scholarly journals Autonomic regulation of cutaneous vascular resistance in the bullfrog Rana catesbeiana

1990 ◽  
Vol 152 (1) ◽  
pp. 425-439
Author(s):  
G. M. Malvin ◽  
C. Riedel
Keyword(s):  
Vascular Resistance ◽  
Cranial Nerve ◽  
Sympathetic Ganglion ◽  
Rana Catesbeiana ◽  
Sympathetic Nerves ◽  
Plasma Catecholamine ◽  
Skin Preparation ◽  
Beta Adrenoceptors ◽  
Cutaneous Vascular Resistance ◽  
Stimulation Of

To gain a better understanding of the regulation of cutaneous blood flow in the bullfrog, the vascular innervation, vasoactivity and adrenoceptor types of the cutaneous vasculature were investigated using a pump-perfused skin preparation. Stimulation of cranial nerve I, the vagal ganglion, sympathetic ganglion 1 and sometimes sympathetic ganglion 2 caused cutaneous vascular resistance (CVR) to increase. Stimulation of cranial nerve IX and spinal nerves 1 and 2 had no effect on CVR. The response to stimulation of sympathetic ganglion 1 was antagonized by phentolamine but not by atropine. Phentolamine, atropine and alpha,beta-methylene ATP had no effect on the response to vagal stimulation. Both epinephrine (EPI) and norepinephrine (NE) increased CVR, with EPI being more potent than NE. The minimum concentrations of EPI and NE required for a significant change in CVR were much higher than plasma catecholamine levels reported for resting bullfrogs. Phentolamine antagonized, but propranolol had no effect on, the responses to the catecholamines. Isoproterenol caused small decreases in CVR which were abolished by propranolol. Acetylcholine was a weak vasodilator. The results indicate that the cutaneous vasculature has two types of vasomotor nerves: sympathetic nerves that are probably adrenergic, and other nerves that are non-adrenergic/non-cholinergic and which do not use ATP as a transmitter. Although catecholamines are vasoactive, the sensitivity of the cutaneous vasculature to EPI and NE is probably too low to allow a direct regulatory role of these hormones on CVR. There is no evidence for cholinergic regulation of CVR. Both alpha- and beta-adrenoceptors are present in the cutaneous vasculature. alpha-Adrenoceptors mediate the constrictor responses to sympathetic nerve stimulation and catecholamine administration. It is unlikely that beta-adrenoceptors play a significant role in regulating CVR.

Localization of intrahepatic portal vascular resistance

1986 ◽  
Vol 251 (3) ◽  
pp. G375-G381 ◽  
Author(s):  
W. W. Lautt ◽  
C. V. Greenway ◽  
D. J. Legare ◽  
H. Weisman
Keyword(s):  
Pressure Drop ◽  
Portal Vein ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Vena Cava ◽  
Sympathetic Nerves ◽  
Hepatic Veins ◽  
Pressure Changes ◽  
Stimulation Of ◽  
Anesthetized Cat

The pressure drop from the portal vein to the vena cava occurs primarily across a postsinusoidal site localized to a narrow segment (less than 0.5 cm) of hepatic veins (roughly 1.5 mm diam) in the anesthetized cat. Portal venous pressure (PVP = 8.9 +/- 0.3 mmHg) and lobar hepatic venous pressure (LVP = 8.7 +/- 0.4 mmHg) are insignificantly different, and pressure changes imposed from the presinusoidal or postsinusoidal side are equally transmitted to both pressure sites. Several types of experiments were done to validate the LVP measurement. The portal vein, hepatic sinusoids, and hepatic veins proximal to the resistance site are all under a similar pressure. Previously reported calculations of hepatic vascular resistance are in error because of incorrect assumptions of sinusoidal pressure and localization of the portal resistance site as presinusoidal. Stimulation of hepatic sympathetic nerves for 3 min caused LVP and PVP to increase equally, showing that the increased "portal" resistance is postsinusoidal across the same region of the hepatic veins that was previously localized as the site of resistance in the basal state.

