Contribution of paraventricular nucleus to afferent renal nerve pressor response

1988 ◽  
Vol 254 (3) ◽  
pp. R531-R543 ◽  
Author(s):  
M. M. Caverson ◽  
J. Ciriello
Keyword(s):  
Paraventricular Nucleus ◽  
Pressor Response ◽  
Sensory Information ◽  
Sympathetic Nerves ◽  
Firing Frequency ◽  
Procaine Hydrochloride ◽  
Renal Nerve ◽  
Neurosecretory Neurons ◽  
Electrolytic Lesions ◽  
Alpha Chloralose

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.

Effect of stimulation of afferent renal nerves on plasma levels of vasopressin

1987 ◽  
Vol 252 (4) ◽  
pp. R801-R807 ◽  
Author(s):  
M. M. Caverson ◽  
J. Ciriello
Keyword(s):  
Pressor Response ◽  
Plasma Concentrations ◽  
Sensory Information ◽  
Plasma Osmolality ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Autonomic Blockade ◽  
Component Plasma ◽  
Alpha Chloralose ◽  
Stimulation Of

Experiments were done in alpha-chloralose-anesthetized, paralyzed and artificially ventilated cats with vagus, cervical sympathetic, aortic depressor, and carotid sinus nerves cut bilaterally to investigate the effect of afferent renal nerve (ARN) stimulation on circulating levels of vasopressin (AVP). Electrical stimulation of ARN elicited a pressor response that had two components, a primary (1 degree) component locked in time with the stimulus and a secondary (2 degree) component that had a long onset latency and that outlasted the stimulation period. The 1 degree and 2 degree components of the pressor response were largest at stimulation frequencies of 30 and 40 Hz, respectively. Autonomic blockade with hexamethonium bromide and atropine methylbromide abolished the 1 degree component. Administration of the vasopressin V1-vascular receptor antagonist d(CH2)5VAVP during autonomic blockade abolished the 2 degree component. Plasma concentrations of AVP measured by radioimmunoassay increased from control levels of 5.2 +/- 0.9 to 53.6 +/- 18.6 pg/ml during a 5-min period of stimulation of ARN. Plasma AVP levels measured 20-40 min after stimulation (13.6 +/- 7.0 pg/ml) were not significantly different from control values. Plasma osmolality was not altered during the course of the experiment. These data demonstrate that sensory information originating in the kidney alters the release of vasopressin from the neurohypophysis and suggest that ARN are an important component of the neural circuitry involved in homeostatic mechanisms controlling arterial pressure.

Afferent renal inputs to paraventricular nucleus vasopressin and oxytocin neurosecretory neurons

1998 ◽  
Vol 275 (6) ◽  
pp. R1745-R1754 ◽  
Author(s):  
John Ciriello
Keyword(s):  
Electrical Stimulation ◽  
Paraventricular Nucleus ◽  
Discharge Rate ◽  
Sensory Information ◽  
Renal Nerves ◽  
Spontaneous Discharge ◽  
Unit Recording ◽  
Neurosecretory Neurons ◽  
Discharge Patterns ◽  
Stimulation Of

Extracellular single-unit recording experiments were done in pentobarbital sodium-anesthetized rats to investigate the effects of electrical stimulation of afferent renal nerves (ARN) and renal vein (RVO) or artery (RAO) occlusion on the discharge rate of putative arginine vasopressin (AVP) and oxytocin (Oxy) neurons in the paraventricular nucleus of the hypothalamus (PVH). PVH neurons antidromically activated by electrical stimulation of the neurohypophysis were classified as either AVP or Oxy secreting on the basis of their spontaneous discharge patterns and response to activation of arterial baroreceptors. Ninety-eight putative neurosecretory neurons in the PVH were tested for their response to electrical stimulation of ARN: 44 were classified as putative AVP and 54 as putative Oxy neurons. Of the 44 AVP neurons, 52% were excited, 7% were inhibited, and 41% were nonresponsive to ARN stimulation. Of the 54 Oxy neurons, 43% were excited, 6% inhibited, and 51% were not affected by ARN. An additional 45 neurosecretory neurons (29 AVP and 16 Oxy neurons) were tested for their responses to RVO and/or RAO. RVO inhibited 42% of the putative AVP neurons and 13% of the putative Oxy neurons. On the other hand, RAO excited 33% of the AVP and 9% of the Oxy neurons. No AVP or Oxy neurons were found to be excited by RVO or inhibited by RAO. These data indicate that sensory information originating in renal receptors alters the activity of AVP and Oxy neurons in the PVH and suggest that these renal receptors contribute to the hypothalamic control of AVP and Oxy release into the circulation.

