Effect of adenosine and glucagon on hepatic blood volume responses to sympathetic nerves

1991 ◽  
Vol 69 (1) ◽  
pp. 43-48 ◽  
Author(s):  
W. Wayne Lautt ◽  
Joshua Schafer ◽  
Dallas J. Legare
Keyword(s):  
Blood Volume ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Liver Weight ◽  
Maximal Response ◽  
Venous Capacitance ◽  
Resistance Vessels ◽  
Capacitance Vessels

Hepatic blood volume responses were studied in cats using in vivo plethysmography. The maximal response (Rmax) to sympathetic nerve stimulation and to infusions of norepinephrine into the hepatic artery or portal vein was similar (12–14 mL expelled per liver in 2.9-kg cats; average liver weight, 76.8 ± 6.8 g). The ED50 for norepinephrine intraportal (0.44 ± 0.13) and intrahepatic arterial infusions (0.33 ± 0.08 μg∙kg−1∙min−1) were similar indicating equal access of both blood supplies to the capacitance vessels. Adenosine (2.0 mg∙kg−1∙min−1) did not cause significant volume changes but produced a mild (27%) suppression of Rmax due to nerve stimulation with no change in the frequency (3.4 Hz) needed to produce 50% of Rmax. Rmax tended (not statistically significant) to decrease during glucagon (1.0 μg∙kg−1∙min−1) infusion but the nerve frequency needed to produce 50% of Rmax rose to 5.6 Hz. Thus both adenosine and glucagon produced modulation of sympathetic nerve-induced capacitance responses without having significant effects on basal blood volume. Adenosine, by virtue of its marked effects on arterial resistance vessels (at substantially lower doses than those used here) and the relative lack of effect on venous capacitance vessels, may be useful for producing clinical afterload reduction without venous pooling.Key words: blood volume, capacitance, sympathetic nerves, adenosine, glucagon.

Effects of nifedipine on hepatic blood volume in cats: indirect venoconstriction and absence of inhibition of postsynaptic α2-adrenoceptor responses

1986 ◽  
Vol 64 (5) ◽  
pp. 615-620 ◽  
Author(s):  
R. Segstro ◽  
K. L. Seaman ◽  
I. R. Innes ◽  
C. V. Greenway
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Intravenous Administration ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Adrenal Glands ◽  
Sympathetic Nerves ◽  
Direct Effects ◽  
Sympathetic Nerve Stimulation ◽  
Α2 Adrenoceptor

Intravenous administration of hypotensive doses (30–200 μg/kg) of nifedipine to cats anesthetized with pentobarbital caused an increase in cardiac output accompanied by hepatic venoconstriction. The hepatic venoconstriction and the increase in cardiac output were abolished in animals in which the hepatic sympathetic nerves were cut, the adrenal glands were excluded, and the kidneys were removed. This contrasts with the indirect hepatic venoconstrictor action of isoproterenol which was shown previously not to be abolished by these procedures. Further experiments showed that the hepatic venoconstrictor effect of nifedipine was blocked by removal of the kidneys, but not by removal of the hepatic sympathetic nerves and adrenals. These results support the hypothesis that venoconstriction plays an important role when drugs produce increased cardiac output. In nephrectomized animals, nifedipine had no direct effects on hepatic blood volume and it did not alter the effects of infusions of norepinephrine on hepatic blood volume, which have previously been shown to be mediated through α2-adrenoceptors. However, it did reduce the hepatic venous responses to hepatic sympathetic nerve stimulation by 30%.

Influence of sympathetic discharge pattern on norepinephrine and neuropeptide Y release

1989 ◽  
Vol 257 (3) ◽  
pp. H866-H872 ◽  
Author(s):  
J. Pernow ◽  
J. Schwieler ◽  
T. Kahan ◽  
P. Hjemdahl ◽  
J. Oberle ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Impulse Activity ◽  
Sympathetic Nerve Stimulation ◽  
Vasoconstrictor Response ◽  
Neuropeptide Y Release ◽  
Sympathetic Discharge ◽  
Stimulation Pattern

The effects of sympathetic nerve stimulation on vasoconstrictor responses and overflow of norepinephrine (NE) and neuropeptide Y-like immunoreactivity (NPY-LI) were studied in the dog gracilis muscle and pig spleen in vivo. A continuous regular impulse activity was compared with irregular human sympathetic and regular bursting patterns. During control conditions, stimulation with the irregular activity induced larger peak vasoconstriction than the regular activity at 0.59 Hz, but not at higher frequencies in the muscle, at 0.59 and 2.0 Hz in the spleen. The nerve stimulation-evoked overflow of NE and NPY-LI from the muscle were not influenced by the pattern of stimulation. The overflow of NPY-LI, but not that of NE, from the spleen was enhanced by the irregular activity at 0.59 and 2.0 Hz, and both NPY-LI and NE overflows were enhanced by regular burst activity at 2.0 Hz. After blockade of alpha- and beta-adrenoceptors by phenoxybenzamine and propranolol, respectively, which enhanced nerve stimulation-evoked overflow of both NE and NPY-LI, the NE overflow from the muscle evoked by the irregular activity was slightly larger at 0.59 Hz but smaller at higher frequencies compared with that evoked by regular activity, whereas the detectable overflow of NPY-LI was not largely influenced by the stimulation pattern. In conclusion, both the vasoconstrictor response and the overflow of NPY-LI and NE seem to be influenced by the pattern and frequency of sympathetic nerve stimulation.

