Effect of stimulation of nucleus raphe dorsalis on carotid blood flow. I. The monkey

The dorsal raphe nucleus (DRN) and surrounding midbrain of 16 anaesthetized monkeys were stimulated electrically, and carotid blood flows were measured with electromagnetic flow probes. Stimulation of the DRN caused a frequency-dependent decrease (vasodilatation) in both internal and external carotid vascular resistance, which was abolished in both circulations by bilateral section of the facial nerve intracranially. These vasodilator responses were unaltered by intravenous administration of muscarinic cholinergic or by alpha- or beta-adrenoceptor antagonists. A postdilatation constrictor response, observed in the external carotid circulation, was blocked by the alpha-adrenoceptor antagonist phentolamine. It is concluded that projections of the DRN through the greater superficial petrosal branch of the facial nerve mediate vasodilatation in both internal and external carotid circulations.

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Effect of stimulation of nucleus raphe dorsalis on carotid blood flow. II. The cat

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1985.248.2.r263 ◽

1985 ◽

Vol 248 (2) ◽

pp. R263-R269 ◽

Cited By ~ 2

Author(s):

P. J. Goadsby ◽

R. D. Piper ◽

G. A. Lambert ◽

J. W. Lance

Keyword(s):

Intravenous Administration ◽

Spinal Cord Section ◽

Homocysteic Acid ◽

Alpha Adrenoceptor ◽

Adrenoceptor Antagonist ◽

Adrenoceptor Blocker ◽

Raphe Dorsalis ◽

Constrictor Response ◽

The Brain ◽

Stimulation Of

The dorsal raphe nucleus (DRN) and surrounding midbrain of 74 cats were stimulated both electrically and chemically, and carotid flows were measured with electromagnetic flow probes. Stimulation of the DRN caused a frequency-dependent decrease in common carotid vascular resistance, which was abolished by bilateral section of the facial nerve intracranially. Injection of DL-homocysteic acid into the DRN reproduced the effect of electrical stimulation, indicating that the responses arose from excitation of cell bodies within the DRN, not from fibers of passage. The responses were mediated entirely within the brain stem since they remained intact after high spinal cord section. The vasodilator response was blocked by the intravenous administration of the nicotinic ganglion blocker hexamethonium but not by the alpha-adrenoceptor blocker phentolamine. The responses were unaffected by intravenous administration of methysergide but were markedly reduced after depletion of central serotonin by pretreatment with the serotonin depletor, p-chlorophenylalanine. A poststimulus constrictor response was mediated by release of catecholamines from the adrenal medulla and was blocked by the alpha-adrenoceptor antagonist phentolamine. No response involved supracollicular mechanisms since they persisted after decerebration.

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Cephalic carotid pressure as a measure of transmission through cervical ganglion

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1985.248.6.h867 ◽

1985 ◽

Vol 248 (6) ◽

pp. H867-H875

Author(s):

R. S. Tuttle

Keyword(s):

Action Potentials ◽

Carotid Sinus ◽

External Carotid Artery ◽

External Carotid ◽

Nictitating Membrane ◽

Beta Adrenoceptor ◽

Adrenoceptor Antagonist ◽

Cervical Ganglion ◽

Ganglionic Transmission ◽

Stimulation Of

Cephalic or cranial pressure, i.e., pressure recorded craniad from the external carotid artery, was recorded in the cat during stimulation of the pre- and postganglionic trunks of the superior cervical ganglion (SCG) as was tension developed by the nictitating membrane under these situations. The influence of distension of the carotid sinus and of metoprolol on hemodynamic and tension responses was compared with control responses. Distension of the sinus with an indwelling balloon produced an increase of cephalic pressure evoked by stimulation of the SCG. Tension developed by the nictitating membrane was unaffected. Metoprolol reduced the increase in pressure resulting from stimulation of the preganglionic trunk of the SCG at 1.0 Hz but enhanced the pressure increase in the cranial circulation evoked by postganglionic stimulation of the SCG at 5.0 Hz. Action potentials, recorded postganglionically from the SCG, could be roughly grouped by height and latency into three populations. The height of the M3 population increased with distension of the carotid sinus. This study provides evidence that cephalic pressure can be used as a measure of the influence of various factors on the transmission of impulses through the SCG. This parameter appears to be a more sensitive measure of transmission than that of tension developed by the nictitating membrane. Distension of the carotid sinus is one factor that facilitates ganglionic transmission, whereas the beta-adrenoceptor antagonist metoprolol depresses it.