V1a and V1b Vasopressin Receptors Within the Paraventricular Nucleus Contribute to Hypertension in Male Rats Exposed to Chronic Mild Unpredictable Stress

2020 ◽  
Author(s):  
Dragana Komnenov ◽  
Harrison Quaal ◽  
Noreen F. Rossi
Keyword(s):  
Heart Rate ◽  
Paraventricular Nucleus ◽  
Rat Model ◽  
Pressor Response ◽  
Traditional Risk Factor ◽  
Male Rats ◽  
Mild Stress ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Vasopressin Receptors

Depression is an independent non-traditional risk factor for cardiovascular disease and mortality. The chronic unpredictable mild stress (CMS) rat model is a validated model of depression. Within the paraventricular nucleus (PVN), vasopressin (VP) via V1aR and V1bR have been implicated in stress and neurocardiovascular dysregulation. We hypothesized that in conscious, unrestrained CMS rats vs control, unstressed rats, PVN VP results in elevated arterial pressure (MAP), heart rate and renal sympathetic nerve activity (RSNA) via activation of V1aR and/or V1bR. Male rats underwent four weeks of CMS or control conditions. They were then equipped with hemodynamic telemetry transmitters, PVN cannula, and left renal nerve electrode. V1aR or V1bR antagonism dose-dependently inhibited MAP after VP injection. V1aR or V1bR blockers at their ED50 doses did not alter baseline parameters in either control or CMS rats, but attenuated the pressor response to VP microinjected into PVN by ~50%. Combined V­1aR and V1bR inhibition completely blocked the pressor response to PVN VP in control but not CMS rats. CMS rats required combined maximally inhibitory doses to block either endogenous VP within the PVN or responses to microinjected VP. Compared with unstressed control rats, CMS rats had higher plasma VP levels and greater abundance of V1aR and V1bR transcripts within PVN. Thus, the CMS rat model of depression results in higher resting MAP, heart rate and RSNA which can be mitigated by inhibition of vasopressinergic mechanisms involving both V1aR and V1bR within the PVN. Circulating VP may also play a role in the pressor response.

Afferent renal nerve stimulation excites supraoptic vasopressin neurons

1985 ◽  
Vol 249 (3) ◽  
pp. R368-R371 ◽  
Author(s):  
T. A. Day ◽  
J. Ciriello
Keyword(s):  
Activity Patterns ◽  
Sensory Information ◽  
Response Duration ◽  
Firing Frequency ◽  
Onset Latency ◽  
Unit Recording ◽  
Renal Nerve ◽  
Afferent Information ◽  
Vasopressin Neurons ◽  
Body Fluid Balance

Single-unit recording experiments were performed in pentobarbital-anesthetized rats to investigate the effects of afferent renal nerve (ARN) stimulation on the activity of neurosecretory vasopressin cells of the supraoptic nucleus (SON). Neurosecretory SON cells were identified by antidromic invasion from the neurohypophysis and classified either as vasopressin (AVP) or oxytocin (OXY) secreting on the basis of their spontaneous activity patterns and response to activation of arterial baroreceptors. Fifty-three spontaneously active units were identified bilaterally in the SON: 40 putative AVP and 13 putative OXY neurons. Most putative AVP neurons (14/14 contralateral, 18/26 ipsilateral) were excited by ARN stimulation (mean onset latency 189 +/- 5 ms, mean response duration 237 +/- 17 ms). In contrast, ARN stimulation had no effect on the firing frequency of the 13 putative OXY neurons. These data indicate that sensory information originating in the kidney selectively alters the activity of SON AVP neurons and suggest that afferent information from the kidney is important in the coordination of neural and hormonal activity concerned with body fluid balance and the regulation of arterial pressure.

Involvement of the paraventricular nucleus of the hypothalamus in the pressor response to chemoreflex activation in awake rats

2001 ◽  
Vol 895 (1-2) ◽  
pp. 167-172 ◽  
Author(s):  
Marcelo V. Olivan ◽  
Leni G.H. Bonagamba ◽  
Benedito H. Machado
Keyword(s):  
Paraventricular Nucleus ◽  
Pressor Response ◽  
Awake Rats

Neurotransmission in the medulla mediating insular cortical and lateral hypothalamic sympathetic responses

1998 ◽  
Vol 76 (7-8) ◽  
pp. 737-746 ◽  
Author(s):  
Kenneth S Butcher ◽  
David F Cechetto
Keyword(s):  
Receptor Antagonist ◽  
Sympathetic Nerve ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Bipolar Electrode ◽  
Hypothalamic Area ◽  
Renal Nerve ◽  
Lateral Hypothalamic ◽  
Baseline Activity ◽  
Sympathetic Responses

