Biomedical subjects

J Ciriello

Publications and source records attributed to J Ciriello.

At least 37 records · Page 2Linked to original sources

PubMed1996

Neurotensin projections to subfornical organ from arcuate nucleus.

Two series of experiments were done in the rat to investigate whether neurons in arcuate nucleus of the hypothalamus (Arc) containing neurotensin (NT)-like immunoreactivity projected to subfornical organ (SFO). In the first series, the anterograde tract-tracer Phaseolus vulgaris leucoagglutinin (PHA-L) was microiontrophoresed into the region of Arc that contains NT neurons. After a 9-12 day survival period the animals were sacrificed and forebrain sections that contained SFO were processed for combined PHA-L and NT immunoreactivity. In the second series of experiments, unilateral or bilateral electrolytic lesions of Arc were made and after a 10-17 day survival period SFO was examined to determine the relative contribution of NT Arc neurons to NT immunoreactivity within SFO. PHA-L labelled fibers with terminal-like boutons were found in SFO primarily on the side ipsilateral to the site of injection. A small number of the PHA-L labelled fibers in the lateral aspect of SFO was also immunoreactive to NT. Unilateral lesions reduced, whereas bilateral lesions of Arc eliminated most of the NT-like immunoreactivity within SFO. These data demonstrate the existence of a direct pathway from Arc to SFO that contains the putative neurotransmitter NT. These results suggest that this pathway may function in the modulation of neural and/or humoral events related to cardiovascular regulation and body fluid homeostasis by influencing the activity of SFO neurons.

Animals↗

PubMed1995

Convergence of ventrolateral medulla and aortic baroreceptor inputs onto amygdala neurons.

Experiments were done to investigate the effect of stimulation of neurons in ventrolateral medulla (VLM) and aortic baroreceptors on the discharge rate of amygdala neurons. The region of central nucleus of the amygdala (ACe) was explored for spontaneously active single units that altered their discharge rate to electrical stimulation of VLM in the alpha-chloralose anesthetized rat. Responsive units were also assessed for their response to electrical stimulation of the aortic depressor nerve (ADN). Stimulation of VLM altered the discharge rate of 47% (43/92) of the units tested in and around the region of ACe. Of these units, 60% (26/43) were excited (mean latency, 13.6 +/- 3.6 ms) and 40% (17/43) were inhibited (mean latency, 23.1 +/- 4.3 ms) by VLM stimulation. Of the 43 units that responded to stimulation of VLM, 19 (44%) also responded to ADN stimulation with a mean latency of 32.5 +/- 7.6 ms. These data demonstrate that inputs from VLM and ADN converge onto ACe neurons and suggest that VLM may function as a relay for cardiovascular afferent information to the amygdala.

Afferent Pathways↗

PubMed1995

Glutamate stimulation of arcuate nucleus inhibits responses of subfornical organ neurons to plasma hypernatremia and angiotensin II.

Experiments were done in urethane anesthetized rats to investigate the effect of glutamate (Glu) stimulation of arcuate nucleus of the hypothalamus (Arc) on the discharge rate of subfornical organ (SFO) neurons during changes in plasma sodium concentration and angiotensin II (ANG II) levels. Extracellular recordings were made from 67 histologically verified single neurons within SFO. Of these, 17 (25.4%) were excited by intracarotid infusion of hypertonic NaCl and 21 (31.3%) by intracarotid ANG II infusion. Five (29.4%) of the units excited by hypertonic NaCl were also excited by Glu stimulation of Arc. Similarly, seven (33.3%) of the units excited by ANG II were also excited by Arc stimulation. Additionally, four (19.0%) of the units excited by ANG II were inhibited by Glu stimulation of Arc. The remaining SFO units did not alter their discharge rate to activation of Arc neurons. The response of units to hypertonic NaCl or to ANG II was attenuated during simultaneous activation of Arc. These data suggest that Arc may be involved in modulating the activity of SFO neurons that function in the detection of blood-borne signals from the depletion of intra- and extracellular fluid volumes.

Analysis of Variance↗

PubMed1995

Plasma hypernatremia induces c-fos activity in medullary catecholaminergic neurons.

