Nervous release of vasoactive intestinal polypeptide from the feline uterus: pharmacological characteristics.

Fahrenkrug, Jan; Ottesen, Bent

doi:10.1113/jphysiol.1982.sp014382

Cited by 38 publications

(7 citation statements)

References 22 publications

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“…In contrast, the present study has extended our previous electrophysiological work (Jobling et al 2003) to demonstrate directly that neurones projecting from mid‐lumbar spinal cord via the lumbar splanchnic and hypogastric nerves provide the major neural pathway for vasodilatation of pelvic arteries supplying the internal reproductive organs of female guinea‐pigs. This is consistent with reports of hypogastric nerve stimulation but not pelvic nerve stimulation increasing venous outflow and VIP release from the cat uterus (Fahrenkrug & Ottesen, 1982). The relative large magnitude of vasodilatations produced by stimulation of the ipsilateral hypogastric or lumbar splanchnic nerves compared with the L3 ventral roots is likely to reflect the extensive bilateral projection of lumbar preganglionic neurones down both hypogastric nerves (McLachlan, 1985).…”

Section: Discussionsupporting

confidence: 93%

Post‐stimulus potentiation of transmission in pelvic ganglia enhances sympathetic dilatation of guinea‐pig uterine artery in vitro

Morris

Gibbins

Jobling

2005

The Journal of Physiology

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Vasodilatation produced by stimulation of preganglionic neurones in lumbar and sacral pathways to pelvic ganglia was studied using an in vitro preparation of guinea-pig uterine artery and associated nerves in a partitioned bath allowing selective drug application to the ganglia or artery. Arterial diameter was monitored using real time video imaging. Vasodilatations produced by hypogastric nerve stimulation (HN; 300 pulses, 10 Hz) were significantly larger and longer in duration than with pelvic nerve stimulation (N = 18). Stimulation of ipsilateral lumbar splanchnic nerves or ipsilateral third lumbar ventral roots also produced prolonged vasodilatations. Blockade of ganglionic nicotinic receptors (0.1-1 mM hexamethonium) delayed the onset and sometimes reduced the peak amplitude of dilatations, but slow dilatations persisted in 16 of 18 preparations. These dilatations were not reduced further by 3 µM capsaicin applied to the artery and ganglia, or ganglionic application of 1 µM hyoscine, 30-100 µM suramin or 10 µM CNQX. Dilatations were reduced slightly by ganglionic application of NK1 and NK3 receptor antagonists (SR140333, SR142801; 1 µM), but were reduced significantly by bathing the ganglia in 0.5 mM Ca 2+ and 10 mM Mg 2+ . Intracellular recordings of paracervical ganglion neurones revealed fast excitatory postsynaptic potentials (EPSPs) in all neurones on HN stimulation (300 pulses, 10 Hz), and slow EPSPs (3-12 mV amplitude) in 25 of 37 neurones. Post-stimulus action potential discharge associated with slow EPSPs occurred in 16 of 37 neurones (firing rate 9.4 ± 1.5 Hz). Hexamethonium (0.1-1 mM) abolished fast EPSPs. Hexamethonium and hyoscine (1 µM) did not reduce slow EPSPs and associated post-stimulus firing in identified vasodilator neurones (with VIP immunoreactivity) or non-vasodilator paracervical neurones. These results demonstrate a predominantly sympathetic origin of autonomic pathways producing pelvic vasodilatation in females. Non-cholinergic mediators of slow transmission in pelvic ganglia produce prolonged firing of postganglionic neurones and long-lasting dilatations of the uterine artery. This mechanism would facilitate maintenance of pelvic vasodilatation on stimulation of preganglionic neurones during sexual activity.

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Section: Discussionsupporting

confidence: 93%

Post‐stimulus potentiation of transmission in pelvic ganglia enhances sympathetic dilatation of guinea‐pig uterine artery in vitro

Morris

Gibbins

Jobling

2005

The Journal of Physiology

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“…Similarly, reflex or psychogenic erections in male rats also occur predominantly via sacral outflow through the pelvic nerve (Cruz et al, 1999;Giuliano et al, 1997). However, release of VIP-IR from the feline uterus occurs following both pelvic and hypogastric nerve stimulation (Fahrenkrug and Ottesen, 1982). Furthermore, these authors reported that hypogastric, but not pelvic nerve stimulation, was associated with an increase in uterine venous outflow consistent with uterine vasodilation.…”

Section: Vasodilator Neurons Receive Synaptic Input Via Pelvic and Hymentioning

confidence: 94%

Functional organization of vasodilator neurons in pelvic ganglia of female guinea pigs: Comparison with uterine motor neurons

