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J Ciriello

Publications and source records attributed to J Ciriello.

At least 55 records · Page 3Linked to original sources

Contribution of nucleus medianus to the drinking and pressor responses to angiotensin II acting at subfornical organ.

The contribution of neurons in the nucleus medianus (NM) in mediating the drinking and pressor responses elicited by administration of angiotensin II (AII) either directly into the subfornical organ (SFO) or intravenously was investigated in conscious, unrestrained rats. Microinjection of AII into the SFO elicited a robust drinking (7.9 +/- 0.8 ml in 15 min; n = 24) and pressor (peak rise in mean arterial pressure (MAP), 15 +/- 1 mm Hg; n = 20) response. On the other hand, intravenous infusion of AII elicited an increase in MAP (36 +/- 3 mm Hg; n = 14) accompanied by a marked reflex bradycardia (134 +/- 18 beats/min), but not a significant drinking response. Lesions of NM cells, dorsal to the anterior commissure and between the fornical columns, with the neurotoxin kainic acid significantly (P less than 0.05) attenuated the drinking response (prelesion volume, 8.3 +/- 0.8 ml in 15 min; postlesion volume, 1.9 +/- 1.4 ml in 15 min; n = 7), but did not alter the pressor response to AII injected directly into the SFO. Similarly, kainic acid lesions of NM cells did not significantly effect the pressor response or the associated reflex bradycardia to intravenous administration of AII. Sham lesions of NM cells or control kainic acid lesions of adjacent structures did not alter the AII-induced drinking or pressor responses. These data suggest that neurons in the dorsal NM are part of a forebrain neuronal circuit that is involved in the drinking, but not the pressor responses to AII acting at the SFO in the conscious rat.

Angiotensin II↗

Effect of preganglionic stimulation or chronic decentralization on neurotensin-like immunoreactivity in sympathetic ganglia of the cat.

In pentobarbital-anesthetized cats, supramaximal stimulation (40 Hz, 2 h) of the preganglionic input to the acutely decentralized right stellate (RSG) or superior cervical (RSCG) ganglion resulted in a decrease in neurotensin (NT)-like immunoreactivity (IR), by 83% in the SG and by 46% in the SCG, as determined by radioimmunoassay. Chronic (7 days) decentralization of the ganglia resulted in a similar depletion of NT-like IR (SG: 86%; SCG: 76%). Supramaximal stimulation (40 Hz, 2 h) of the intact postganglionic outflow of either ganglion had no effect on NT-like IR. These data suggest that NT in the SG and SCG is present in preganglionic axons and is released by activation of these axons.

Animals↗

Organization of ventrolateral medullary afferents to the hypothalamus.

In summary, these anatomical and electrophysiological data have provided evidence to support the suggestion that VLM neurons project directly to regions of the hypothalamus that contain magnocellular neurosecretory neurons. In addition, these results support the suggestion that pathways ascending from the VLM to the hypothalamus function, in part, in the control of the release of the neurohypophyseal hormones by PVH and SON magnocellular neurosecretory neurons during activation of peripheral cardiovascular receptors.

Afferent Pathways↗

Contribution of afferent renal nerves to the metabolic activity of central structures involved in the control of the circulation.

Afferent renal nerves (ARN) are thought to be an important link in the pathogenesis of hypertension because of their influence on neuronal circuits involved in the control of arterial pressure and body fluid homeostasis. However, the central neural pathways involved in mediating ARN information have not been completely elucidated. In the present study, regions of the brainstem and forebrain, whose metabolic activity was altered after renal denervation, were functionally identified using hexokinase histochemistry in the rat. No differences in arterial pressure or heart rate were observed in either the 3-day or 13-day ARN-transected (tARN) animals compared with the respective sham ARN-transected (sARN) groups. Significant increases in the hexokinase reaction product were seen in the parvocellular component of the paraventricular nucleus of the hypothalamus, the supraoptic nucleus, the arcuate nucleus, the subfornical organ, the median preoptic nucleus, and the medial nucleus of the amygdala in both the 3-day and 13-day tARN animals. The bed nucleus of the stria terminalis was observed to have a significant decrease in hexokinase activity in the tARN groups, as were the caudal and medial aspects of the nucleus of the solitary tract. In the 3-day tARN group only, a significant decrease in hexokinase activity was observed in the region of the brainstem containing the A5 cell group, compared with sARN animals. The magnocellular component of the paraventricular nucleus of the hypothalamus and the lateral hypothalamus was seen to have increased hexokinase activity in the 13-day tARN animals only.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The herbal medicine tian ma gou teng yen alters the development of high blood pressure in the spontaneously hypertensive rat.