Experiments were done in conscious rats to investigate the effect of intravenous infusion of hypertonic saline on the induction of the phosphoprotein Fos in brainstem catecholaminergic neurons. Fos induction, detected immunohistochemically, was used as a marker for neuronal activation. Infusions of 165 mM or 1.4 M NaCl solutions into the jugular vein resulted in Fos-like immunoreactivity in approximately the caudal two thirds of nucleus of the solitary tract (NTS), the caudal and rostral ventrolateral medulla (VLM), and in the lateral aspects of the parabrachial nucleus (PBN). Within caudal NTS a small number (7.9 +/- 1.8%) of Fos labelled neurons were found also to contain tyrosine hydroxylase (TH) or dopamine beta-hydroxylase (DBH) immunoreactivity. In rostral NTS no Fos labelled cells were found to contain phenylethanolamine N-methyltransferase (PNMT) immunoreactivity, although a few (8.5 +/- 2.3%) were immunoreactive to TH. Similarly, in VLM, most of the Fos labelled cells in caudal VLM (65.9 +/- 2.7%) contained either TH or DBH immunoreactivity, whereas in the rostral VLM, 32.2 +/- 4.6% of the Fos labelled cells were also immunoreactive to TH or DBH. However, no Fos cells were found in either the caudal or rostral VLM that were immunoreactive to PNMT. Little or no Fos-like immunoreactive neurons were detected in the brainstem after intravenous infusions of physiological (143 mM) or hypotonic (106 mM) NaCl solutions. These data suggest that noradrenergic neurons of the caudal NTS and VLM are components of central circuits that are involved in osmoregulation and cardiovascular function.

Animals↗

PubMed1994

Collateral axonal projections from ventrolateral medullary non-catecholaminergic neurons to central nucleus of the amygdala.

Retrograde tract-tracing techniques were used to investigate whether catecholaminergic neurons in the ventrolateral medulla (VLM) send collateral axonal projections to both central nuclei of the amygdala (ACe) in the rat. Rhodamine-labelled latex microspheres or fluorogold (2%) were microinjected into the region of either the right or left ACe. After a survival period of 10-12 days, the rats were sacrificed and transverse sections of the brainstem were processed immunohistochemically for the identification of cell bodies containing the catecholamine biosynthetic enzymes tyrosine hydroxylase (TH) or phenylethanolamine-N-methyltransferase (PNMT). Neuronal perikarya containing the retrogradely transported tracers were observed throughout the rostrocaudal extent of VLM, bilaterally. Approximately 10% of the retrogradely labelled neurons were observed to contain both retrograde tracers. The majority (79 +/- 6.8%) of these double labelled neurons were located within the caudal VLM and their number decreased rostrally. In addition, the proportion of double labelled neurons to single labelled neurons in VLM decreased rostrally; approximately 11% in the caudal VLM and 6% in the rostral VLM. Furthermore, approximately 21% of all VLM neurons that projected to ACe were found to be catecholaminergic: 75% of these were immunoreactive to TH and 25% to PNMT. However, no neurons were found in VLM that contained both retrograde tracers and immunoreactivity to TH or PNMT. These data demonstrate that axons originating from non-catecholaminergic neurons in VLM bifurcate to innervate ACe bilaterally. Although the function of these VLM neurons that project to both ACe is not known, they may be the anatomical substrate by which VLM neurons relay simultaneously autonomic and/or visceral sensory information to influence the activity of ACe.

Amygdala↗

PubMed1994

Cardiovascular effects of NaCl microinjections into the nucleus of the solitary tract.

The nucleus of the solitary tract (NTS) was systematically explored in the alpha-chloralose-anesthetized rat for sites that elicited changes in mean arterial pressure (MAP) and heart rate (HR) during microinjections (20 nl) of phosphate-buffered saline (PBS; pH 7.2-7.4) or NaCl solutions containing various concentrations of NaCl (104-326 mM). Decreases in MAP (range 7-83 mmHg) and HR (range 10-70 bpm) were consistently elicited from sites in the caudal medial and commissural subnuclei of NTS. Microinjection of PBS or NaCl into other NTS subnuclei or area postrema did not elicit cardiovascular responses. Microinjection of LiCl in PBS elicited cardiovascular responses that were significantly smaller than those elicited by microinjection of NaCl in PBS at the same NTS site. Injections of either a hyperosmotic (400 mOsm/kg) or a hyposmotic (204 mOsm/kg) solution of mannitol into NaCl-sensitive sites did not elicit cardiovascular responses. Finally, most of the sites in NTS that elicited cardiovascular responses during microinjection of glutamate (1 M) did not respond to microinjections of PBS. Administration of atropine methyl bromide had no effect on the magnitude of the depressor response to injections of PBS into NTS, but significantly attenuated (32%) the HR response. Subsequent administration of the ganglionic blockers hexamethonium bromide or arfonad abolished both the depressor and bradycardic responses. These data suggest that within a restricted region of the caudal NTS there exists a pool of neurons sensitive to changes in extracellular Na+ concentrations that, when activated by the sodium, elicit vasodepressor responses as a result of sympathoinhibition and bradycardia as a result of vagal excitation and sympathoinhibition.