Decreased carotid arterial resistance in cats in response to trigeminal stimulation

1984 ◽  
Vol 61 (2) ◽  
pp. 307-315 ◽  
Author(s):  
Geoffrey A. Lambert ◽  
Nikolai Bogduk ◽  
Peter J. Goadsby ◽  
John W. Duckworth ◽  
James W. Lance
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Trigeminal Nerve ◽  
Cranial Nerve ◽  
Antidromic Activation ◽  
Carotid Blood Flow ◽  
Seventh Cranial Nerve ◽  
Trigeminal Stimulation ◽  
Arterial Blood ◽  
Stimulation Of

✓ Stimulation of the trigeminal nerve or ganglion in the cat caused a frequency-dependent reduction in carotid vascular resistance. Systemic arterial blood pressure (SABP) decreased at low frequencies (0.2 to 5 sec−1) and increased at higher frequencies, thus increasing carotid blood flow at the higher frequencies. The effect on resistance was predominantly ipsilateral and was unaltered by cervical sympathectomy, but was abolished or substantially reduced by section of the trigeminal root proximal to the ganglion. Diminution of carotid vascular resistance was replicated by stimulation of the greater superficial petrosal (GSP) nerve without any change in SABP. Section of the seventh cranial nerve reduced or abolished the response to stimulation of the trigeminal nerve but not that from the GSP nerve. The trigeminal response was prevented by ganglion-blocking drugs in seven out of eight cats. The resistance response was unaffected by noradrenergic, cholinergic, serotonergic, and histamine-2 blocking agents. No neural connection could be demonstrated between the GSP and the trigeminal ganglion, and the vascular response to GSP stimulation persisted after trigeminal section. It is concluded that activation of the trigeminal system increases carotid blood flow by a pathway involving the seventh cranial nerve, the GSP and Vidian nerves, and a parasympathetic synapse employing an unconventional transmitter. A varying proportion of the response (greatest in the third division) may be mediated by antidromic activation of trigeminal nerves. These findings may have clinical implications for the vascular changes of migraine and other facial pain.

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.

Molecular characterization and functional expression of a substance P receptor from the sympathetic ganglion of Rana catesbeiana

Neuroscience ◽  
1997 ◽  
Vol 79 (4) ◽  
pp. 1219-1229 ◽  
Author(s):  
M.A Simmons ◽  
R.M Brodbeck ◽  
V.V Karpitskiy ◽  
C.R Schneider ◽  
D.P.A Neff ◽  
...  
Keyword(s):  
Substance P ◽  
Molecular Characterization ◽  
Sympathetic Ganglion ◽  
Rana Catesbeiana ◽  
Functional Expression ◽  
Substance P Receptor

Effects of intravenous anesthetic agents on left ventricular function in dogs

1977 ◽  
Vol 232 (1) ◽  
pp. H44-H48
Author(s):  
L. D. Horwitz
Keyword(s):  
Left Ventricular Pressure ◽  
Cardiovascular Effects ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Intravenous Anesthetic ◽  
First Derivative ◽  
Anesthetic Agents ◽  
Thiopental Sodium ◽  
Stimulation Of ◽  
Mean Heart Rate

The cardiovascular effects of ketamine hydrochloride and thiopental sodium were studied in 11 dogs. During anesthesia, mean heart rate rose to 185 beats/min with ketamine and 147 beats/min with thiopental. Cardiac output was increased with ketamine but unchanged by thiopental. The maximum first derivative of the left ventricular pressure (dP/dt max) fell by 14% with thiopental but did not change significantly with ketamine. Propranolol resulted in attenuation of the tachycardia and a fall of 10% in dP/dt max with ketamine but had little effect on the response to thiopental. Phentolamine had no consistent effects on either drug. With pentolinium both drugs decreased dP/dt max. Intracoronary injection of ketamine decreased dP/dt max. Adrenalectomy had little effect on the responses to either anesthetic. The results lead to the conclusion that both ketamine and thiopental have myocardial depressant effects, but, whereas thiopental does not alter sympathetic tone, the depressive effects of ketamine are obscured by stimulation of cardiac sympathetic nerves.