In this study, the effect of the herbal prescription Tian Ma Gou Teng Yen (TGY), which is traditionally used to treat certain diseases associated with elevated arterial pressure (AP), on the general development of hypertension was investigated in the spontaneously hypertensive rat (SHR). An aqueous extract of TGY was given orally (0.5 ml/100g body weight) to 5 week old SHR twice a day for six consecutive days followed by one day without herbal therapy. The herbal prescription was administered until the SHR were 16 weeks of age. Administration of TGY significantly altered the development and prevented hypertension in SHR. On the other hand, heart rate, body weight, food and water intake, and urine volume and electrolytes were not altered. These data suggest that the effect of TGY on AP was through an action of TGY on sympathetic vasomotor activity.

Animals↗

Renal denervation alters forebrain hexokinase activity in neurogenic hypertensive rats.

The effect of afferent renal nerve transection (tARN) on the metabolic activity of forebrain structures the activity of which was altered after aortic depressor nerve transection (tADN) was studied using the hexokinase (HK) histochemical method in the rat. In tADN-sham (s) ARN rats, increases in HK activity were observed in the medial septum (MS), median preoptic nucleus (MnPO), subfornical organ, supraoptic nucleus, nucleus circularis (Nc), magnocellular, and dorsal and medial (mpPVH) parvocellular components of paraventricular nucleus, the anterior, lateral, and dorsomedial (DMH) hypothalamus, and in the central and medial nuclei of the amygdala. In addition, a decrease in HK activity was seen in the dorsal arcuate nucleus (dArc). Similarly, increases in HK activity were seen in sADN-tARN rats in all the above structures except MS, Nc, and DMH, where no changes were observed, and dArc, where an increase in HK activity was noted. The bed nucleus of the stria terminalis, lateral preoptic nucleus (POA), and ventral (v) Arc also showed elevated HK activity. In contrast, the increased HK activity after either tADN or tARN alone was returned to levels not different from sADN-sARN rats in all structures in the tADN-tARN rats, except MnPO, mpPVH, and dArc, where the level of HK activity was only attenuated, and MS, POA, and vArc, where it remained elevated. These data suggest that similar forebrain structure are associated with the hypertension after tADN and are involved in the integration of ARN information and that these sites of interaction are involved in the maintenance and the reversal of the neurogenic hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

Afferent renal nerve effects on plasma vasopressin and oxytocin in conscious rats.

Experiments were done in conscious, unrestrained, baroreceptor-intact rats to investigate the effects of afferent renal nerve (ARN) stimulation on circulating levels of arginine vasopressin (AVP) and oxytocin (OXY). Electrical stimulation of ARN elicited a rise in arterial pressure (AP) of 12 +/- 2 mmHg and no significant change in heart rate (HR). Plasma concentrations of AVP and OXY measured by radioimmunoassay were significantly increased immediately after the stimulation period. AVP increased from control levels of 1.89 +/- 0.72 to 4.59 +/- 1.19 pg/ml after stimulation of ARN and OXY increased from 4.3 +/- 0.35 to 10.0 +/- 1.00 pg/ml. AVP remained significantly elevated at 1 h after stimulation and gradually returned to control levels by 3 h after stimulation. On the other hand, OXY values were at control levels at 1 h after stimulation. Stimulation of ARN, after cutting ARN proximal to the stimulating electrode, and sham ARN stimulation did not alter AP, HR, or plasma levels of AVP and OXY. Plasma osmolality was not altered during the experiments. These data demonstrate that, in the conscious rat, afferent information from the kidney alters the release of AVP and OXY from the neurohypophysis and suggests that ARNs are important components of a neuronal circuit that modulates differentially the release of these hormones, which function in the homeostatic regulation of AP and fluid balance.