Animals↗

PubMed1994

Collateral axonal projections to limbic structures from ventrolateral medullary A1 noradrenergic neurons.

Experiments were done to investigate whether catecholaminergic neurons within the ventrolateral medulla (VLM) send collateral axonal projections to the central nucleus of the amygdala (ACe) and the bed nucleus of the stria terminalis (BST). Unilateral microinjections of the fluorescent retrograde tracers fluorogold (FG) or rhodamine labelled latex micro-beads (Rd) were made into either ACe or BST in the rat. Brainstem sections were then processed immunohistochemically for the identification of cell bodies containing the catecholamine biosynthetic enzymes tyrosine hydroxylase, dopamine beta-hydroxylase (DBH) or phenylethanolamine-N-methyltransferase (PNMT). Retrogradely labelled cell bodies projecting to either ACe or BST were found throughout the rostrocaudal extent of VLM, bilaterally. Approximately 44% of these retrogradely labelled neurons were found to contain both retrograde tracers. In addition, approximately 91% of the VLM neurons that send collateral axonal projections to ACe and BST were also immunoreactive to DBH. None were found to contain PNMT immunoreactivity. These results demonstrate that noradrenergic neurons of the A1 cell group in VLM innervate ACe and BST via collateral axonal projections and suggest that these VLM neurons may be directly involved in relaying cardiovascular afferent and/or visceral afferent information directly to these limbic structures.

Amygdala↗

PubMed1994

Effects of plasma hypernatremia on nucleus tractus solitarius neurons.

Experiments were done in chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of plasma hypernatremia and baroreceptor activation on the excitability of nucleus tractus solitarius (NTS) neurons. Extracellular, single unit recordings were made from 67 histologically verified neurons in the region of NTS. The firing frequency of 29 (43%) NTS neurons was increased by the intracarotid infusion of hypertonic saline (0.5 M). The acute activation of baroreceptors after the intravenous infusion of phenylephrine resulted in the excitation of seven (31.8%) or the inhibition of five (22.7%) of the units responsive to plasma hypernatremia. Thirteen of the hypertonic saline-responsive neurons were recorded in animals in which the organum vasculosum lamina terminalis and subfornical organ were lesioned and/or the left vagus nerve was cut. These data suggest that within NTS there exists a pool of neurons that alter their discharge rate in response to changes in plasma sodium levels and that these neurons may also function in cardiovascular regulation.

Animals↗

PubMed1993

C-fos expression in arcuate nucleus following intracerebroventricular hypertonic saline injections.

Experiments were done in conscious rats to investigate the effect of i.c.v. infusions of hypertonic NaCl solutions on the induction of the protein Fos in the arcuate nucleus (Arc). Neurons containing Fos-like immunoreactivity were observed throughout the rostrocaudal extent of Arc after i.c.v. infusions of hypertonic saline solutions (337-744 mM). However, most of the labelled neurons were confined to the middle third of the nucleus, in the region of the dorsomedial and ventromedial subnuclei. Few, if any Fos-labelled neurons were observed in Arc of animals that received i.c.v. infusions of isotonic (142 mM) or mild hypertonic (173 mM) saline solutions or a hyperosmotic (660 mOsm/kg) saline solution of mannitol. No Fos-labelled neurons were found in the subfornical organ, although a few were observed scattered throughout the organum vasculosum laminae terminalis (OVLT) in all the animals studied. The density nor the distribution pattern of Fos-labelled neurons in OVLT was altered in animals receiving i.c.v. infusions of hypertonic saline or hyperosmotic solutions. These data demonstrate that Arc neurons are activated during a hypertonic saline challenge and suggest that Arc may function as a sodium-sensitive structure that is involved in body-fluid and circulatory homeostasis.

Animals↗

PubMed1993

Fos induction in brainstem neurons by intravenous hypertonic saline in the conscious rat.

