Involvement of the median preoptic nucleus in the regulation of paraventricular vasopressin neurons by the subfornical organ in the rat

Summary Extracellular recordings in urethane-anesthetized male rats indicated that electrical stimulation of the subfornical organ (SFO) alters the activity of 54 out of 62 phasically firing neurosecretory neurons in the hypothalamic paraventricular nucleus (PVN); 44 cells demonstrate an increase in excitability; 10 cells display a depression in their activity. In 14 out of 38 PVN cells tested, SFO stimulation-evoked excitations were abolished by pretreatment with the angiotensin II (ANG II) antagonist, saralasin (Sar), in the region of the median preoptic nucleus (MnPO). Inhibitory responses (n=7) were not affected. Microinjection of ANG II into the region of the SFO produced either a facilitation (n=28) or no effect (n=6) on the excitability of phasically active PVN neurosecretory cells and the facilitatory effect of 9 out of 23 cells tested was prevented by pretreatment with Sar in the region of the MnPO. All the PVN cells which had excitatory responses to either electrical (n=7) or chemical (n=9) stimulation of the SFO that were blocked following the pretreatment could also be activated by intravenous administration of ANG II. Furthermore, this activation was blocked (n=10) or attenuated (n=6) by pretreatment with Sar in the region of the MnPO. These results show an involvement of both the MnPO and the SFO for the regulation of excitability of putative vasopressin (VP)-secreting PVN neurons, and suggest that MnPO neurons sensitive to ANG II may relay activation of SFO neurons by circulating ANG II to putative VP-secreting PVN neurons which result in enhanced excitability.     

Lateral hypothalamic area and paraventricular nucleus connections with subfornical organ neurons: an electrophysiological study in the rat

The neural pathways from the lateral hypothalamic area (LHA) to the hypothalamic paraventricular nucleus (PVN) mediated by subfornical organ (SFO) neurons were examined in urethane-anesthetized male rats in order to determine the excitability of vasopressin (VP)-secreting neurons in the PVN. Microinjection of angiotensin II (AII) into the LHA excited the activity of nearly half (n = 8) of the SFO neurons (n = 18) activated antidromically by electrical stimulation of the PVN. Microinjection of AII into the LHA also caused excitation of approximately one-quarter (n = 11) of putative VP-secreting neurons (n = 45) in the PVN while the excitatory responses of the putative VP-secreting neurons were blocked or attenuated by pretreatment with the AII antagonist, saralasin (Sar), in the SFO. Electrical stimulation of the LHA, on the other hand, produced excitation (n = 17) or inhibition (n = 14) of the putative VP-secreting neurons (n = 52) in the PVN. About half of the excitatory responses to LHA stimulation were blocked or attenuated by pretreatment with Sar in the SFO, whereas the inhibitory responses were not affected. These results show some possible connections between the LHA and PVN, and suggest that AII-sensitive LHA neurons with efferent projections to the SFO may act to enhance the excitability of putative VP-secreting neurons in the PVN via an excitatory influence on the AII-sensitive SFO neurons.     

Efferent pathways from the region of the subfornical organ to hypothalamic paraventricular nucleus: an electrophysiological study in the rat

Summary Twenty-three neurons in the region of the subfornical organ (SFO) were antidromically activated by electrical stimulation of the hypothalamic paraventricular nucleus (PVN) in male rats under urethane anesthesia. Microiontophoretically (MIPh) applied angiotensin II (AII) excited the activity of all units in the region of the SFO and the effect of AII was blocked by MIPh applied saralasin (Sar), an AII antagonist, but not by atropine (Atr), a muscarinic antagonist. In these units, 12 were also excited by MIPh applied acetylcholine (ACh) while 11 were not affected and the effect of ACh was attenuated by not only MIPh applied Atr, but also Sar, suggesting that not only neurons specific for AII, but also neurons sensitive to both AII and ACh project to the PVN in the region of the SFO. Intravenously administered AII excited the activity of both types of units in the region of the SFO. Microinjected AII or ACh into the region of the SFO excited the activity of putative vasopressin (VP)-secreting units in the PVN. These results suggest that neurons projecting to the PVN in the region of the SFO may act to enhance the activity of putative VP-secreting neurons in the PVN in response to circulating AII.     

