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.

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.

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

1989 ◽  
Vol 256 (6) ◽  
pp. R1240-R1244 ◽  
Author(s):  
J. K. Simon ◽  
N. W. Kasting ◽  
J. Ciriello
Keyword(s):  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Conscious Rat ◽  
Renal Nerve ◽  
Plasma Vasopressin ◽  
Afferent Information ◽  
Stimulation Period ◽  
Circulating Levels ◽  
Stimulation Of ◽  
Intact 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.

Ventilatory effects of stimulation of phrenic afferents

1987 ◽  
Vol 63 (3) ◽  
pp. 1063-1069 ◽  
Author(s):  
J. D. Road ◽  
N. H. West ◽  
B. N. Van Vliet
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Sensory Innervation ◽  
Respiratory Muscle Fatigue ◽  
Pentobarbital Sodium ◽  
Arterial Blood ◽  
Afferent Activation ◽  
Ventilatory Drive ◽  
Alpha Chloralose ◽  
Stimulation Of

The diaphragm, a ventilatory muscle, has abundant sensory innervation. The effects of phrenic afferent activation on ventilation have been varied. In this study the proximal end of the phrenic nerve was electrically stimulated, and the effects on ventilation were measured in supine dogs anesthetized with either alpha-chloralose or pentobarbital sodium. We found a maximum increase in ventilation of 45 +/- 4% in the alpha-chloralose group and an increase in mean arterial blood pressure of 18 +/- 4%. This response was obtained at high stimulus intensities (60 times twitch threshold). Stimulation of the proximal end of the gastrocnemius nerve produced a similar ventilatory response (61 +/- 10%) but at lower stimulus intensities. During pentobarbital sodium anesthesia both the hyperventilation and the pressor response were produced; however, ventilation was increased by an increase in respiratory frequency. The reflex was abolished by sectioning of the cervical dorsal roots (C4-C7). Proximal cold blockade of the nerve abolished the response at a perineural temperature of 1.35 +/- 0.64 degrees C. The main effect of activation of phrenic afferents was an increase in ventilation and blood pressure that was mediated by unmyelinated fibers and possibly thin myelinated fibers. This response is similar to skeletal muscle afferent activation and may play a role in ventilatory drive during such conditions as exercise and respiratory muscle fatigue.

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.

Spinoreticular cell responses to renal venous and ureteral occlusion

1988 ◽  
Vol 254 (2) ◽  
pp. R268-R276
Author(s):  
W. S. Ammons
Keyword(s):  
Renal Vein ◽  
Cardiovascular Responses ◽  
Cardiovascular Reflexes ◽  
Renal Nerves ◽  
Mechanical Stimuli ◽  
Medullary Reticular Formation ◽  
Renal Nerve ◽  
Pressor Responses ◽  
Alpha Chloralose ◽  
Ureteral Occlusion

Responses of 65 thoracolumbar spinoreticular neurons to renal vein or ureteral occlusion were studied in 40 alpha-chloralose-anesthetized cats. Cells were antidromically activated from the medial medullary reticular formation and all responded to somatic stimuli as well as renal nerve stimulation. Renal vein occlusion excited 17 of 40 cells. Activity increased from 6 +/- 1 to 13 +/- 2 spikes/s, with little adaptation. Depressor responses occurred in 9 cats and pressor responses in 12 cats. Pressor responses, but not depressor responses, were abolished by renal denervation. Ureteral occlusion increased activity of 28 of 50 cells. Responses were always rapid in onset but were either nonadapting, slowly adapting, or completely adapting. Activity increased from 7 +/- 1 to a peak of 17 +/- 3 spikes/s. Pressor responses occurred in 22 of 25 cats and tachycardia in 15 cats. Transection of renal nerves abolished cardiovascular responses. Twenty-five cells were tested for responses for both stimuli. Ten were excited by both, six by only ureteral occlusion, and nine failed to respond to either. The responding group of cells had a significantly greater incidence of A delta- and C-fiber renal input compared with nonresponding cells. Nonresponding cells tended to have only A delta-input. The results show that renal and ureteral mechanical stimuli which evoke cardiovascular reflexes excite spinoreticular cells. These cells may be part of supraspinal reflex arcs initiated by renal receptors.

