Interaction of histamine with noradrenergic constrictory mechanisms in cat cerebral arteries and veins

1983 ◽  
Vol 61 (7) ◽  
pp. 756-763 ◽  
Author(s):  
Paul M. Gross ◽  
A. Murray Harper ◽  
Graham M. Teasdale
Keyword(s):  
Cerebral Arteries ◽  
Sympathetic Nerves ◽  
Histamine Receptor ◽  
Inhibitory Influence ◽  
Sympathetic Nerve Stimulation ◽  
Pial Arteries ◽  
Simultaneous Application ◽  
Arteries And Veins ◽  
Stimulation Of

We examined responses of pial arteries and veins in situ to noradrenergic stimuli in the presence of histamine. Electrical stimulation of sympathetic nerves and perivascular microapplication of norepinephrine in mock cerebrospinal fluid produced constriction of arteries and veins in anesthetized cats. During simultaneous perivascular injection of histamine, these noradrenergic responses were attenuated or reversed. In both arteries and veins, constriction from sympathetic nerve stimulation was prevented by simultaneous application of the histamine receptor agonists, pyridylethylamine (H1) or impromidine (H2), results that suggest interference involving both types of histamine receptors. In arteries, impromidine, but not pyridylethylamine, inhibited constriction resulting from exogenous norepinephrine. Our findings indicate that histamine may have an inhibitory influence, exerted through both receptor types, on noradrenergic mechanisms in cerebral vessels.

scholarly journals Effects of Kininase II Inhibitors on the Vasomotor Response to Bradykinin of Feline Intracranial and Extracranial Arteries in vitro and in situ

1983 ◽  
Vol 3 (3) ◽  
pp. 339-345 ◽  
Author(s):  
Michael Wahl ◽  
Alan R. Young ◽  
Lars Edvinsson ◽  
Franz Wagner
Keyword(s):  
Cerebral Arteries ◽  
Surrounding Tissue ◽  
Experimental Conditions ◽  
Pial Arteries ◽  
Simultaneous Application ◽  
Kininase Ii ◽  
Middle Cerebral Arteries ◽  
Prostaglandin F

Bradykinin is known to effect a vasodilatation of feline cerebral arteries in situ and of both human and feline pial arteries in vitro. In order to demonstrate whether kininase II (localized within the vessel wall or in the surrounding tissue or fluid) influences the response to bradykinin, two different inhibitors of this bradykinin degradation enzyme were tested. Perivascular microapplication of potentiator C (10−10–10−4 M) or captopril (10−10–10−3 M) did not, by itself, change the diameter of feline pial arteries (87–305 μm) in situ. In a similar investigation, the dilating action of bradykinin (10−8–10−5 M) was not modified by the simultaneous application of potentiator C or captopril (10−5 M). Furthermore, the relaxing effect of bradykinin (10−10–10−4 M) on isolated feline middle cerebral arteries (preconstricted with 5-hydroxytryptamine or prostaglandin F2α) was not influenced by the presence of captopril (10−7 M). In contrast, when studied on isolated extracranial vessel segments (feline sublingual artery), bradykinin caused a concentration-dependent constriction of the artery. This constriction was completely reversed to dilatation in the presence of captopril (10−7 M). Moreover, the characteristic effect of kininase II inhibition was demonstrated in the isolated guinea pig ileum preparation. In this instance, bradykinin induced a concentration-dependent contraction that was enhanced by potentiator C or captopril. We conclude, therefore, that bradykinin exerts variable responses on vascular smooth muscle, depending on the species used, the muscle location and experimental conditions. Finally, the in situ and in vitro findings for pial and middle cerebral arteries demonstrate that kininase II does not modify the dilating effect of bradykinin under our experimental conditions.

scholarly journals Changes in Cerebral Arterial, Tissue and Venous Oxygenation with Evoked Neural Stimulation: Implications for Hemoglobin-Based Functional Neuroimaging