Subfornical organ neurons act to enhance the activity of paraventricular vasopressin neurons in response to intravenous angiotensin II

The effects of pretreatment of the angiotensin II (ANGII) antagonist, saralasin (Sar), in the subfornical organ (SFO) on intravenous ANGII-induced responses of the activity of phasically firing paraventricular nucleus (PVN) neurons (n = 23) antidromically identified as projecting to the posterior pituitary were examined in urethane-anesthetized rats. The activity of the majority (n = 18) of identified PVN neurons was excited by intravenously administered ANGII, whereas the remaining neurons (n = 5) were not affected. The excitatory responses (n = 13) to ANGII were prevented by pretreatment with Sar, but not by isotonic saline (n = 3), in the SFO. These results suggest that ANGII-sensitive SFO neurons may act to enhance the excitability of putative vasopressin (VP)-secreting neurons in the PVN in response to circulating ANGII.     

Alpha-adrenergic control of ANG II-induced drinking in the rat median preoptic nucleus

The present study was carried out to investigate the contribution of angiotensinergic and catecholaminergic systems in the median preoptic nucleus (MnPO) to the drinking response elicited by activation of the subfornical organ (SFO) following injections of angiotensin II (ANG II) in the awake unrestrained rat. Microinjection of ANG II into the SFO caused the drinking response. The water intake caused by ANG II injected into the SFO was significantly enhanced by previous injections of phenylephrine, an alpha-adrenoceptor agonist, but not by isoprenaline, a beta-adrenoceptor agonist. Previous injections of either saralasin, a specific ANG II antagonist, or phentolamine, an alpha-adrenoceptor antagonist, into the MnPO significantly attenuated the water intake caused by the ANG II injection into the SFO. Similar injections of timolol, a beta-adrenoceptor antagonist, or the vehicle into the MnPO had no significant effect on the drinking response. These results show the involvement of both angiotensinergic and alpha-adrenergic systems in the MnPO in the drinking response induced by ANG II acting at the SFO, and imply that the alpha-adrenergic system may serve to enhance the neural inputs including the angiotensinergic inputs from the SFO, thereby causing increased dipsogenic response.     

Subfornical organ efferents enhance extracellular noradrenaline concentrations in the median preoptic area in rats

The present study was carried out to examine whether angiotensinergic pathways from the subfornical organ (SFO) regulate the noradrenergic system in the median preoptic nucleus (MnPO). Intracerebral microdialysis techniques were used to quantify the extracellular concentration of noradrenaline (NA) in the MnPO area. In urethane-anesthetized male rats, electrical stimulation (5–20 Hz, 0.6 mA) of the SFO significantly increased the NA concentration in the MnPO area, and the increase was significantly diminished by pretreatment with the angiotensin II (ANG II) antagonist saralasin (Sar; 5 μg), into the third ventricle (3V). Injections of ANG II (5 μg) into the 3V significantly enhanced NA release in the MnPO area. The data imply that the angiotensinergic pathways from the SFO to the MnPO may act to enhance NA release in the MnPO area.     

Losartan blocks the excitatory effect of peripheral hypertonic stimulation on vasopressinergic neurons in hypothalamic paraventricular nucleus in rats: electrophysiological and immunocytochemical evidence

The effect of peripheral hypertonic stimulation on the neurons of hypothalamic paraventricular nucleus (PVN) was investigated in the present study with both electrophysiological and immunocytochemical methods. The discharge frequency of the neurons with phasic activity in PVN could be increased by intraperitoneal (i.p.) injection of hypertonic saline (HS, 1.5M NaCl) (from 2.8 +/- 0.5 Hz to 5.4 +/- 0.9 Hz, P<0.001). The Fos expression in PVN could be enhanced (from 21.2 +/- 12.9 to 217.3 +/- 38.5 Fos-positive neurons, P<0.001) by i.p. HS and the majority of AVP-positive neurons expressing Fos (91.7 +/- 3.6%) was in magnocellular subdivision of PVN. After intracerebroventricular (i.c.v.) injection of losartan, angiotensin II type 1 (AT1) receptor antagonist (5 microg/microl), the excitatory effect of peripheral hypertonic stimulation on PVN neurons with phasic activity was inhibited significantly, and the number of the neurons co-expressing Fos and AVP in PVN decreased significantly (P<0.001) as well. The result demonstrated that the vasopressinergic neurons in PVN could be excited by peripheral hypertonic stimulation, and this excitation might be mediated by angiotensin II fibers projecting from subfornical organ to PVN.     

