β-Adrenergic receptors in the hepatic arterial bed of the anesthetized cat

1969 ◽  
Vol 47 (5) ◽  
pp. 415-419 ◽  
Author(s):  
C. V. Greenway ◽  
Anne E. Lawson
Keyword(s):  
Adrenergic Receptors ◽  
Electromagnetic Flowmeter ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Arterial Infusion ◽  
Arterial Blood ◽  
Basal Tone ◽  
Β Receptor ◽  
Β Adrenergic Receptors ◽  
Stimulation Of

The hepatic arterial blood flow of cats anesthetized with pentobarbital was recorded with an electromagnetic flowmeter. Administration of isoprenaline by close arterial infusion caused a vasodilatation which was blocked after propranolol. Adrenaline caused a variable change but after propranolol it consistently produced vasoconstriction, and after phenoxybenzamine, vasodilatation. One hour after phenoxybenzamine, stimulation of the sympathetic nerves caused a marked vasodilatation which was blocked by propranolol. It is concluded that both α and β adrenergic receptors are present in the hepatic arterial bed. However, β receptor responses may be difficult to elicit if the basal tone of the vascular bed is already reduced by prior procedures.

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.

Adrenergic modulation of reactive hyperemia in rat gut

1991 ◽  
Vol 261 (3) ◽  
pp. G392-G400 ◽  
Author(s):  
W. W. Pawlik ◽  
O. D. Hottenstein ◽  
E. D. Jacobson
Keyword(s):  
Adrenergic Receptors ◽  
Reactive Hyperemia ◽  
Arterial Occlusion ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Dependent Manner ◽  
Alpha Adrenergic Receptors ◽  
Arterial Blood ◽  
Adrenergic Modulation ◽  
Rat Gut

The hypothesis was tested that peripheral, adrenergic nerves modulate reactive hyperemia (RH) in the intestinal circulation. In anesthetized rats, anterior mesenteric arterial occlusion for 30-120 s elicited subsequent RH responses, including 63-118% increases in the velocity of arterial blood flow, even greater increases in conductance, and durations of 64-139 s. The longer the period of arterial occlusion, the greater the magnitude of RH. Electrical stimulation of postganglionic, sympathetic nerves reduced RH responses in a frequency-dependent manner. RH responses were enhanced by pretreatment with hexamethonium and phenoxybenzamine and were diminished by pretreatment with propranolol. Propranolol also prevented the enhanced RH responses caused by hexamethonium and phenoxybenzamine. Reserpine prevented the enhanced RH responses to hexamethonium, but bilateral adrenalectomy did not. These findings support the hypothesis that peripheral sympathetic nerves modulate RH in rat gut, with alpha-adrenergic receptors restricting and beta-adrenergic receptors enhancing the hyperemia.

α-Adrenergic receptor modulation of the intrathoracic efferent sympathetic nervous system regulating the canine heart

1989 ◽  
Vol 67 (10) ◽  
pp. 1199-1204 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Blocking Agent ◽  
Sympathetic Ganglia ◽  
Canine Heart ◽  
Receptor Modulation ◽  
Adrenergic Antagonist ◽  
Cervical Ganglia ◽  
Β Adrenergic Receptors ◽  
Stimulation Of

The augmentation of ventricular inotropism induced by electrical stimulation of acutely decentralized efferent sympathetic preganglionic axons was reduced, but still present, following administraiton of hexamethonium (10 mg/kg i.v.). While hexamethonium continued to be administered, the cardiac augmentations so induced were enhanced significantly following administration of the α-adrenergic receptor blocking agent, phentolamine myselate (1 mg/kg i.v.). Stimulation of the sympathetic efferent postganglionic axons in cardiopulmonary nerves induced cardiac augmentations that were unchanged following administration of these agents singly or together. The cardiac augmentations induced by stimulation of efferent preganglionic sympathetic axons were unchanged when phentolamine was administered alone. The augmentations of cardiac inotropism induced by efferent postganglionic sympathetic axonal stimulation were decreased following local administration of the β-adrenergic antagonist timolol into the ipsilateral stellate and middle cervical ganglia. Thereafter, these augmentations were unchanged following the subsequent intravenous administration of phentolamine. It is concluded that the activation of cardiac neurons in the stellate and middle cervical ganglia by stimulation of efferent preganglionic sympathetic axons can be modified by α-adrenergic receptors and that these effects are dependent upon β-adrenergic receptors, not nicotinic ones, in intrathoracic ganglia.Key words: α-adrenergic inotropism, sympathetic ganglia, hexamethonium, phentolamine.