Stimulation of parabrachial neurons elicits a sympathetically mediated pressor response in cats

1988 ◽  
Vol 255 (6) ◽  
pp. H1349-H1358 ◽  
Author(s):  
J. S. Hade ◽  
S. W. Mifflin ◽  
T. S. Donta ◽  
R. B. Felder
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Electrical Stimulus ◽  
Respiratory Drive ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Low Intensity ◽  
Stimulation Of

We examined the role of the parabrachial neuronal mass in mediating the pressor response to electrical stimulation of parabrachial nucleus (PBN). In anesthetized cats, 100 mM L-glutamate (L-glu) was microinjected into PBN at sites from which low-intensity (25 microA) electrical stimulation evoked a pressor response. Arterial pressure, heart rate, and, in some animals, renal or phrenic nerve activity were monitored. Microinjection of L-glu caused an increase in arterial pressure that was comparable with that elicited by low-intensity electrical stimulation. Electrical stimulation, and to a lesser extent L-glu microinjection, caused an increase in renal sympathetic nerve activity but no significant change in heart rate. No consistent change in central respiratory drive accompanied the pressor response. These responses were preserved after baroreceptor denervation but were blocked by intravenous administration of the alpha-adrenergic receptor antagonist phentolamine. Microinjection into PBN of 2 mM kainic acid, which selectively depolarizes neurons but spares axons, reversibly blocked the arterial pressure and renal nerve responses to the 25-microA electrical stimulus. We conclude that the pressor response elicited by electrical stimulation of PBN in the anesthetized cat is mediated by cellular elements in PBN, not by fibers of passage. Because phentolamine completely blocked the pressor response, we suggest that it is subserved peripherally by sympathetic alpha-adrenergic rather than humoral (e.g., angiotensin, vasopressin) vasoconstrictor mechanisms. Finally, our data indirectly suggest that PBN stimulation may differentially engage efferent components of the sympathetic nervous system to elicit the pressor response.

Regional responsiveness of renal perfusion to activation of the renal nerves

2002 ◽  
Vol 283 (5) ◽  
pp. R1177-R1186 ◽  
Author(s):  
Sarah-Jane Guild ◽  
Gabriela A. Eppel ◽  
Simon C. Malpas ◽  
Niwanthi W. Rajapakse ◽  
Alistair Stewart ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Stimulus Frequency ◽  
Renal Medulla ◽  
Renal Perfusion ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Vascular Elements ◽  
Doppler Flux ◽  
Stimulation Of

We tested for regional differences in perfusion responses, within the renal medulla and cortex, to renal nerve stimulation in pentobarbital sodium-anesthetized rabbits. Laser-Doppler flux (LDF) was monitored at various depths below the cortical surface (1–15 mm). Basal cortical LDF (1–3 mm, ∼200–450 U) was greater than medullary LDF (5–15 mm, ∼70–160 U), but there were no statistically significant differences in basal LDF within these regions. The background LDF signal during aortic occlusion was similar in the cortex (2 mm, 31 U) and outer medulla (7 mm, 31 U), but slightly greater in the inner medulla (12 mm, 44 U). During electrical stimulation of the renal nerves (0.5–8 Hz), cortical LDF and total renal blood flow were similarly progressively reduced with increasing stimulus frequency. Medullary LDF (measured between 5 and 15 mm) was overall less responsive than cortical LDF. For example, 4-Hz stimulation reduced inner medullary LDF (9 mm) by 19 ± 6% but reduced cortical LDF (1 mm) by 54 ± 11%. However, medullary LDF responses to nerve stimulation were similar at all depths measured. Our results indicate that while the vascular elements controlling medullary perfusion are less sensitive to the effects of electrical stimulation of the renal nerves than are those controlling cortical perfusion, sensitivity within these vascular territories appears to be relatively homogeneous.

Responses of thoracolumbar spinal neurons to renal artery occlusion

1989 ◽  
Vol 256 (6) ◽  
pp. H1515-H1523 ◽  
Author(s):  
W. S. Ammons ◽  
R. Sinha
Keyword(s):  
Electrical Stimulation ◽  
Renal Artery ◽  
Artery Occlusion ◽  
Renal Ischemia ◽  
Renal Nerves ◽  
Spinal Neurons ◽  
Renal Artery Occlusion ◽  
C Fiber ◽  
Alpha Chloralose ◽  
Stimulation Of