2009 ◽  
Vol 30 (2) ◽  
pp. 428-439 ◽  
Author(s):  
Alberto L Vazquez ◽  
Mitsuhiro Fukuda ◽  
Michelle L Tasker ◽  
Kazuto Masamoto ◽  
Seong-Gi Kim
Keyword(s):  
Brain Function ◽  
Functional Neuroimaging ◽  
Sensory Stimulation ◽  
Average Diameter ◽  
Neural Stimulation ◽  
Blood Oxygen ◽  
Pial Arteries ◽  
Small Arteries ◽  
Arteries And Veins ◽  
Stimulation Of

Little is known regarding the changes in blood oxygen tension (PO2) with changes in brain function. This work aimed to measure the blood PO2 in surface arteries and veins as well as tissue with evoked somato-sensory stimulation in the anesthetized rat. Electrical stimulation of the forepaw induced average increases in blood flow of 44% as well as increases in the tissue PO2 of 28%. More importantly, increases in PO2 throughout pial arteries (resting diameters=59 to 129 μm) and pial veins (resting diameters=62 to 361 μm) were observed. The largest increases in vascular PO2 were observed in the small veins (from 33 to 40 mm Hg) and small arteries (from 78 to 88 mm Hg). The changes in oxygen saturation (SO2) were calculated and the largest increases were observed in small veins (Δ=+11%) while its increase in small arteries was small (Δ=+4%). The average diameter of arterial vessels was observed to increase by 4 to 6% while that of veins was not observed to change with evoked stimulation. These findings show that the increases in arterial PO2 contribute to the hyper-oxygenation of tissue and, mostly likely, also to the signal changes in hemoglobin-based functional imaging methods (e.g. BOLD fMRI).

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.

Neuropeptide Y: Immunocytochemical localization to and effect upon feline pial arteries and veins in vitro and in situ

1984 ◽  
Vol 122 (2) ◽  
pp. 155-163 ◽  
Author(s):  
LARS EDVINSSON ◽  
PIERS EMSON ◽  
JAMES McCULLOCH ◽  
KAZUHIKO TATEMOTO ◽  
ROLF UDDMAN
Keyword(s):  
Neuropeptide Y ◽  
Immunocytochemical Localization ◽  
Pial Arteries ◽  
Arteries And Veins

Augmentation of alpha-adrenergic contractions in the trachealis muscle of living dogs

1983 ◽  
Vol 54 (6) ◽  
pp. 1558-1566 ◽  
Author(s):  
J. K. Brown ◽  
R. Shields ◽  
C. Jones ◽  
W. M. Gold
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Nerves ◽  
Cholinergic Agonists ◽  
Short Acting ◽  
In Situ Preparation ◽  
Anesthetized Dogs ◽  
Long Acting ◽  
Trachealis Muscle ◽  
Stimulation Of

Discrepancies exist between reported effects of histamine on the alpha-adrenergic responsiveness of the canine trachealis muscle. Therefore, using an in situ preparation described recently (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 49: 84–94, 1980), we tested the effects of histamine and other agents on alpha-adrenergic responses in the trachealis muscle of 34 anesthetized dogs. Under basal conditions, maximum alpha-adrenergic responses were small [3 +/- 1 (SE) g/cm] compared with those induced by a supramaximal parasympathetic stimulus (45 +/- 3 g/cm). After exposure of the muscle to histamine, responsiveness increased markedly to alpha-adrenergic stimuli, which included tracheal arterial injections of norepinephrine and phenylephrine or electrical stimulation of sympathetic nerves. Augmented alpha-adrenergic responsiveness persisted for 20 min after the end of contractions induced by histamine. Serotonin and long-acting, but not short-acting, cholinergic agonists also potentiated alpha-adrenergic responsiveness. We concluded that exposure of the trachealis muscle in living dogs to a variety of constrictor stimuli potently augmented its alpha-adrenergic responsiveness.