Gastric afferents to the paraventricular nucleus in the rat

Summary Extracellular recordings were made from vasopressin (AVP) and oxytocin (OXT)-secreting cells in the paraventricular nucleus (PVN) of the hypothalamus in rats anesthetized with urethane-chloralose to determine the effects of electrical stimulation of vagal gastric nerves and gastric distension on their activity. Electrical stimulation of gastric branches of the vagus nerves inhibited 5 and excited 10 of 32 phasically firing neurosecretory cells. Approximately one third of the phasically firing neuro-secretory cells (9 out of 29 cells) were transiently inhibited by gastric distension; an effect which was completely abolished by bilateral cervical vagotomy. In contrast, gastric nerve stimulation excited 45 of 72 non-phasically firing paraventricular cells. Thirteen of 77 non-phasically firing cells tested were excited by gastric distension. We conclude that there are some sensory afferent inputs originating from gastric receptors and transmitted by gastric vagal afferents which inhibit the activity of AVP- secreting neurons in the PVN although other inputs excite the cells. Similar inputs also excite some of the putative OXT-secreting neurons in the PVN.     

Neurons in the nucleus of the solitary tract with ascending projections to the subfornical organ in the rat

Thirty-one neurons in the region of the nucleus of the solitary tract (NTS) were antidromically activated by electrical stimulation of the subfornical organ (SFO) in male rats under urethane anesthesia. The activity of these identified neurons was tested for a response to activation of peripheral baroreceptors, achieved by rising arterial blood pressure with an intravenous administration of the alpha-agonist metaraminol. Of the neurons tested, 17 displayed an increase and 6 exhibited a reduction in neuronal firing that accompanied a 40- to 60-mmHg elevation in mean arterial pressure, while 8 were unresponsive. The results suggest that neurons projecting to the SFO in the region of the NTS may be important for carrying peripheral baroreceptor information to the SFO.     

Attenuated drinking response induced by angiotensinergic activation of subfornical organ projections to the paraventricular nucleus in estrogen-treated rats

The present study was carried out to examine whether estrogen modulates the drinking response caused by activation of neural pathways from the subfornical organ (SFO) to the hypothalamic paraventricular nucleus (PVN) in the female rat. Microinjection of angiotensin II (ANG II) into the SFO elicited drinking in ovariectomized female rats that were treated with either propylene glycol (PG) vehicle or estradiol benzoate (EB). The amount of water intake induced by the ANG II injection was significantly greater in the PG-treated than in the EB-treated animals. In both groups, previous injections of either saralasin, an ANG II antagonist, or phentolamine, an alpha-adrenoceptor antagonist, bilaterally into the PVN resulted in the significant attenuation of the drinking response to ANG II, whereas similar injections of saline vehicle into the PVN were without effect. These results suggest that the circulating estrogen may act to reduce the drinking response that is mediated through angiotensinergic and alpha-adrenergic mechanisms in the PVN in response to angiotensinergic activation of SFO efferent projections.     

Region-specific projections from the subfornical organ to the paraventricular hypothalamic nucleus in the rat

Neurons in the subfornical organ (SFO) project to the paraventricular hypothalamic nucleus (PVN) and there, in response to osmolar and blood pressure changes, regulate vasopressin neurons in the magnocellular part (mPVN) or neurons in the parvocellular part (pPVN) projecting to the cardiovascular center. The SFO is functionally classified in two parts, the dorsolateral peripheral (pSFO) and ventromedial core parts (cSFO). We investigated the possibility that neurons in each part of the SFO project region-specifically to each part of the PVN, using anterograde and retrograde tracing methods. Following injection of an anterograde tracer, biotinylated dextran amine (BDX) in the SFO, the respective numbers of BDX-uptake neurons in the pSFO and cSFO were counted and the ratio of the former to the latter was obtained. In addition, the respective areas occupied by BDX-labeled axons per unit area of the mPVN and pPVN were measured and the ratio of the former to the latter was obtained. Similarly, following injection of the retrograde tracer in the PVN, the respective areas occupied by tracer per unit area of the mPVN and pPVN were measured and the ratio of the former to the latter was obtained. The respective numbers of retrogradely labeled neurons in the pSFO and cSFO were also counted and the ratio of the former to the latter was obtained. It became clear by statistical analyses that there are strong positive correlations between the ratio of BDX-uptake neuron number in the SFO and the ratio of BDX-axon area in the PVN in anterograde experiment (correlation coefficient: 0.787) and between the ratio of retrograde neuron number in the SFO and the ratio of tracer area in the PVN in retrograde experiment (correlation coefficient: 0.929). The result suggests that the SFO projects region-specifically to the PVN, the pSFO to the mPVN and the cSFO to the pPVN.     