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Hypothalamic adrenoceptors mediate sympathoadrenal activity in exercising rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1990.259.3.r470 ◽

1990 ◽

Vol 259 (3) ◽

pp. R470-R477 ◽

Cited By ~ 9

Author(s):

A. J. Scheurink ◽

A. B. Steffens ◽

R. P. Gaykema

Keyword(s):

Ventromedial Hypothalamus ◽

Plasma Corticosterone ◽

Plasma Norepinephrine ◽

Hypothalamic Area ◽

Beta Adrenoceptor ◽

Alpha Adrenoceptor ◽

Adrenoceptor Antagonist ◽

Sympathoadrenal Activity ◽

The Central Nervous System ◽

Exercise Induced

The role of hypothalamic adrenoceptors in the exercise-induced alterations of plasma norepinephrine (NE), epinephrine (E), and corticosterone concentrations was investigated in rats. Exercise consisted of strenuous swimming against a counter-current for 15 min. Before, during, and after swimming, blood samples were withdrawn through a permanent heart catheter for determination of E, NE, and corticosterone. In control rats E, NE, and corticosterone levels were all increased during exercise. Infusion of the alpha-adrenoceptor antagonist phentolamine through permanent bilateral cannulas into the ventromedial hypothalamus (VMH) immediately before exercise reduced the exercise-induced increase in plasma E without affecting NE. Infusion of the beta-adrenoceptor antagonist timolol into the VMH enhanced plasma E and attenuated plasma NE increases. Infusion of phentolamine into the lateral hypothalamic area (LHA) led to enhanced NE and unchanged E concentrations, whereas infusion of timolol into the LHA caused a potentiation of the increase in plasma E without an effect on NE. Plasma corticosterone concentrations were not affected. The results suggest that 1) alpha- and beta-adrenoceptors in the hypothalamus influence peripheral catecholamine release, and 2) E and NE responses to exercise can be dissociated by interference of the central nervous system.

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The dose dependency of the alpha-adrenoceptor antagonist and beta- adrenoceptor partial agonist activity of dilevalol and labetalol in man.

British Journal of Clinical Pharmacology ◽

10.1111/j.1365-2125.1993.tb04225.x ◽

1993 ◽

Vol 36 (3) ◽

pp. 251-256 ◽

Cited By ~ 3

Author(s):

TC Tham ◽

JP McKaigue ◽

S Guy ◽

RG Shanks ◽

JG Riddell

Keyword(s):

Partial Agonist ◽

Agonist Activity ◽

Dose Dependency ◽

Beta Adrenoceptor ◽

Alpha Adrenoceptor ◽

Adrenoceptor Antagonist ◽

Partial Agonist Activity

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Effect of compound D-600 (methoxyverapamil) on gluconeogenesis and on acceleration of the process by α-adrenergic stimuli in rat kidney tubules

Biochemical Journal ◽

10.1042/bj1900283 ◽

1980 ◽

Vol 190 (2) ◽

pp. 283-291 ◽

Cited By ~ 9

Author(s):

E D Saggerson ◽

C A Carpenter

Keyword(s):