Experiments were performed to examine responses of spinal neurons to activation of renal chemoreceptors during renal artery occlusion (RAO). One hundred twenty-two spinal neurons were studied in 33 cats that were anesthetized with alpha-chloralose. Cells studied in the L2-T11 segments were excited by electrical stimulation of the renal nerves and responded to stimulation of somatic structures. RAO (90 s) excited 67 cells (55%). Twenty-eight cells were excited at the onset of occlusion (from 5 +/- 1 to 27 +/- 5 spikes/s) and then either completely or partially adapted (ON responses). Another 39 cells were excited at the onset of occlusion, adapted to varying degrees, and then exhibited a second increase in activity beginning 41 +/- 7 s into the occlusion period [onset-ischemic (ON/IS) responses]. The secondary increase reached a peak of 15 +/- 2 spikes/s 65 s after occlusion. Among the responding cells, ON responses were associated with cells receiving A delta only or with cells with A delta- and C-fiber renal inputs. In contrast, 100% of cells with ON/IS response received both A delta- and C-fiber inputs. Probability of finding responding cells was greatest in the most rostral segments. We conclude that ON responses to RAO are due to activation of mechanoreceptors in the renal artery. ON/IS responses must have resulted from activation of mechanoreceptors followed by activation of renal chemoreceptors in association with development of renal ischemia. These data provide evidence for activation of spinal neurons by RAO. These neurons may be important for renal reflexes of chemoreceptor origin.

Cholinergic stimulation of the hypothalamus and natriuresis in rats: role of the renal nerves

1986 ◽  
Vol 250 (2) ◽  
pp. F322-F328 ◽  
Author(s):  
C. R. Silva-Netto ◽  
R. H. Jackson ◽  
R. E. Colindres
Keyword(s):  
Renal Plasma Flow ◽  
Isotonic Saline ◽  
Renal Perfusion ◽  
Renal Nerves ◽  
Cholinergic Stimulation ◽  
Renal Nerve ◽  
Water Excretion ◽  
Before And After ◽  
Stimulation Of

The role of the renal nerves in the natriuresis seen after cholinergic stimulation of the hypothalamus was studied in anesthetized rats treated with injection into the lateral hypothalamus (LH) of 1 microgram of carbamylcholine chloride (carbachol) in 1 microliter of 0.15 M NaCl or NaCl alone. Injection of carbachol exhibited diuresis and natriuresis both in acutely denervated kidneys (P less than 0.01) and in contralateral innervated kidneys (P less than 0.01) without changes in glomerular filtration rate (GFR) or renal plasma flow (RPF) (n = 10). Salt and water excretion was unchanged in 10 rats after injection of NaCl. Micropuncture studies in denervated kidneys showed that, after carbachol injection, tubular fluid-to-plasma inulin concentration ratio [(F/P)In] in the late proximal tubule fell from 1.86 +/- 0.08 to 1.64 +/- 0.07 (P less than 0.01) without changes in single-nephron GFR. In nine other carbachol-treated rats in which renal perfusion pressure was maintained low and constant, diuresis and natriuresis, although attenuated, were again observed both in denervated (P less than 0.01) and in contralateral innervated kidneys (P less than 0.05). In another group of 11 animals, efferent renal nerve activity (ERNA) was recorded before and after LH injection of carbachol and isotonic saline. ERNA was significantly depressed for 30 min, only after carbachol injection. Our results suggest that the renal nerves, although involved, are not essential for the natriuretic response after cholinergic stimulation of LH. By exclusion, other factors, presumably hormones, must contribute to the response.

Multisegmental spinal sympathetic reflexes originating from the heart

1983 ◽  
Vol 245 (3) ◽  
pp. R345-R352 ◽  
Author(s):  
L. C. Weaver ◽  
H. K. Fry ◽  
R. L. Meckler ◽  
R. S. Oehl
Keyword(s):  
Cervical Spinal Cord ◽  
Sympathetic Nerves ◽  
Spinal Reflexes ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Afferent Stimulation ◽  
Spinal Pathways ◽  
Afferent Nerves ◽  
Before And After ◽  
Stimulation Of

Activation of cardiac sympathetic afferent nerves can initiate excitatory cardiocardiac reflexes through pathways that are exclusively spinal. In addition, stimulation of the same nerves also causes lower thoracic and lumbar sympathetic excitation, but the contribution of spinal pathways to these reflexes is unknown. Therefore experiments were performed to compare cardiac, splenic, and renal sympathetic responses to cardiac sympathetic afferent stimulation before and after cervical spinal cord transection in anesthetized, vagotomized, sinoaortic-denervated cats. Electrical stimulation of afferent cardiac sympathetic nerves produced excitatory responses in cardiac and renal nerves before transection but only cardiac nerve responses after transection. In contrast, afferent stimulation by epicardially applied bradykinin excited cardiac, renal, and splenic nerves before and after cord transection. Splenic nerve responses were greater than renal nerve responses in intact and spinal cats. These results demonstrate that spinal reflexes initiated by activation of cardiac sympathetic afferent nerves are not limited to cardiocardiac pathways. The similarity of patterns of responses in intact and spinal cats suggests that spinal pathways contribute significantly to the reflex excitation observed in intact animals.

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