Uptake and re-use of sympathetic transmitter in the cat’s spleen

1969 ◽  
Vol 174 (1034) ◽  
pp. 51-68 ◽  
Keyword(s):  
Sympathetic Nerve ◽  
Present Method ◽  
Sympathetic Nerves ◽  
Homologous Blood ◽  
Progressive Decline ◽  
The Relationship ◽  
Frequency Of Stimulation ◽  
Sympathetic Transmitter ◽  
Stimulation Of

The output of transmitter resulting from stimulation of the sympathetic nerves of the cat’s spleen, perfused with homologous blood, is described and compared with similar results obtained from the spleen in situ . Transmitter overflows are somewhat lower in the spleen perfused by the present method, but the relationship between overflow and frequency of stimulation is the same as in the spleen in situ . Noradrenaline added to the perfusate at rates as high as 6 μ g/min is taken up by the spleen which shows no sign of saturation even at these high levels of presentation. Loss of transmitter from the spleen causes a progressive decline in the overflow of transmitter produced by successive trains of stimuli. Evidence is presented to support the hypothesis that the continued effectiveness of a sympathetic nerve depends upon the uptake and re-use of the transmitter that it liberates.

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.

Peripheral muscarinic control of norepinephrine release in the cardiovascular system

1980 ◽  
Vol 239 (6) ◽  
pp. H713-H720 ◽  
Author(s):  
E. Muscholl
Keyword(s):  
Physiological Role ◽  
Sympathetic Nerves ◽  
Adrenergic Nerve ◽  
Sequence Of Events ◽  
Adrenergic Response ◽  
Adrenergic Nerve Terminals ◽  
Muscarinic Cholinergic ◽  
Related Compounds ◽  
Stimulation Of

Activation of muscarinic cholinergic receptors located at the terminal adrenergic nerve fiber inhibits the process of exocytotic norepinephrine (NE) release. This neuromodulatory effect of acetylcholine and related compounds has been discovered as a pharmacological phenomenon. Subsequently, evidence for a physiological role of the presynaptic muscarinic inhibition was obtained on organs known to be innervated by the autonomic ground plexus (Hillarp, Acta. Physiol. Scand. 46, Suppl. 157: 1-68, 1959) in which terminal adrenergic and cholinergic axons run side by side. Thus, in the heart electrical vagal stimulation inhibits the release of NE evoked by stimulation of sympathetic nerves, and this is reflected by a corresponding decrease in the postsynaptic adrenergic response. On the other hand, muscarinic antagonists such as atropine enhance the NE release evoked by field stimulation of tissues innervated by the autonomic ground plexus. The presynaptic muscarine receptor of adrenergic nerve terminals probably restricts the influx of calcium ions that triggers the release of NE. However, the sequence of events between recognition of the muscarinic compound by the receptor and the process of exocytosis still remains to be clarified.

Effects of indomethacin and prostacyclin on isolated human pial arteries contracted by CSF from patients with aneurysmal SAH

1981 ◽  
Vol 55 (6) ◽  
pp. 877-883 ◽  
Author(s):  
Lennart Brandt ◽  
Bengt Ljunggren ◽  
Karl-Erik Andersson ◽  
Bengt Hindfelt ◽  
Tore Uski
Keyword(s):  
Cerebrospinal Fluid ◽  
Arachidonic Acid ◽  
Vessel Wall ◽  
Cerebral Arteries ◽  
Pial Arteries ◽  
Content Type ◽  
Cerebral Vasoconstriction ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites ◽  
Fine Print

✓ In small human cerebral arteries preincubated with indomethacin, contractions induced by cerebrospinal fluid (CSF), from patients with subarachnoid hemorrhage were markedly increased. Also contractions induced by noradrenaline, but not 5-hydroxytryptamine, were augmented. Prostacyclin and its metabolite 6-keto-prostaglandin (PG)E1 reversed the contractions induced by CSF, as well as by noradrenaline, 5-hydroxytryptamine, and PGF2α. The findings suggest that these substances are able to counteract the influence of vasoconstrictor material in hemorrhagic CSF. If the capacity to synthesize these “protective” arachidonic acid metabolites is reduced, the resulting imbalance between contractile and relaxant forces acting on the vessel wall may lead to sustained cerebral vasoconstriction.

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