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.

Escape from vasoconstriction in the gastric microcirculation

1975 ◽  
Vol 228 (6) ◽  
pp. 1893-1895 ◽  
Author(s):  
Paul H. Guth ◽  
Esther Smith
Keyword(s):  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
System Response ◽  
In Vivo Microscopy ◽  
Adrenergic Stimulation ◽  
Resistance Vessels ◽  
Autoregulatory Escape ◽  
Splanchnic Nerve Stimulation ◽  
Gastric Microcirculation

Escape of splanchnic resistance vessels from vasoconstriction due to adrenergic stimulation has been attributed to increasing submucosal blood flow due to dilation of submucosal arteriovenous anastomoses (shunts). This postulate, as applied to the rat gastric microcirculation, was studied by in vivo microscopy. Using an image-splitting TV microscope recording system, response of gastric submucosal arterioles (13–33 µm) to 3 min of left splanchnic nerve stimulation, norepinephrine superfusion, and vasopressin superfusion was measured. All stimuli produced initial vasoconstriction. Escape occurred in all rats with nerve stimulation and norepinephrine, but in only one of five with vasopressin. No shunts were seen. The study demonstrates that the gastric submucosal arterioles exhibit an escape phenomenon, suggesting that "autoregulatory escape" in other splanchnic beds also may be due to relaxation of constricted vessels and not to opening of shunts.

Presynaptic inhibitory effects of sotalol, propranolol, and acebutolol on noradrenaline release upon cardiac sympathetic nerve stimulation in anesthetized dogs

1986 ◽  
Vol 64 (8) ◽  
pp. 1076-1084 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Michel Naud ◽  
Daniel Lamontagne ◽  
Reginald Nadeau ◽  
Jacques de Champlain
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Inhibitory Effect ◽  
Cardiac Sympathetic Nerve ◽  
Sympathetic Nerve Stimulation ◽  
Flow Response ◽  
Anesthetized Dogs ◽  
Na Release

Effect of sotalol (STL) was compared with that of (±)-propranolol, (+)-propranolol (PPL), and acebutolol (ABL) on noradrenaline (NA) release as measured in coronary sinus (CS) blood during postganglionic stimulation (2 Hz, 30 s) of the left cardiac sympathetic nerves in anesthetized dogs. In control dogs receiving saline, increasing responses of CS-NA concentration, mean CS blood flow, and CS-NA output to repetitive stimulation were relatively stable throughout a given experimental period. Both STL (1, 2.5, and 5 mg/kg, i.v.) and (±)-PPL (0.5 and 2.5 mg/kg, i.v.) diminished the increased CS-NA concentration by approximately 35 (P < 0.05) to 60% (P < 0.01) in a dose-dependent fashion. However, (+)-PPL (0.02–2.5 mg/kg, i.v.) and ABL (0.5–5 mg/kg, i.v.) did not significantly alter the increasing response of CS-NA concentration upon stimulation. STL, (±)-PPL, and ABL markedly inhibited the CS blood flow response to stimulation at all doses tested, while (+)-PPL did not significantly diminish the flow response even at the highest dose tested. Consequently, CS-NA output decreased significantly (p < 0.01) in the presence of STL, (±)-PPL, and ABL at all doses tested but not with (+)-PPL at any dose tested. The inhibitory effect of STL and (±)-PPL on the increasing response of CS-NA concentration upon stimulation could be related to their beta-blocking effect, which exerts presumably on postulated presynaptic β-adrenoceptors, as (+)-PPL did not at all diminish the response. On the other hand, ABL does not seem to exert a similar presynaptic inhibitory effect, owing presumably either to its β-1 selectivity or to its intrinsic sympathetic activity. The results support the existence of facilitatory presynaptic β-adrenoceptors in the normal dog heart under in vivo conditions. The findings also suggest that NA release upon cardiac sympathetic nerve stimulation may be reflected more precisely by CS-NA concentration than by NA output.