Afferent Pathways↗

Renal and cardiovascular afferent inputs to hypothalamic paraventriculo-spinal neurons.

Experiments were done in chloralose-anesthetized cats to identify single units in the paraventricular nucleus of the hypothalamus (PVH) that responded to stimulation of afferent renal nerves (ARN) and the buffer nerves (carotid sinus (CSN) and aortic depressor (ADN) nerves), and whose axons projected directly to thoracic spinal sympathetic areas. Of 426 single units tested in the PVH region, 20 were antidromically activated by stimulation of the spinal cord. Sixteen of these antidromic units (80%) responded orthodromically to stimulation of ARN and/or the buffer nerves; 6 units (30%) were excited by ARN stimulation only, 2 units (10%) were excited by both ARN and buffer nerve stimulation, and 6 units were excited and 2 inhibited by buffer nerve stimulation only. These data demonstrate that sensory information originating in renal and cardiovascular receptors alters the firing rate of PVH-spinal projecting neurons and suggest that this long renal-PVH reflex loop may contribute to the elevation of arterial pressure (AP) during conditions when ARN are activated.

Animals↗

Vestibular nucleus inputs to paramedian reticulospinal neurons in the cat.

Experiments were done in chloralose-anesthetized cats to identify single units in the paramedian reticular nucleus (PRN) that responded to stimulation of pressor sites in the vestibular nucleus complex (VNC) and that projected directly to the intermediate gray (IG) region of the upper thoracic cord. Forty-seven units responded orthodromically to stimulation of the ipsilateral VNC with a mean latency of 6.3 +/- 0.6 ms: 44 were excited and 3 were inhibited. Of these 47 units, 29 (62%) also were antidromically activated by stimulation of the ipsilateral IG at the level of T2. These data provide electrophysiological evidence for the existence of neurons in PRN that receive VNC inputs and project directly to spinal autonomic areas, and suggest that this pathway may be involved in mediating vestibulosympathetic reflex responses associated with postural adjustments.

Action Potentials↗

Cardiovascular afferent and fastigial nucleus inputs to paramedian reticulospinal neurons.

In chloralose anesthetized, paralyzed and artificially ventilated cats, the region of the paramedian reticular nucleus (PRN) was systematically explored for single units antidromically activated by electrical stimulation of histologically verified sites in the intermediate gray region of the upper thoracic cord (T2). These antidromically identified units were then tested for their orthodromic responses to electrical stimulation of ipsilateral carotid sinus nerve (CSN) and of pressor sites in the contralateral fastigial nucleus (FN). Sixty-two histologically verified single units, located predominantly in the caudal half of the ventral PRN, were antidromically activated with latencies corresponding to a mean conduction velocity of 36.4 +/- 2.1 m/s. Of these units 25 (40%) were excited orthodromically by stimulation of the CSN and/or FN: 5 to stimulation of the CSN only (mean latency, 18.3 +/- 9.9 ms), 6 to stimulation of the FN only (mean latency, 7 +/- 1.7 ms), and 14 to stimulation of both the CSN and FN (mean latencies, 12.3 +/- 2.9 ms and 8.4 +/- 1 ms, respectively). These data provide electrophysiological evidence for the existence of PRN reticulo-spinal neurons that integrate and relay cardiovascular afferent information from the CSN and FN to spinal autonomic neurons.

Action Potentials↗

Neuropeptide and serotonin immunoreactive neurons in the cat ventrolateral medulla.