Cardiac arrhythmias of sympathetic origin in the dog

1977 ◽  
Vol 233 (5) ◽  
pp. H535-H540
Author(s):  
L. S. D'Agrosa
Keyword(s):  
Cardiac Arrhythmias ◽  
Sympathetic Nerves ◽  
Nerve Fibers ◽  
Cardiac Contraction ◽  
Cardiac Rate ◽  
Atrioventricular Junction ◽  
Cardiac Nerve ◽  
Sympathetic Nerve Fibers ◽  
Beta Receptors ◽  
Stimulation Of

The effects of ventrolateral and ventromedial cardiac nerve (left sympathetics) stimulation on cardiac force, on rate, and on arrhythmogenic responses were characterized and quantitated. The stimulation of left sympathetic nerves produced augmentation in cardiac contraction in 45% of the experiments, an augmentation of both a cardiac rate and force in 47%, and in cardioacceleration alone in 8%. Two characteristic patterns of arrhythmogenic responses were elicited from stimulations of 100 sympathetic nerves. The two types of neurally induced arrhythmias were atrioventricular junctional or ventricular in origin. The onset and duration of the arrhythmias were quantitated. Both types of neurally induced arrhythmias were prevented either by blocking the beta receptors with propranolol or by preventing the neural release of norepinephrine with bretylium tosylate. The neurally induced arrhythmias were probably the result of enhanced automaticity in the atrioventricular junction area and in the ventricles produced by stimulating the sympathetic nerve fibers. This report thus implicates the ventromedial cardiac nerve in the genesis of cardiac arrhythmias.

Orbital Nerves

2012 ◽  
Author(s):  
David Jordan ◽  
Louise Mawn ◽  
Richard L. Anderson
Keyword(s):  
Lacrimal Gland ◽  
Cranial Nerve ◽  
Motor Nerve ◽  
Rectus Muscle ◽  
Abducens Nerve ◽  
Sympathetic Nerves ◽  
Lower Eyelid ◽  
Infraorbital Nerve ◽  
Ciliary Ganglion ◽  
Orbital Surgery

The orbit contains a vast array of motor, sensory, sympathetic, and parasympathetic nerve fibers. Some of these fibers can be seen during eyelid or orbital surgery and are often landmarks of one’s location within the orbit. It is important to know the various nerve pathways, appreciate that there might be some individual variation, and preserve these pathways during orbital surgery. The discussion of nerves begins with their superficial brainstem origin, proceeds to their intracranial course, and ends with their intraorbital course and eventual termination. The following nerves enter the orbit: 1. Optic nerve (cranial nerve II). 2. Oculomotor nerve (cranial nerve III). This motor nerve gives fibers to the levator, inferior oblique, and three of the four rectus muscles. It carries parasympathetic fibers destined for the ciliary ganglion. These fibers will eventually synapse in the ciliary ganglion and then travel to the iris sphincter muscles (sphincter pupillae). Sympathetic fibers have also been recently identified in this nerve. 3. Trochlear nerve (cranial nerve IV). This motor nerve distributes fibers to the superior oblique muscle. Sympathetic fibers have recently been identified within this nerve. 4. Trigeminal nerve (cranial nerve V). a. Ophthalmic division (V 1 ) . This sensory division gives fibers to the eyeball (iris, ciliary body, cornea), lacrimal gland, conjunctiva, and eyelids, as well as to the forehead. It also carries sympathetic nerves. b. Maxillary division (V 2 ) . As it enters the orbit, the maxillary division is known as the infraorbital nerve and lies beneath the periorbita. It gives off the zygomatic nerve, which is an important branch carrying parasympathetic and sympathetic fibers to the lacrimal gland. Within the infraorbital canal, alveolar nerves arise and provide sensation to the incisor and canine teeth. The infraorbital nerve provides sensation to the lower eyelid, nose, cheek area, and upper lip. 5. Abducens nerve (cranial nerve VI). This motor nerve goes to the lateral rectus muscle. Sympathetic fibers have recently been identified within this nerve.

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