Experiments were done in conscious rats to investigate the effect of intravenous infusion of hypertonic saline on the induction of the protein Fos, in brainstem neurons. Neurons containing Fos-like immunoreactivity were observed in the caudal nucleus of the solitary tract (NTS), the caudal and rostral ventrolateral medulla, and parabrachial nucleus after an infusion of solutions containing 1.4 M NaCl. Little or no expression of Fos was detected in brainstem neurons after intravenous infusions of either physiological (143 mM) or hypotonic (106 mM) NaCl solutions. These data provide evidence for the involvement of brainstem structures in osmoregulatory functions and suggest that brainstem neuronal circuits that function in cardiovascular regulation may also be shared by those involved in body fluid homeostasis.

Animals↗

PubMed1993

Effect of arcuate nucleus activation on neuronal activity in subfornical organ.

Experiments were done in urethane anesthetized rats to investigate the effect of activation of the arcuate nucleus (Arc) on the discharge rate of single units in the subfornical organ (SFO). Extracellular recordings were made from 51 spontaneously active neurons histologically verified in the SFO. Of these units, 19 (37%) were inhibited (mean latency 7.3 +/- 1.1 ms) and 14 (28%) were excited (mean latency 12.8 +/- 3.2 ms) during electrical stimulation of the Arc. The remaining 18 units did not alter their firing frequency during stimulation of the Arc. These data suggest that the Arc may be involved in the modulation of neural and humoral events related to body fluid homeostasis and cardiovascular regulation by altering the activity of SFO neurons.

Animals↗

PubMed1993

Innervation of the amygdaloid complex by catecholaminergic cell groups of the ventrolateral medulla.

The projections to the amygdaloid complex (AMG), originating in the catecholaminergic cell groups of the ventrolateral medulla (VLM), were studied in the rat by using either the retrograde tracer fluoro-gold (FG) or the anterograde tracer Phaseolus vulgaris leucoagglutinin (PHA-L) in combination with tyrosine hydroxylase (TH) and/or phenylethanolamine-N-methyltransferase (PNMT) immunohistochemistry. In the first series of experiments, injections of FG were made into regions of the central nucleus of the amygdala (ACe) where dense TH and PNMT immunoreactivity was previously observed, and then sections of the brainstem were processed for TH and PNMT immunoreactivity. FG retrogradely labelled neuronal cell bodies were observed throughout the rostrocaudal extent of VLM, bilaterally, with a contralateral predominance. Approximately 44% of the FG labelled cell bodies in VLM were also immunoreactive to the catecholamine biosynthetic enzymes TH and/or PNMT. Most of these catecholaminergic neurons were part of the A1 noradrenergic cell group in the caudal VLM and to a lesser extent part of the C1 adrenergic cell group in the rostral VLM. In the second series of experiments, PHA-L was iontophoresed into VLM at different rostrocaudal levels where in the previous series of experiments FG retrogradely labelled cell bodies were observed. Transverse sections of the forebrain and brainstem were then processed for the demonstration of PHA-L and either TH or PNMT immunoreactivity in cell bodies, axons, and presumptive axon terminals. PHA-L injection sites within either the caudal or rostral VLM resulted in labelled axons and terminal bouton-like swellings primarily in the contralateral AMG and to a lesser extent in the ipsilateral AMG. The ACe was observed to receive the greatest innervation from either VLM site. Additionally, PHA-L labelled fibers and presumptive terminal boutons were observed within the intercalated, medial, basomedial, and basolateral nuclei of the AMG. Most of the PHA-L labelled fibers and presumptive terminal boutons in the AMG after a caudal VLM (A1 region) injection also displayed TH immunoreactivity, whereas after a PHA-L injection into the rostral VLM (C1 region) all of the labelled axons and axon terminals in the AMG also were immunoreactive to PNMT. These data demonstrate that catecholaminergic neurons in A1 and C1 regions of VLM innervate the AMG and suggest that these VLM neurons may be involved in relaying afferent information directly to the AMG which influences the activity of AMG neurons controlling autonomic, endocrine, and behavioural functions.

Afferent Pathways↗

PubMed1993

Contribution of caudal ventrolateral medulla to the cardiovascular responses elicited by activation of bed nucleus of the stria terminalis.