The distribution of cell bodies containing serotonin (5-HT)-, substance-P (SP)-, neurotensin (NT)-, and somatostatin (SS)-like immunoreactivity (IR) in ventrolateral medulla (VLM) of the cat was studied immunohistochemically after administration of colchicine into the cisterna magna. Perikarya containing 5-HT-, SP-, NT- or SS-IR were found throughout the rostrocaudal extent of the VLM. Although neurons containing the different neuroactive substances appeared to have an overlapping distribution in VLM, some distinct differences were observed. In the caudal VLM most of the immunoreactive cell bodies observed contained 5-HT-IR. These neurons were found primarily in the region medial to lateral reticular nucleus (LRN) around the exiting intramedullary rootlets of the hypoglossal nerve (12N). In the intermediate region of VLM, perikarya containing 5-HT- and SP-IR were observed primarily near the ventrolateral surface of the medulla in the region around the exiting rootlets of the 12N. In contrast, most of the cells containing NT- and SS-IR were consistently observed to occupy a region in the medullary reticular formation immediately dorsal to that where 5-HT- and SP-IR perikarya were found. Finally, most of the immunoreactive perikarya were found in the rostral VLM; perikarya containing 5-HT- and SP-IR were observed throughout the nucleus paragigantocellularis lateralis (PGL) near the ventrolateral surface of the medulla. These data indicate that neurons immunoreactive to either 5-HT or several different neuropeptides were located in regions of VLM which have previously been implicated in the control of arterial pressure. As regions of VLM containing these neuroactive substances in neuronal perikarya have been shown to have direct connections with spinal sympathetic areas it is likely that these VLM cells are components of neuronal circuits involved in homeostatic mechanisms controlling the circulation.

Animals↗

Contribution of paraventricular nucleus to afferent renal nerve pressor response.

Experiments were done in alpha-chloralose-anesthetized, paralyzed, and artificially ventilated cats to determine the effect of afferent renal nerve (ARN) stimulation on the firing frequency of neurons in the paraventricular nucleus of the hypothalamus (PVH), whose axons project directly to the neurohypophysis (NH), and the contribution of these neurons to the pressor response elicited by ARN stimulation. In the first series of experiments, 474 single units were extracellularly recorded in the PVH region. Of these units 86 were antidromically excited by stimulation of the NH. Seventeen of the antidromic units (20%) responded orthodromically to ARN stimulation; 10 responded to ARN stimulation only, and 7 units responded to both ARN and buffer nerve stimulation. All PVH-NH-projecting neurons that responded to ARN stimulation were excited. In the second series the contribution of PVH neurons to the pressor response elicited by ARN stimulation was investigated in animals with the aortic depressor, carotid sinus, vagus, and cervical sympathetic nerves cut bilaterally. The ARN pressor response has previously been shown to be due to the activation of the sympathetic nervous system and to the release of arginine vasopressin (AVP). The primary and secondary (AVP component) components of the pressor response were attenuated by 51 and 69%, respectively, by bilateral injections of procaine hydrochloride into PVH or bilateral electrolytic lesions of PVH. Control injections of saline into PVH or electrolytic lesions of hypothalamic regions anterior, dorsal, or ventral to PVH did not alter the ARN pressor response. These experiments demonstrate that sensory information originating in renal receptors excites magnocellular neurosecretory neurons in PVH and suggest that this renal-paraventricular reflex loop may contribute to the elevated arterial pressure and AVP release during conditions when ARN are activated.

Afferent Pathways↗

Effects of plasma angiotensin II and hypernatremia on subfornical organ neurons.

