic response occurs at postreceptor sites in the smooth muscle cell.

Glucagon inhibition of hepatic arterial responses to hepatic nerve stimulation

1977 ◽  
Vol 233 (6) ◽  
pp. H647-H654 ◽  
Author(s):  
P. D. Richardson ◽  
P. G. Withrington
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Perfusion Pressure ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Arterial Responses ◽  
Sympathetic Discharge ◽  
Glucagon Concentration

The hepatic arterial vascular bed of the chloaralose-urethan-anesthetized dog was perfused with blood from a cannulated femoral artery. Hepatic arterial blood flow and perfusion pressure were measured. The hepatic periarterial postganglionic sympathetic nerves were stimulated supramaximally at 0.1, 0.5, 1, 2, 5, 10, and 20 Hz; this caused frequency-dependent rises in the calculated hepatic arterial vascular resistance at all frequencies above the threshold of 0.1 or 0.5 Hz. Glucagon was infused intra-arterially in dosese from 0.25 to 10 microgram/min; glucagon antagonized both the vasoconstrictor effects of hepatic nerve stimulation and of intra-arterial injections of norepinephrine. The degree of antagonism of these responses was significantly correlated with the calculated hepatic arterial glucagon concentration. It is possible that glucagon released physiologically in stress and hypoglycemia may protect the hepatic arterial vasculature from the effects of increased sympathetic discharge.

scholarly journals Pancreatic and extrapancreatic galanin release during sympathetic neural activation

1990 ◽  
Vol 258 (3) ◽  
pp. E436-E444 ◽  
Author(s):  
B. E. Dunning ◽  
P. J. Havel ◽  
R. C. Veith ◽  
G. J. Taborsky
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Sympathetic Nerves ◽  
Neural Activation ◽  
Anesthetized Dogs ◽  
Basal Insulin Secretion ◽  
Peripheral Arterial ◽  
Splanchnic Nerve Stimulation ◽  
Stimulation Of

To address the hypothesis that the neutropeptide, galanin, functions as a sympathetic neurotransmitter in the endocrine pancreas, we sought to determine if galanin is released from pancreatic sympathetic nerves during their direct electrical stimulation in halothane-anesthetized dogs. During bilateral thoracic splanchnic nerve stimulation (BTSNS), both peripheral arterial and pancreatic venous levels of galanin-like immunoreactivity (GLIR) increased (delta at 10 min = +92 +/- 31 and +88 +/- 25 fmol/ml, respectively). Systemic infusions of synthetic galanin demonstrated that 1) the increment of arterial GLIR observed during BTSNS was sufficient to modestly restrain basal insulin secretion and 2) only 25% of any given increment of arterial GLIR appears in the pancreatic vein, suggesting that the pancreas extracts galanin, as it does other neurotransmitters. By use of 75% for pancreatic extraction of circulating galanin, it was calculated that pancreatic galanin spillover (output) increased by 410 +/- 110 fmol/min during BTSNS. To reinforce the conclusion that pancreatic sympathetic nerves release galanin, GLIR spillover was next measured during direct local stimulation of the pancreatic sympathetic input produced by electrical stimulation of the mixed autonomic pancreatic nerves (MPNS) in the presence of the ganglionic blocker, hexamethonium. During this local pancreatic sympathetic nerve stimulation, arterial GLIR remained unchanged, but pancreatic venous GLIR increased by 123 +/- 34 fmol/ml. Thus pancreatic GLIR spillover increased by 420 +/- 110 fmol/min during MPNS in the presence of hexamethonium. We conclude that galanin is released from both pancreatic and extrapancreatic sources during sympathetic neural activation in dogs.

scholarly journals Heart Rate Variability and Hemodynamic Change in the Superior Mesenteric Artery by Acupuncture Stimulation of Lower Limb Points: A Randomized Crossover Trial

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Soichiro Kaneko ◽  
Masashi Watanabe ◽  
Shin Takayama ◽  
Takehiro Numata ◽  
Takashi Seki ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Superior Mesenteric Artery ◽  
Lower Limb ◽  
Mesenteric Artery ◽  
Low Frequency ◽  
Autonomic Nerve ◽  
Nerve Activity ◽  
Acupuncture Stimulation ◽  
Stimulation Of

Objective. We investigated the relationship between superior mesenteric artery blood flow volume (SMA BFV) and autonomic nerve activity in acupuncture stimulation of lower limb points through heart rate variability (HRV) evaluations.Methods. Twenty-six healthy volunteers underwent crossover applications of bilateral manual acupuncture stimulation at ST36 or LR3 or no stimulation. Heart rate, blood pressure, cardiac index, systemic vascular resistance index, SMA BFV, and HRV at rest and 30 min after the intervention were analyzed.Results. SMA BFV showed a significant increase after ST36 stimulation (0% to 14.1% ± 23.4%,P=0.007); very low frequency (VLF), high frequency (HF), low frequency (LF), and LF/HF were significantly greater than those at rest (0% to 479.4% ± 1185.6%,P=0.045; 0% to 78.9% ± 197.6%,P=0.048; 0% to 123.9% ± 217.1%,P=0.006; 0% to 71.5% ± 171.1%,P=0.039). Changes in HF and LF also differed significantly from those resulting from LR3 stimulation (HF: 78.9% ± 197.6% versus −18.2% ± 35.8%,P=0.015; LF: 123.9% ± 217.1% versus 10.6% ± 70.6%,P=0.013).Conclusion. Increased vagus nerve activity after ST36 stimulation resulted in increased SMA BFV. This partly explains the mechanism of acupuncture-induced BFV changes.

Direct evidence for the role of neuropeptide Y in sympathetic nerve stimulation-induced vasoconstriction

1998 ◽  
Vol 274 (1) ◽  
pp. H290-H294 ◽  
Author(s):  
Songping Han ◽  
Chun-Lian Yang ◽  
Xiaoli Chen ◽  
Linda Naes ◽  
Bryan F. Cox ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Perfusion Pressure ◽  
Biological Action ◽  
Sympathetic Nerve Stimulation ◽  
Low Frequencies ◽  
Vascular Bed ◽  
Potentiation Effect ◽  
Mesenteric Vascular Bed

Neuropeptide Y (NPY) is a vasoconstrictor peptide and a cotransmitter with norepinephrine (NE) in sympathetic nerve terminals and is thought to be involved in sympathetic nerve stimulation (SNS)-induced vasoconstriction. Using BIBP-3226, a Y1 receptor selective antagonist, we examined this hypothesis in the isolated and perfused mesenteric vascular bed. SNS produced a frequency-dependent increase in perfusion pressure and concomitant overflow of NPY immunoreactivity in the perfusate. [Leu31,Pro34]NPY potentiated NE-induced and ATP-induced vasoconstriction, indicating the presence and biological action of Y1 receptors in this vascular bed. The potentiation effect of [Leu31,Pro34]NPY of the increase in perfusion pressure by NE, ATP, or SNS was prevented by BIBP-3226. In addition, SNS-induced vasoconstriction at both high and low frequencies was significantly attenuated by BIBP-3226 at a concentration that completely blocked the [Leu31,Pro34]NPY-induced potentiation of the NE- or ATP-induced vasoconstrictor effect. These results suggest that ∼30% of vasoconstriction produced by SNS depends on NPY in the mesenteric vascular bed.

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