The contribution of caudal ventrolateral medulla (cVLM) to the mean arterial pressure (MAP) and heart rate (HR) responses elicited by microinjections of L-glutamate (GLU) into the cardiovascular responsive region of bed nucleus of the stria terminalis (BST) was investigated in the chloralose-anesthetized, paralysed and artificially ventilated rat. Unilateral injections of GLU into BST elicited decreases in MAP of -25 +/- 3 mmHg (n = 10) and HR of -13 +/- 3 bpm (n = 10). These cardiovascular responses were not altered after a 100 nl microinjection of 0.9% NaCl into cVLM. However, the magnitudes of the decreases in MAP and HR were attenuated (-11 +/- 3 mmHg and HR, -4 +/- 1 bpm, respectively) 5 min after a 100 nl microinjection of the reversible synaptic blocker cobalt chloride (CoCl2) into cVLM. Restimulation of BST 40 min after the 100 nl microinjection of CoCl2 in cVLM elicited cardiovascular responses that were not significantly different in magnitude from those evoked before the microinjection of CoCl2 (MAP, -23 +/- 4 mmHg; HR, -12 +/- 5 bpm). In an additional series of experiments (n = 3), restimulation of BST 1 h after an ipsilateral electrolytic lesion in cVLM elicited decreases in MAP (-11 +/- 2 mmHg) and HR (-8 +/- 4 bpm) that were significantly smaller than those elicited prior to cVLM lesion. These data suggest that a component of the pathways originating in BST involved in mediating depressor responses and cardiac slowing relays in cVLM.

Animals↗

PubMed1993

Contribution of bed nucleus of the stria terminalis to the cardiovascular responses elicited by stimulation of the amygdala.

Anatomical and physiological studies were done in the rat to investigate the possibility that the cardiovascular responses elicited by stimulation of central nucleus of the amygdala (ACe) were mediated via projections to bed nucleus of the stria terminalis (BST). In the first series, to determine the distribution of neurons in ACe that projected to the cardiovascular region of BST, the retrograde tracer Fluorogold (FG) or rhodamine latex micro-beads (Rd) were injected into BST. FG and Rd injections that overlapped the cardiovascular region of BST resulted in retrogradely labelled neurons throughout the amygdala. In ACe, retrogradely labelled neurons were observed primarily in the lateral subdivision of the rostral ACe compared to the caudal ACe. The medial subdivision of ACe was found to have very few retrogradely labelled neurons. In the second series, the effect of either blocking synaptic transmission in BST with CoCl2, chemical lesions of BST with ibotenic acid (IBO), or electrolytic lesions of BST on the depressor response elicited by either electrical or chemical stimulation of ACe was investigated in the chloralose-anesthetized, artificially ventilated and paralysed rat. Microinjections of CoCl2 into BST significantly attenuated the depressor responses to stimulation of the rostral components of the lateral subnucleus of ACe, but not those to stimulation of the caudal and medial components of ACe. Microinjections of IBO into BST or electrolytic lesions of BST resulted in similar effects on the depressor responses to ACe stimulation. Taken together, these data indicate that neurons within the rostral components of the lateral subnucleus of ACe project to the cardiovascular region of BST and mediate in part the depressor responses to stimulation of the rostral ACe. On the other hand, the depressor responses elicited from the caudal ACe are not mediated through BST. These results suggest that at least two independent pathways originate in the ACe that influence the circulation.

Amygdala↗

PubMed1993

Effect of glutamate stimulation of bed nucleus of the stria terminalis on arterial pressure and heart rate.

Experiments were done in the chloralose-anesthetized, paralyzed, and artificially ventilated rat to determine the cardiovascular responses elicited during chemical stimulation of bed nucleus of the stria terminalis (BST) and to investigate the components of the peripheral autonomic nervous system that mediate these responses. Neurons in BST were selectively stimulated by the microinjection (10-20 nl) of the excitatory amino acid L-glutamate (1 M). Stimulation of BST elicited decreases in mean arterial pressure (n = 105) of -6 to -55 mmHg. These depressor responses were on occasion (n = 60) accompanied by decreases in heart rate ranging between -10 and -40 beats/min. The largest depressor responses were consistently elicited from a crescent-shaped region of BST around the dorsolateral, lateral, and ventrolateral surfaces of the anterior commissure. Intravenous administration of the muscarinic receptor blocker, atropine methylbromide, had no affect on the magnitude of the mean arterial pressure and heart rate responses. On the other hand, administration (intravenous) of the nicotinic receptor blocker, hexamethonium bromide or arfonad, abolished both the depressor response and cardiac slowing during stimulation of BST. These data suggest that the BST depressor and the bradycardia responses are mediated by inhibition of both sympathetic vasoconstrictor fibers to the vasculature and cardioacceleratory fibers to the heart, respectively.

Animals↗

PubMed1992

Caudal ventrolateral medullary projections to the nucleus of the solitary tract in the cat.