Electrophysiology of supraoptico-paraventricular nucleus connections in the rat

Summary In an attempt to clarify the mechanisms involved during synchronous discharge of magnocellular neurosecretory cells of the supraoptic and paraventricular nuclei, extracellular action potentials were recorded from 149 single units located in the rat paraventricular nucleus. Responses of the cells to stimulation of the ipsilateral supraoptic nucleus were recorded and it was observed that 7% of paraventricular nucleus neurones could be antidromically identified as projecting to the supraoptic nucleus. Excitatory responses were recorded from 40% of cells tested and were probably mediated by an interneurone population. Inhibitory responses were recorded from 37% of the cells and may have been mediated by direct projections from the supraoptic nucleus. No differences in responses were recorded from cells identified as projecting to the median eminence or neurohypophysis as compared with the rest of the population tested. However, more of the phasically firing putative vasopressin-secreting cells, (58%) were excited than were continuously active cells (38%). Delivery of short trains of high-frequency stimulation induced bursts of discharge from 93% of cells so tested, regardless of response to single shock stimulation. These burst discharges showed a late onset as compared with responses following single shock stimulation. The results suggest that a complex of intra- and internuclear interactions serve to regulate the neurosecretory activity of magnocellular cells within the supraoptic and paraventricular nuclei.     

The A1 noradrenergic region enhances the responsivity of hypothalamic paraventricular neurohypophyseal neurons to inputs from the subfornical organ in the rat

Summary The action of the A1 noradrenergic neurons of the ventrolateral medulla on the responsiveness of neurohypophyseal neurons in the rat hypothalamic paraventricular nucleus (PVN) to inputs from the subfornical organ (SFO) was examined in antidromically identified PVN neurons that respond to electrical stimulation of both the SFO and A1 region. In both putative vasopressin (VP)- and oxytocin (OXY)-secreting PVN neurons that were classified according to their spontaneous firing patterns and their responsivity to baroreceptor activation, prior stimulation of the A1 region did not affect the short latency brief duration excitatory response induced by SFO stimulation. Simultaneous stimulation of the A1 region significantly enhanced the long latency prolonged excitatory response induced by SFO stimulation and the enhancement was blocked by microiontophoretically applied phentolamine, and -adrenoceptor antagonist, but not by timolol, a -adrenoceptor antagonist. Simultaneous stimulation of the A1 region also significantly enhanced the inhibitory response induced by SFO stimulation and the enhancement was blocked by microiontophoretically applied timolol, but not by phentolamine. These results suggest that the A1 region may act to enhance the partial excitatory (via an -adrenoceptor mechanism) and inhibitory SFO inputs (via a -adrenoceptor mechanism) to the PVN neurohypophyseal neurons as a modulatory action.     

Involvement of the septum in the regulation of paraventricular vasopressin neurons by the subfornical organ in the rat

Extracellular recordings were obtained from 58 phasically active neurosecretory neurons in the hypothalamic paraventricular nucleus (PVN) of urethane-anesthetized male rats. Of these PVN neurons, 39 exhibited an increase and 11 displayed a reduction in ongoing activity following electrical stimulation of the subfornical organ (SFO), while the remaining neurons were unresponsive. Microinjection of the local anesthetic lidocaine into the medial septum reversibly abolished the SFO stimulus-evoked reduction in 7 out of 9 PVN neurons tested, whereas similar injection was without effect on the stimulus-evoked increase in 18 out of 20 PVN neurons tested. These results suggest that the SFO efferents through the medial septum to the PVN exert a predominantly inhibitory influence on the excitability of putative vasopressin (VP)-secreting neurons in the PVN.     