Renal Cortex ◽

Rat Kidney ◽

Sodium Lactate ◽

Kidney Tubules ◽

Alpha Adrenoceptor ◽

Adrenoceptor Antagonist ◽

Adrenoceptor Agonist ◽

Adrenoceptor Blocker ◽

Glucose Formation ◽

Stimulation Of

1. Tubule fragments were isolated from renal cortex of fed rats and glucose formation was measured after incubation with 5 mM-sodium lactate. 20 Compound D-600 (10-100 microM) decreased gluconeogenesis from lactate. This inhibition of the process by compound D-600 increased with increasing extracellular Ca2+ concentration, was overridden by noradrenaline and diminished by starvation for 24 h. 3. Inhibition of lactate-supported gluconeogenesis by compound D-600 was not prevented by the alpha 1-adrenoceptor antagonist thymoxamine. 4. Compound D-600 had little effect on gluconeogenesis from 2-oxoglutarate and increased gluconeogenesis from succinate. 5. Compound D-600 opposed stimulation of gluconeogenesis by noradrenaline or oxymetazoline (a selective alpha-adrenoceptor agonist) in a manner suggesting that compound D-600 is an alpha-adrenoceptor blocker. Oxymetazoline was more sensitive than noradrenaline to blockade by both compound D-600 and by the conventional alpha-adrenoceptor antagonist phentolamine. Noradrenaline became more sensitive to blockade by compound D-600 when extracellular Ca2+ was decreased. 6. Compound D-600 did not block stimulation of gluconeogenesis by angiotensin or cyclic AMP.

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Nerve-induced nonadrenergic vasoconstriction and vasodilatation in skeletal muscle

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.258.5.h1334 ◽

1990 ◽

Vol 258 (5) ◽

pp. H1334-H1338 ◽

Cited By ~ 2

Author(s):

A. Ohlen ◽

M. G. Persson ◽

L. Lindbom ◽

L. E. Gustafsson ◽

P. Hedqvist

Keyword(s):

High Frequency ◽

Motor Nerve ◽

Low Frequency ◽

High Frequency Stimulation ◽

Alpha Adrenoceptor ◽

Adrenoceptor Antagonist ◽

Stimulation Parameters ◽

Low Frequency Stimulation ◽

Frequency Stimulation ◽

Stimulation Of

Intravital microscopy was used to study the effect of motor nerve stimulation on microvessel diameters in the rabbit tenuissimus muscle. Stimulation of the motor nerve (0.5-5 ms, 2-20 Hz, 5-15 V) evoked pulse duration- and frequency-dependent constriction of transverse and terminal arterioles. The vasoconstriction induced by low-frequency stimulation (2 Hz) was abolished by the alpha-adrenoceptor antagonist phentolamine, whereas high-frequency stimulation (10-20 Hz) resulted in a response that was only partially inhibited by phentolamine. However, desensitization of the tissue to the vasoconstrictor effects of neuropeptide Y (NPY) changed the response remaining after phentolamine into vasodilatation. Independent of stimulation parameters, pretreatment of the tissue with the adrenergic neuron blocker guanethidine reversed the constriction into dilatation that was resistant to propranolol, atropine, and indomethacin. The results document the functional presence of both vasoconstrictor and vasodilator fibers in the rabbit tenuissimus muscle motor nerve, and they suggest that part of the nerve-induced vasoconstriction at higher stimulation frequencies is caused by neuronally released NPY.

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Paraventricular hypothalamic adrenoceptors and energy metabolism in exercising rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1990.259.3.r478 ◽

1990 ◽

Vol 259 (3) ◽

pp. R478-R484 ◽

Cited By ~ 3

Author(s):

A. J. Scheurink ◽

A. B. Steffens ◽

R. P. Gaykema

Keyword(s):