Previous evidence has shown sympathetic nerve responses to insular cortical (IC) stimulation are mediated by synapses within the lateral hypothalamic area (LHA) and ventrolateral medulla (VLM). The present study was aimed at determining the neurotransmitter(s) and receptor(s) involved at the synapse in the VLM. Twenty male Wistar rats were instrumented for renal nerve, arterial pressure, and heart rate recording. The IC or the LHA was stimulated with a bipolar electrode (200-1000 µA; 2 ms; 0.8 Hz) to elicit sympathetic nerve responses. Antagonists were then pressure-injected into the VLM (300 nL). Bilateral and unilateral kynurenate (25 mM) resulted in 100% block of IC- and LHA-stimulated sympathetic nerve responses. Bilateral injection of the non-NMDA (N-methyl-D-aspartate) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 200 µM) also resulted in up to 100% block of IC and LHA sympathetic responses. In addition, unilateral injections of CNQX were made in two animals, resulting in 100 and 83% block of LHA sympathetic responses. Bilateral injection of the NMDA receptor antagonist DL-2-amino-5-phosphonopentanoic acid (AP5; 200µM) did not affect the response to IC or LHA stimulation. Kynurenate, CNQX, and AP5 all resulted in an elevation of baseline sympathetic nerve activity and a pressor response. Kynurenate resulted in a 263 ± 79% increase in baseline activity, while CNQX and AP5 resulted in 83 ± 19% and 91 ± 21% increases, respectively. Bilateral injections of antagonists for GABAA (bicuculline; 0.1 µM), acetylcholine (atropine; 0.1 µM) and catecholaminergic alpha and beta receptors (phentolamine and propranolol: 0.1 µM) had no effect on LHA sympathetic responses. Thus, sympathetic responses originating in the IC and LHA are mediated by a non-NMDA receptors in the VLM, which are likely AMPA receptors.Key words: insular cortex, ventrolateral medulla, glutamate, sympathetic activity.

Synchronization of cardiac-related discharges of sympathetic nerves with inputs from widely separated spinal segments

1995 ◽  
Vol 268 (6) ◽  
pp. R1472-R1483 ◽  
Author(s):  
G. L. Gebber ◽  
S. Zhong ◽  
S. M. Barman
Keyword(s):  
Phase Angle ◽  
Cervical Spinal Cord ◽  
Sympathetic Nerves ◽  
Time Interval ◽  
Renal Nerve ◽  
Cardiac Nerve ◽  
Spinal Segments ◽  
The Difference ◽  
Decerebrate Cats ◽  
Inferior Cardiac Nerve

We used phase spectral analysis to study the relationships between the cardiac-related discharges of pairs of postganglionic sympathetic nerves in urethan-anesthetized or decerebrate cats. Phase angle when converted to a time interval should equal the difference in conduction times from the brain to the nerves (i.e., transportation lag) if their cardiac-related discharges have a common central source. Transportation lag was estimated as the difference in the onset latencies of activation of the nerves by electrical stimulation of the medulla or cervical spinal cord. The phase angle for the cardiac-related discharges of two nerves was not always equivalent in time to the transportation lag. For example, in some cases the cardiac-related discharges of the renal nerve were coincident with or led those of the inferior cardiac nerve. In contrast, the electrically evoked responses of the renal nerve lagged those of the inferior cardiac nerve by > or = 32 ms. These observations are consistent with a model of multiple and dynamically coupled brain stem generators of the cardiac-related rhythm, each controlling a different sympathetic nerve or exerting nonuniform influences on different portions of the spinal sympathetic outflow.

A Slow Transient Potassium Current Expressed in a Subset of Neurosecretory Neurons of the Hypothalamic Paraventricular Nucleus

2000 ◽  
Vol 84 (4) ◽  
pp. 1814-1825 ◽  
Author(s):  
Jason A. Luther ◽  
Katalin Cs. Halmos ◽  
Jeffrey G. Tasker
Keyword(s):  
Paraventricular Nucleus ◽  
Potassium Current ◽  
Outward Current ◽  
Retrograde Transport ◽  
Neurosecretory Cells ◽  
Firing Frequency ◽  
Hypothalamic Paraventricular Nucleus ◽  
Transient Outward Current ◽  
Type I ◽  
Double Labeling

Type I putative magnocellular neurosecretory cells of the hypothalamic paraventricular nucleus (PVN) express a prominent transient outward rectification generated by an A-type potassium current. Described here is a slow transient outward current that alters cell excitability and firing frequency in a subset of type I PVN neurons (38%). Unlike most of the type I neurons (62%), the transient outward current in these cells was composed of two kinetically separable current components, a fast activating, fast inactivating component, resembling an A-type potassium current, and a slowly activating [10–90% rise time: 20.4 ± 12.8 (SE) ms], slowly inactivating component (time constant of inactivation: τ = 239.0 ± 66.1 ms). The voltage dependence of activation and inactivation and the sensitivity to block by 4-aminopyridine (5 mM) and tetraethylammonium chloride (10 mM) of the fast and slow components were similar. Compared to the other type I neurons, the neurons that expressed the slow transient outward current were less excitable when hyperpolarized, requiring larger current injections to elicit an action potential (58.5 ± 13.2 vs. 15.4 ± 2.4 pA; 250-ms duration; P < 0.01), displaying a longer delay to the first spike (184.9 ± 15.7 vs. 89.7 ± 8.8 ms with 250- to 1,000-ms, 50-pA current pulses; P < 0.01), and firing at a lower frequency (18.7 ± 4.6 vs. 37.0 ± 5.5 Hz with 100-pA current injections; P < 0.05). These data suggest that a distinct subset of type I PVN neurons express a novel slow transient outward current that leads to a lower excitability. Based on double labeling following retrograde transport of systemically administered fluoro-gold and intracellular injection of biocytin, these cells are neurosecretory and are similar morphologically to magnocellular neurosecretory cells, although it remains to be determined whether they are magnocellular neurons.

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