Neural inputs from the uterus to the paraventricular magnocellular neurons in the rat

Extracellular action potentials were recorded from antidromically identified, tonically firing cells in the hypothalamic paraventricular nucleus (PVN) of ovariectomized, estrogen-treated female rats under urethane anesthesia. Genital or somatic sensory stimuli, or electrical stimulation of the nerves innervating the pelvis were applied. Uterine horn or vaginal distension each excited 33% of the neurons tested. Probing of the cervix had no effect. Hindpaw pinch produced excitation in 39% and inhibition in 11% of the neurons tested. Non-noxious somatic stimuli had no effect. Stimulation of the uterine afferent nerves, the hypogastric and pelvic nerves, excited 55% and 30% of the neurons tested, respectively. Stimulation of a somatic nerve of the hindleg, the sciatic nerve, activated 80% of the neurons tested. These results indicate that specific sensory afferents arrive at the PVN from the uterus; in addition, somatic afferents converge in this hypothalamic nucleus.     

Glutamate mediates an excitatory influence of the paraventricular hypothalamic nucleus on the dorsal motor nucleus of the vagus

Data have shown that the paraventricular nucleus of the hypothalamus (PVN) and the dorsal motor nucleus of the vagus (DMNV) play important roles in the regulation of gastrointestinal function and eating behavior. Anatomical studies have demonstrated direct projections from the PVN to the DMNV and physiological studies showed that the DMNV mediates many of the effects of PVN stimulation and electrical current stimulation of the PVN excites a subset of DMNV neurons. The aim of this study was to characterize the role of glutamate receptors in the excitatory influence of the PVN on gut-related DMNV neurons. Using single-cell recording techniques, we determined the effects of kynurenic acid, 6-cyano-7-nitroquinoxalene-2,3-dione (CNQX), and DL-2-amino-5-phosphonopentanoic acid (DL-AP5) on the increase in firing rate due to electrical current stimulation of the PVN. In initial experiments, we studied 24 DMNV neurons excited by electrical current stimulation of the PVN. Kynurenic acid, a broad-spectrum glutamate receptor antagonist, prevented the PVN effect in 22 neurons and significantly attenuated the effect in the other cells. Nine of these neurons demonstrated an inhibition in firing rate with PVN stimulation after pretreatment with kynurenic acid. In a separate group of 12 neurons, we determined the effects of CNQX (1.2 nmol) injected into the DMNV. This AMPA receptor antagonist completely blocked the excitatory response to PVN stimulation of six DMNV neurons and significantly attenuated the response of the other six DMNV neurons. The addition of 1.2 nmol DL-AP5, a N-methyl-D-aspartate (NMDA) receptor antagonist, further attenuated the response to PVN stimulation in four of the five DMNV neurons that were still excited after CNQX treatment. The fifth neuron demonstrated PVN- induced inhibition of firing rate after treatment with CNQX and DL-AP5. In a separate group of 11 DMNV neurons excited by electrical stimulation of the PVN, DL-AP5 partially attenuated the excitatory responses of only four DMNV neurons and did not block the excitation of any cells. The mean latency (14 neurons tested) from the PVN to the DMNV was 37.71 +/- 2.40 (SE) ms. Monosynaptic action potentials and excitatory postsynaptic potentials were demonstrated in three DMNV neurons by intracellular recording. Our results indicate that glutamate released from PVN neurons projecting to the DMNV excite the gut-related vagal motor neurons by acting predominantly on the AMPA receptor. The NMDA receptor plays only a minor role in the excitatory effect.     

Angiotensin II excites paraventricular nucleus neurons that innervate the rostral ventrolateral medulla: an in vitro patch-clamp study in brain slices