Blood Glucose ◽

Plasma Corticosterone ◽

Plasma Norepinephrine ◽

Alpha Adrenoceptors ◽

Beta Adrenoceptor ◽

Alpha Adrenoceptor ◽

Glucose Levels ◽

Adrenoceptor Antagonist ◽

Exercise Induced ◽

Induced Changes

The role of adrenoceptors in the paraventricular nucleus (PVN) in the exercise-induced changes in plasma norepinephrine (NE), epinephrine (E), corticosterone, free fatty acids (FFA), and blood glucose was investigated in rats. Exercise consisted of strenuous swimming against a countercurrent for 15 min. Before, during, and after swimming, blood samples were withdrawn through a permanent heart catheter for determination of E, NE, corticosterone, FFA, and glucose, In control rats receiving artificial cerebrospinal fluid through permanent bilateral cannulas into the PVN, the levels of all blood components increased during exercise. Infusion of the alpha-adrenoceptor antagonist phentolamine into the PVN completely reduced the exercise-induced increases in blood glucose and plasma corticosterone concentrations. Plasma NE, E, and FFA were not affected. Infusion of the beta-adrenoceptor antagonist timolol into the PVN reduced blood glucose and plasma NE concentrations. Plasma E, corticosterone, and FFA remained unchanged. It is concluded that alpha- and beta-adrenergic receptors in the PVN are involved in the central nervous regulation of blood glucose levels during exercise, partly by influencing sympathetic outflow. alpha-Adrenoceptors in the PVN play an important role in the release of corticosterone during exercise.

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Adrenergic inhibition of carbon dioxide excretion by trout red blood cells in vitro is mediated by activation of Na+/H+ exchange

Journal of Experimental Biology ◽

10.1242/jeb.157.1.367 ◽

1991 ◽

Vol 157 (1) ◽

pp. 367-380

Author(s):

S. F. Perry ◽

C. M. Wood ◽

S. Thomas ◽

P. J. Walsh

Keyword(s):

Carbon Dioxide ◽

Blood Cell ◽

Red Blood Cell ◽

Beta Adrenoceptor ◽

Alpha Adrenoceptor ◽

Adrenoceptor Antagonist ◽

Exchange Inhibitor ◽

Adrenoceptor Agonist ◽

Co2 Excretion

We have used a sensitive new technique to assess the mechanism(s) of adrenergic inhibition of rainbow trout (Oncorhynchus mykiss) red blood cell (RBC) carbon dioxide excretion in vitro. The effect was only apparent using blood acidified to simulate metabolic acidosis. Red blood cell CO2 excretion was inhibited in a dose-dependent manner by physiologically relevant concentrations of noradrenaline (10–1000 nmol l-1) or adrenaline (100–1000 nmol l-1). The beta-adrenoceptor antagonist propranolol abolished the inhibitory effect of adrenaline, whereas the alpha-adrenoceptor antagonist phentolamine was without effect. The action of noradrenaline on RBC CO2 excretion was mimicked by the beta-adrenoceptor agonist isoproterenol, but not by the alpha-adrenoceptor agonist phenylephrine. Therefore, adrenergic inhibition of CO2 excretion is mediated by RBC beta-adrenoceptors, presumably of the beta 1 subtype. The Na+/H+ exchange inhibitor amiloride effectively blocked adrenergic stimulation of Na+/H+ exchange (as indicated from measurements of pHe and RBC pHi) and entirely prevented the inhibition of CO2 excretion. Noradrenaline significantly reduced the rate of CO2 excretion even in the presence of the Cl-/HCO3- exchange inhibitor SITS. Therefore, adrenergic inhibition of CO2 excretion is accomplished via activation of RBC Na+/H+ exchange rather than by a direct inhibition of Cl-/HCO3- exchange. The observed relationship between CO2 excretion rates and the RBC transmembrane pH difference (pHe-pHi) and the occurrence of the inhibition only at low pHe provide further evidence of the linkage with RBC Na+/H+ exchange. We suggest that adrenergic activation of RBC Na+/H+ exchange impedes CO2 excretion by causing a rise in intracellular HCO3- levels concurrent with a reduction of intracellular PCO2. The net result is a reduced gradient for HCO3- entry into the RBC in conjunction with a diminution of the outwardly directed PCO2 gradient. Thus, the rate of formation of CO2 from the dehydration of plasma HCO3- is reduced and, in turn, a portion of this CO2 is not excreted but recycled through the red blood cell.

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