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.

Hemodynamic Effects of CCl4 in the Intact Liver of the Cat

1974 ◽  
Vol 52 (3) ◽  
pp. 727-735 ◽  
Author(s):  
W. W. Lautt ◽  
G. L. Plaa
Keyword(s):  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Sympathetic Nerves ◽  
Causative Factor ◽  
Arterial Infusion ◽  
Total Blood ◽  
Arterial Blood ◽  
Reflex Activation ◽  
Total Blood Flow ◽  
Early Phases

Blood flow in the intact liver of anesthetized cats did not change significantly over a period of 4 h following intraduodenal injection of CCl4 (1 ml/kg). Hepatocellular disruption was well underway by 2 h after the injection. Twenty-four hours following an oral dose of CCl4, the hepatic arterial resistance to blood flow was reduced and total blood flow to the liver was at least as high as in control animals. At this time, the hepatic artery appeared fully dilated and was less responsive to humoral (intra-arterial infusion of noradrenaline) and neural (reflex activation of the sympathetic nerves) constrictor influences. Thus, alterations in hepatic blood flow do not occur during the early phases of CCl4-induced hepatic injury. These data indicate that diminished blood flow is not a causative factor in the initial phases of CCl4-induced liver injury. By 24 h, hepatic blood flow is altered in such a manner that the damaged liver receives a higher proportion of arterial blood and a total blood flow that is not reduced in spite of a generally depressed cardiovascular system.

STIMULATION OF β-ADRENERGIC RECEPTORS INHIBITS TUMOR NECROSIS FACTOR ALPHA RELEASE FROM THE ISOLATED RAT HEART

1999 ◽  
Vol 27 (Supplement) ◽  
pp. A70
Author(s):  
Walter H Newman ◽  
Manuel R Castresana ◽  
Zhongbiao Wang ◽  
Martin L Dalton ◽  
Debra J Warejcka
Keyword(s):  
Tumor Necrosis Factor ◽  
Adrenergic Receptors ◽  
Tumor Necrosis ◽  
Isolated Rat Heart ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Β Adrenergic Receptors ◽  
Necrosis Factor ◽  
Isolated Rat ◽  
Stimulation Of

Response to cardiac sympathetic activation in transgenic mice overexpressing beta 2-adrenergic receptor

1996 ◽  
Vol 271 (2) ◽  
pp. H630-H636 ◽  
Author(s):  
X. J. Du ◽  
E. Vincan ◽  
D. M. Woodcock ◽  
C. A. Milano ◽  
A. M. Dart ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Nerve Stimulation ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Sympathetic Nerves ◽  
Adrenergic Stimulation ◽  
Adrenergic Activity ◽  
Beta 2 ◽  
Stimulation Of

Transgenic mice have been created with 200-fold overexpression of beta 2-adrenergic receptors specifically in the heart. Cardiac function was studied in these transgenic mice and their controls at baseline and during isoproterenol perfusion or sympathetic nerve stimulation. The model used was an in situ buffer-perfused, innervated heart, and the left ventricle maximal derivative of pressure over time (dP/dtmax) and heart rate (HR) were measured. Basal HR and dP/dtmax were 30-40% higher in hearts from transgenic mice than controls. Electrical stimulation of sympathetic nerves (2, 4, and 8 Hz) or infusion of isoproterenol markedly increased HR and dP/dtmax in control hearts. Hearts from transgenic mice did not respond to isoproterenol. However, hearts from transgenic mice retained the HR response to nerve stimulation, and a small increase in dP/dtmax was also detected. Atenolol inhibited the response to nerve stimulation in control hearts but not that in hearts from transgenic mice. ICI-118551 inhibited the response in transgenic hearts. Basal HR and dP/dtmax were decreased by ICI-118551 only in transgenic hearts. Thus overexpression of cardiac beta 2-receptors modifies beta-adrenergic activity, but the responses to endogenous and exogenous adrenergic stimulation are affected differently.

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