Neurons of the hypothalamic paraventricular nucleus (PVN) are key controllers of sympathetic nerve activity and receive input from angiotensin II (ANG II)-containing neurons in the forebrain. This study determined the effect of ANG II on PVN neurons that innervate in the rostral ventrolateral medulla (RVLM)-a brain stem site critical for maintaining sympathetic outflow and arterial pressure. Using an in vitro brain slice preparation, whole cell patch-clamp recordings were made from PVN neurons retrogradely labeled from the ipsilateral RVLM of rats. Of 71 neurons tested, 62 (87%) responded to ANG II. In current-clamp mode, bath-applied ANG II (2 muM) significantly (P < 0.05) depolarized membrane potential from -58.5 +/- 2.5 to -54.5 +/- 2.0 mV and increased the frequency of action potential discharge from 0.7 +/- 0.3 to 2.8 +/- 0.8 Hz (n = 4). Local application of ANG II by low-pressure ejection from a glass pipette (2 pmol, 0.4 nl, 5 s) also elicited rapid and reproducible excitation in 17 of 20 cells. In this group, membrane potential depolarization averaged 21.5 +/- 4.1 mV, and spike activity increased from 0.7 +/- 0.4 to 21.3 +/- 3.3 Hz. In voltage-clamp mode, 41 of 47 neurons responded to pressure-ejected ANG II with a dose-dependent inward current that averaged -54.7 +/- 3.9 pA at a maximally effective dose of 2.0 pmol. Blockade of ANG II AT1 receptors significantly reduced discharge (P < 0.001, n = 5), depolarization (P < 0.05, n = 3), and inward current (P < 0.01, n = 11) responses to locally applied ANG II. In six of six cells tested, membrane input conductance increased (P < 0.001) during local application of ANG II (2 pmol), suggesting influx of cations. The ANG II current reversed polarity at +2.2 +/- 2.2 mV (n = 9) and was blocked (P < 0.01) by bath perfusion with gadolinium (Gd(3+), 100 muM, n = 8), suggesting that ANG II activates membrane channels that are nonselectively permeable to cations. These findings indicate that ANG II excites PVN neurons that innervate the ipsilateral RVLM by a mechanism that depends on activation of AT1 receptors and gating of one or more classes of ion channels that result in a mixed cation current.     

An electrophysiological characterization of projections from the pedunculopontine area to entopeduncular nucleus and globus pallidus in the cat

Stimulation of the pedunculopontine region (PPN), in which neurons are filled by horseradish peroxidase injected into the entopeduncular nucleus (ENTO) or globus pallidus (GP) of the cat, excites ENTO and GP neurons both orthodromically and antidromically. Stimulus threshold mapping experiments and intracellular records of EPSPs provide evidence that the orthodromic excitation may be produced monosynaptically by the axons of PPN neurons. Antidromic excitation of ENTO axons from stimulation in PPN or the thalamus may elicit IPSPs in ENTO neurons via the action of recurrent collaterals. An excitatory synaptic action of PPN neurons on pallidal cells could be a partial basis for the high discharge rate characteristic of these neurons in awake animals.     

Paraventricular neurosecretory neurons: synaptic inputs from the ventrolateral medulla in rats

Effects of electrical stimulation of the ventrolateral medulla on discharge activity of neurosecretory neurons in the paraventricular nucleus (PVN) were studied in male rats anesthetized with urethane-chloralose. Among 35 phasically firing neurosecretory neurons, stimulation of the lateral reticular nucleus and its vicinity produced excitation in 10 and inhibition in 2. The stimulation also enhanced the activity of 40% of the PVN neurosecretory neurons that fired continuously (n = 81); of these responsive neurons, half of the neurons tested (n = 12) were inhibited by i.v. administration of phenylephrine. The result suggests that both vasopressin- and oxytocin-secreting neurons in the PVN receive mainly excitatory synaptic inputs from the ventrolateral medulla.     

Activation within dorsal medullary nuclei following stimulation in the hypothalamic paraventricular nucleus in rats

The influence of the hypothalamic paraventricular nucleus (PVN) on neurones in the dorsal medulla has been examined in 71 urethane/sagatal-anaesthetised rats. Of 536 neurones localised and tested for responses to electrical stimulation of both the vagus and/or the PVN, 378 were synaptically or antidromically activated following vagal stimulation 72 of which were synaptically activated by stimulation within PVN. The majority of those were located at the border between NTS and dorsal motor nucleus of the vagus in caudal NTS. None showed cardiac or ventilatory rhythm. Neurones showing such rhythms were not affected from PVN. Of 89 neurones in dorsal motor nucleus of the vagus, ten were synaptically activated and two synaptically depressed from PVN. PVN activated neurones in NTS tested for responses to stimulation of arterial baroreceptors and carotid body chemoreceptors were either unaffected or inhibited, but gastric inflation excited them. The results suggest a powerful PVN influence on the dorsal medulla, which is largely confined to the ventral and caudal NTS. There is little evidence for an effect on neurones with a cardiovascular function, but the abdominal vagal influence suggests a link with feeding.