Jobling

Gibbins

Morris

2003

J of Comparative Neurology

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Neurons producing vasodilation during reproductive activity constitute a large population of neurons in pelvic autonomic ganglia. We used intracellular recording, dye-filling and multiple-labeling immunohistochemistry to determine the morphology and electrophysiological properties of, and number of synaptic inputs to, vasodilator pelvic neurons in female guinea pigs. Vasodilator neurons, identified by their immunoreactivity for vasoactive intestinal peptide (VIP) and their location in paracervical ganglia, had simple dendritic arbors (1 primary dendrite) compared with nonvasodilator neurons (3 dendrites). Vasodilator neurons had more depolarized resting membrane potentials (-47 mV) than other paracervical neurons (-55 mV) and had smaller apparent cell capacitances (65 pF vs. 110 pF). Vasodilator and nonvasodilator neurons could not be distinguished on the basis of their action potential discharge characteristics or current voltage relationships. Most pelvic neurons ( approximately 70%) had tonic (slowly adapting) discharges. Fifty-five percent of vasodilator and 60% of nonvasodilator neurons showed inward rectification when hyperpolarized below -90 mV. Around 65% of neurons showed evidence of M-current. Both vasodilator and nonvasodilator neurons ( approximately 80%) expressed an A-like current. Vasodilator neurons and nonvasodilator neurons received 1-2 fast synaptic inputs following stimulation of pelvic or hypogastric nerve trunks. Most neurons received a least one strong synaptic input. These results indicate that vasodilator neurons and neighboring neurons projecting to other pelvic targets, primarily in the myometrium, express a similar range of ionic conductances and integrate few synaptic inputs. The similarities between these two populations of neurons may be related to their coactivation as part of spinal somato-pelvic reflexes. Vasodilation and uterine contraction during reproductive behavior in female guinea pigs are likely to involve input from preganglionic neurons at both lumbar and sacral spinal levels.

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“…VIP has been suggested as the mediator of noncholinergic, non-adrenergic vasodilation in several tissues such as the gastrointestinal tract (Fahrenkrug et al 1978b), the salivary glands (Bloom & Edwards 1980, Lundberg et al 1980, Uddman et al 1980b, the nasal mucosa (Lundberg et al 1981), the tongue (Lundberg et a1.1982b) and the female genital tract (Fahrenkrug & Ottesen 1982). It is also a potent coronary vasodilator (Smitherman et al 1982).…”

mentioning

confidence: 99%

Vasoactive intestinal polypeptide (VIP): Effects in the eye and on regional blood flows

Nilsson

Bill

1984

Acta Physiologica Scandinavica

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The effect of vasoactive intestinal polypeptide (VIP) on regional blood flows was studied with labeled microspheres in albino rabbits. Intravenous injection of 500 ng VIP/kg b.w. during 100 s did not change the arterial blood pressure significantly, but caused a rise in intraocular pressure (IOP) and an increase in the choroidal blood flow by 35%, while the blood flow through the anterior uvea was unaffected. The most pronounced vasodilation was observed in the pancreas, the thyroid gland and the parotid gland. In these tissues local blood flow increased by more than 100%. Other tissues, in which this dose of VIP produced vasodilation, were the submandibular gland, the eyelids, the nictitating membrane, the choroid plexus and the heart muscle. Ganglionic or muscarinic blockade had little or no effect on the VIP-induced vasodilation in most of the tissues. Intracameral injection of VIP (1 microgram) produced vasodilation in the iris and the ciliary body, but did not affect IOP. VIP had no apparent effect on the pupil size or the blood-aqueous barrier. In experiments with direct blood flow determination from an opened vortex vein intravenous infusion of VIP, 100 ng X kg-1 X min-1 b.w., during five minutes reduced the uveal vascular resistance by about 50%. This study shows that VIP is a potent vasodilator in many tissues at doses hardly affecting the arterial blood pressure and supports the suggestion, that VIP is responsible for the non-cholinergic vasodilation in the eye caused by facial nerve stimulation.

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Nervous release of vasoactive intestinal polypeptide from the feline uterus: pharmacological characteristics.

Cited by 38 publications

References 22 publications

Post‐stimulus potentiation of transmission in pelvic ganglia enhances sympathetic dilatation of guinea‐pig uterine artery in vitro

Post‐stimulus potentiation of transmission in pelvic ganglia enhances sympathetic dilatation of guinea‐pig uterine artery in vitro

Functional organization of vasodilator neurons in pelvic ganglia of female guinea pigs: Comparison with uterine motor neurons

Vasoactive intestinal polypeptide (VIP): Effects in the eye and on regional blood flows

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