Escape from vasoconstriction in the gastric microcirculation

1975 ◽  
Vol 228 (6) ◽  
pp. 1880-1886 ◽  
Author(s):  
PH Guth ◽  
E Smith
Keyword(s):  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
System Response ◽  
In Vivo Microscopy ◽  
Adrenergic Stimulation ◽  
Resistance Vessels ◽  
Autoregulatory Escape ◽  
Splanchnic Nerve Stimulation ◽  
Gastric Microcirculation

Escape of splanchic resistance vessels from vasconstriction due to adrenergic stimulation has been attributed to increasing submucosal blood flow due to dilation of submucosal arteriovenous anastomes (shunts). This postulate, as applied to the rat gastric microcirculation, was studied by in vivo microscopy. Using an image-splittingTV microscope recording system, response of gastric submucosal arterioles (13-33 mum)to 3 min of left splanchnic nerve stimulation, norepinephrine superfision, and vasopressin superfission was measured. All stimuli produced initial vasoconstriction.Escape occurred in all rats with nerve stimulation and norepinephrine, but in onlyone of five with vasopressin. No shunts were seen. The study demonstrates that thegastric submucosal arterioles exhibit an escape phenomenon, suggesting that "autoregulatory escape" in other splanchic beds also may be due to relaxation of constricted vessels and not to opening of shunts.

Antagonism of vasoconstriction by muscle contraction differs with alpha-adrenergic subtype

1993 ◽  
Vol 264 (3) ◽  
pp. H892-H900 ◽  
Author(s):  
L. R. Dodd ◽  
P. C. Johnson
Keyword(s):  
Muscle Contraction ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Second Order ◽  
Sartorius Muscle ◽  
Receptor Subtypes ◽  
Sympathetic Nerve Stimulation ◽  
Adrenergic Antagonist ◽  
Prejunctional Inhibition

It has been suggested that muscle contraction causes prejunctional inhibition of transmitter release from sympathetic nerves. In accordance with this, we found that second-order (50 microns ID) arterioles of the cat sartorius muscle dilate 40-80% more with muscle contraction during 2-, 4-, or 8-Hz sympathetic nerve stimulation than during equivalent constriction produced by intravenous norepinephrine injection. However, when constriction was to the selective alpha 1-agonist phenylephrine, the magnitude of dilation induced by muscle contraction was similar to that seen with sympathetic nerve stimulation, suggesting that prejunctional inhibition is not involved. Alternatively, different receptor subtypes may be activated by sympathetic nerve stimulation and exogenous norepinephrine. In support of this explanation, we found that approximately 50% of the vasoconstrictor effect of sympathetic nerve stimulation (8 Hz) was blocked by prazosin, an alpha 1-adrenergic antagonist, but no further diminution of tone was seen with addiction of yohimbine, an alpha 2-adrenergic antagonist. In contrast, the vasoconstrictor response to exogenous norepinephrine was not affected by prazosin, while addition of yohimbine almost completely blocked the response. These findings suggest that muscle contraction selectively attenuates vasoconstriction mediated by junctional receptors in second-order arterioles.

Comparative Effects of Prostaglandins A2 and B2 on Vascular and Airway Resistances and Adrenergic Neurotransmission

1974 ◽  
Vol 52 (3) ◽  
pp. 699-705 ◽  
Author(s):  
Stanley Greenberg ◽  
Linda Howard ◽  
William R. Wilson
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Neurotransmitter Release ◽  
Airway Resistance ◽  
Autologous Blood ◽  
Sympathetic Nerve Stimulation ◽  
Systemic Pressure ◽  
Low Concentrations ◽  
Pressor Responses

Prostaglandin B2 (PGB2) may be formed from PGA2in vivo. The following study compares the effects of equivalent concentrations of PGA2 and PGB2 on systemic pressure, heart rate, airway resistance, cutaneous vascular resistance, and responses to sympathetic nerve stimulation and to norepinephrine and tyramine in the acutely denervated canine hind paw perfused with autologous blood at constant flow. Intra-arterial (i.a.) PGB2 (1 and 10 μg/min) produced concentration-dependent vasoconstriction. Fifteen minutes after PGB2 administration the pressor responses of the paw to sympathetic nerve stimulation were enhanced, whereas the pressor responses to norepinephrine and tyramine were unchanged. In contrast, low concentrations of PGA2 produced systemic and transient cutaneous dilation whereas the higher concentration (10 μg/min i.a.) produced systemic dilation and constriction of the acutely denervated paw. The pressor responses of the perfused paw to sympathetic nerve stimulation were enhanced with the higher infusion rate of PGA2. However, the pressor responses to norepinephrine and tyramine were unchanged during PGA2. In addition, PGB2, but not PGA2, increased airway resistance. These results suggest that: (1) PGB2 and PGA2 have different effects on systemic pressure and airway resistance but have similar effects on the cutaneous vascular bed; (2) both PGB2 and PGA2 selectively enhance neurotransmitter release from the catecholamine pool susceptible to activation by the nerve action potential; and (3) PGB2 is more potent in its ability to enhance neurotransmitter release than PGA2. The vasoconstriction and facilitation of sympathetic neurotransmission by PGA2 may be related to formation of PGB2 within the paw.

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