Experiments were done in urethan-anesthetized rats to investigate the effect of plasma angiotensin II (ANG II) and hypernatremia on the excitability of subfornical organ (SFO) neurons projecting directly to paraventricular nucleus of the hypothalamus (PVH), supraoptic nucleus (SON), and nucleus medianus (NM). Extracellular recordings were made from 106 antidromically identified neurons in the SFO. The firing frequency of 53 (50%) was increased by the intracarotid infusion of ANG II and/or 0.5 M hypertonic NaCl. The intracarotid infusion of isotonic saline or the intravenous infusion of phenylephrine did not alter the discharge rate of these SFO neurons. Of 38 PVH projecting neurons, 21 (55%) responded to ANG II and/or hypertonic NaCl: 9 to ANG II only, 8 to hypertonic NaCl only, and 4 to both. Similarly, of 42 SON projecting neurons, 30 (71%) responded to ANG II and/or hypertonic NaCl: 10 to ANG II only, 15 to hypertonic NaCl only, and 5 to both. Finally, of 26 NM projecting neurons, one increased its firing frequency to ANG II and one other to 0.5 M NaCl. An additional eight SFO neurons were found to send collateral axons to both the PVH and SON (n = 6) and PVH and NM (n = 2): four responded in various combinations to intracarotid infusion of ANG II and 0.5 M NaCl. These data suggest that blood-borne ANG II and plasma hypernatremia can influence arterial pressure and the release of vasopressin from the neurohypophysis by altering the discharge rate of SFO neurons projecting to forebrain structures that contain magnocellular neurosecretory vasopressin neurons and neurons that are components of sympathoexcitatory pathways.

Angiotensin II↗

Effect of paraventricular nucleus lesions on drinking and pressor responses to ANG II.

Experiments were done to investigate the contribution of cells of the paraventricular nucleus of the hypothalamus (PVH) to the drinking and pressor responses elicited by microinjection of angiotensin II (ANG II) into the subfornical organ (SFO) in the awake unrestrained rat. Microinjection of ANG II (5 eta g in 0.2 microliter) elicited drinking (7.1 +/- 0.7 ml in 15 min, n = 18) and pressor (19 +/- 1 mmHg, n = 17) responses. Bilateral lesions of the PVH by the administration of kainic acid (KA; 0.2 microgram in 0.2 microliter of phosphate buffer) resulted in the abolition of the drinking response (before, 7.8 +/- 1.8 ml in 15 min; after, 0 ml in 15 min, n = 6) and significant (P less than 0.05) attenuation of the pressor response (before, 15 +/- 1 mmHg; after, 5 +/- 2 mmHg, n = 5). Administration of 0.2 microliter of the phosphate buffer vehicle bilaterally into the PVH and KA into regions adjacent to the PVH had no significant effect on the drinking or pressor responses. KA injections into the PVH resulted in the loss of 70-80% of parvocellular cells in the posterodorsal component of the PVH compared with animals with KA injections into adjacent non-PVH tissue (n = 7) or vehicle injection into the PVH (n = 5). These results suggest that parvocellular cells of the PVH are an important component of the neural circuitry that mediates the drinking and pressor response to ANG II acting at the SFO.

Angiotensin II↗

Contribution of forebrain mechanisms in the maintenance of deoxycorticosterone acetate-salt hypertension.

A considerable amount of experimental evidence exists suggesting that forebrain structures are involved in the pathogenesis of hypertension. In particular, the paraventricular nucleus of the hypothalamus (PVH) has been implicated in the development and maintenance of the elevated arterial pressure (AP) in several different experimental models of hypertension. The present study was done to determine whether the PVH contributed to the maintenance of the increased AP in deoxycorticosterone acetate-salt (DOCA) hypertension in the rat. In the first series of experiments, using the hexokinase histochemical method, increased metabolic activity was observed in the PVH of DOCA-salt hypertensive rats. In addition, the lateral septal nucleus, median preoptic nucleus, bed nucleus of the stria terminalis, subfornical organ, nucleus circularis, supraoptic nucleus and central nucleus of the amygdala were observed to have increased metabolic activity. In the second series of experiments, bilateral lesions of the PVH resulted in a transient reduction in the elevated AP of DOCA-salt hypertensive animals. However, within approximately a week, the level of AP was not significantly different from sham-PVH lesioned DOCA-salt hypertensive rats. These data suggest that the PVH may be one of several forebrain structures that contributes to the elevated sympathetic activity in DOCA-salt hypertension and when absent other pressor systems are recruited to maintain the elevated AP.