The projections of neurons, in and around the A1 noradrenergic cell group of the caudal ventrolateral medulla (VLM), to nucleus of the solitary tract (NTS) were studied in the cat using the anterograde transport of Phaseolus vulgaris leucoagglutinin (PHA-L). PHA-L was micro-iontophoresed into the region of the A1 noradrenergic cell group and after a 7-17 day survival period animals were sacrificed and brainstem sections were processed for PHA-L or tyrosine hydroxylase (TH) immunoreactivity. PHA-L injections within the region of the A1 cell group resulted in labelled fibers with their presumptive terminal boutons primarily in the ipsilateral commissural and medial subnuclei of NTS. A light projection to the ipsilateral parvocellular lateral and ventrolateral subnuclei of the NTS complex was also observed. These data demonstrate that neurons in the region of the A1 noradrenergic cell group project to regions of NTS that receive cardiovascular afferent inputs and suggest that VLM may influence the activity of neurons in NTS involved in the reflex regulation of the circulation.

Animals↗

PubMed1991

Functional identification of central pressor pathways originating in the subfornical organ.

The functional projections from pressor sites in the subfornical organ (SFO) were identified using the 2-deoxyglucose (2-DG) autoradiographic method in urethane-anesthetized, sinoaortic-denervated rats. Autoradiographs of brain and spinal cord sections taken from rats whose SFO was continuously stimulated electrically for 45 min with stereotaxically placed monopolar electrodes (150 microA, 1.5-ms pulse duration, 15 Hz) following injection of tritiated 2-DG were compared with control rats that received intravenous infusions of pressor doses of phenylephrine to mimic the increase in arterial pressure observed during SFO stimulation. Comparisons were also made to autoradiographs from rats in which the ventral fornical commissure (CFV), just dorsal to the SFO, was electrically stimulated. The pressor responses during either electrical stimulation of the SFO or intravenous infusion of phenylephrine were similar in magnitude. On the other hand, stimulation of the CFV did not elicit a significant pressor response. Electrical stimulation of the SFO increased 2-DG uptake, in comparison to the phenylephrine-infused rats, in the nucleus triangularis, septofimbrial nucleus, lateral septal nucleus, nucleus accumbens, bed nucleus of the stria terminalis, dorsal and ventral nucleus medianus (median preoptic nucleus), paraventricular nucleus of the thalamus, hippocampus, supraoptic nucleus, suprachiasmatic nucleus, paraventricular nucleus of the hypothalamus, and the intermediolateral nucleus of and central autonomic area of the thoracic spinal cord. In contrast, in rats whose CFV was stimulated, these nuclei did not demonstrate changes in 2-DG uptake compared with control animals that received pressor doses of phenylephrine. These data have demonstrated some of the components of the neural circuitry likely involved in mediating the pressor responses to stimulation of the SFO and the corrective responses to activation of the SFO by disturbances to circulatory and fluid balance homeostasis.

Animals↗

PubMed1991

Effect of renal denervation on plasma renin activity after aortic baroreceptor deafferentation.

Renal nerves are thought to play an important role in cardiovascular regulation under both normotensive and hypertensive conditions. In the present study the effect of renal denervation on the changes in plasma renin activity (PRA) after aortic baroreceptor deafferentation (tADN) were investigated in the rat. Bilateral renal denervation did not alter arterial pressure (AP, 100 +/- 4 mmHg; 1 mmHg = 133.32 Pa), heart rate (HR, 363 +/- 12 bpm), or PRA (2.9 +/- 0.6 ng.mL-1.h-1) compared with the respective sham renal denervation values of 106 +/- 3 mmHg (AP), 385 +/- 13 bpm (HR), and 3.3 +/- 0.7 ng.mL-1.h-1 (PRA). On the other hand, bilateral tADN resulted in significant increases in AP, HR, and PRA. One and 3 days after tADN, AP was 130 +/- 4 and 127 +/- 6 mmHg, HR was 461 +/- 15 and 463 +/- 20 bpm, and PRA was 9.1 +/- 3.0 and 11.9 +/- 4.5 ng.mL-1.h-1, respectively. Renal denervation before tADN prevented the increases in AP and PRA, but it did not affect the increase in HR. These data indicate that renal denervation does not alter basal PRA in normotensive animals but prevents the increased renin release observed in neurogenic hypertension. These data suggest that the increased PRA may be one of several factors that contributes to the elevated AP after tADN.

Animals↗