Animals↗

Distribution and morphology of vasopressin-, neurophysin II-, and oxytocin-immunoreactive cell bodies in the forebrain of the cat.

Experiments were done to provide a detailed map of the location and a description of morphological characteristics of vasopressin (AVP-IR)-, neurophysin II (NII-IR)- and oxytocin (OXY-IR)-immunoreactive neuronal perikarya in the forebrain of the cat. In addition, the location of cells in the forebrain retrogradely labeled following injections of tracers into the neurohypophysis was determined. The distribution of AVP-IR and NII-IR was similar in all cases studied. Most of the cells containing AVP-IR and OXY-IR were observed in the hypothalamic paraventricular (PVH) and supraoptic (SON) nuclei. In addition, AVP-IR and OXY-IR cell bodies were found in the regions of the nucleus of the diagonal band of Broca, the dorsal chiasmatic nucleus, the anterior hypothalamic-preoptic area, the periventricular area, the nucleus circularis, the perifornical area of the lateral hypothalamus, the accessory SON, the area of the tuber cinereum (Tca), and the medial nucleus of the amygdala. The density of AVP-IR cells was greater than that of OXY-IR cells in these regions. Several forebrain areas were also observed to contain only AVP-IR perikarya: the suprachiasmatic nucleus (Sc), the bed nucleus of the stria terminalis, and the region of the substantia innominata and ventral globus pallidus (SI/GP). In addition, the dorsomedial nucleus of the hypothalamus only contained OXY-IR perikarya. Most of the cells immunoreactive to AVP were multipolar and had spinelike processes over their somata and proximal dendrites. In addition, the majority of cells in the PVH and SON were round or oval, whereas those outside these nuclei were fusiform or triangular. The mean somal area of AVP-IR cells in the region of the SI/GP was significantly (P less than 0.05) larger than that of AVP-IR cells in all other regions examined, whereas the mean somal area of Sc AVP-IR cells was significantly (P less than 0.05) smaller than that of all other groups of AVP-IR cells examined. Most OXY-IR cells were similar morphologically to those immunoreactive to AVP, except that OXY-IR cell bodies and their appendages did not have spinelike processes. In addition, OXY-IR perikarya were generally of uniform size. OXY-IR cells in the PVH and accessory SON were significantly (P less than 0.05) larger than AVP-IR cells in the same regions, but were not different from AVP-IR cells in the lateral hypothalamus and SON.(ABSTRACT TRUNCATED AT 400 WORDS)

Amidines↗

Collateral branching in axonal projections to spinal cord from paramedian reticular nucleus neurons.

Experiments were done in cats to identify neurons in the paramedian reticular nucleus (PRN) sending collateral axons to the region of the intermediolateral nucleus (IML) at different levels of the thoracic cord by using lectin-conjugated horseradish peroxidase (HRP) and double-labeling fluorochrome histochemistry to retrogradely label PRN neurons. Injections of Fast blue (FB) into the spinal cord at the T2 level centered in the region of the IML were coupled with injections of Nuclear yellow (NY) into the ipsilateral cord at either the T4 or T7 levels centered in the region of the IML. Neurons in the PRN retrogradely labeled after diffusion of HRP into the region of the IML at the T2 level were observed throughout the rostrocaudal extent of the ventral PRN. In addition, a few labeled neurons were noted in the ventral portion of the dorsal PRN. About 40% of the neurons in the PRN which were labeled with FB after an injection at the T2 level were also labeled with NY injected into the cord in further caudal segments. These data suggest that the PRN may exert its influence on the cardiovascular system partly through collateral axonal branches to widely separated populations of sympathetic preganglionic neurons in different spinal segmental levels.

Amidines↗