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.

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.

Contribution of renal sympathetic nerves to the urinary excretion of norepinephrine

1982 ◽  
Vol 60 (8) ◽  
pp. 1067-1072 ◽  
Author(s):  
Rodnhy W. Lappe ◽  
David P. Henry ◽  
Lynn R. Willis
Keyword(s):  
Urinary Excretion ◽  
Sympathetic Nerves ◽  
Tubular Secretion ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Group Iii ◽  
Group I ◽  
Renal Nerve Activity ◽  
Renal Sympathetic ◽  
Stimulation Of

Increased activity of the renal sympathetic nerves may result in increased urinary excretion of norepinephrine (NE). In the present study, unilateral electrical stimulation of the renal nerves of the rabbit was employed to test this hypothesis. Stimulation of the renal nerves to one kidney at 2 Hz (group I) produced no significant alteration of plasma NE concentration, glomerular filtration rate (GFR), or NE excretion by either kidney. Stimulation at 4 Hz (group II) caused statistically significant reductions of GFR and urine flow in experimental kidneys, but the urinary excretion of NE, per millilitre GFR, and the CNE/GFR ratios were significantly greater than prestimulation values. In another group of animals (group III), an inhibitor of cation-specific tubular transport, cyanine 863 (6 mg/kg, i.v.), significantly reduced the prestimulation urinary excretion of NE by 60–70% when compared with that of groups I or II. Stimulation of the renal nerves (4 Hz) in the animals of group III caused a significant reduction in GFR in the experimental kidney but did not alter the urinary excretion of NE or the CNE/GFR ratios. The results of these studies indicate that an increase in renal nerve activity causes an increase in the urinary excretion of NE, and that tubular secretion is responsible for the excretion of the neuronally released catecholamine.

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.

Hypothalamic projections of renal afferent nerves in the cat

1980 ◽  
Vol 58 (5) ◽  
pp. 574-576 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Fluid Balance ◽  
Lateral Hypothalamus ◽  
Discharge Rate ◽  
Renal Nerves ◽  
Preoptic Nucleus ◽  
Afferent Nerves ◽  
Stimulation Of

In 10 cats anaesthetized with chloralose the electrical activity of spontaneously active hypothalamic units was recorded for changes in discharge rate during electrical stimulation of renal afferent nerves. The discharge rate of 141 single units was altered by stimulation of either the ipsilateral or contralateral renal nerves. Most of the responsive units were located in the regions of lateral preoptic nucleus, lateral hypothalamus, and paraventricular nucleus. These results demonstrate that renal afferent nerves provide information to hypothalamic structures known to be involved in the regulation of arterial pressure and fluid balance.

scholarly journals Primary Afferent Stimulation Differentially Potentiates Excitatory and Inhibitory Inputs to Spinal Lamina II Outer and Inner Neurons

2004 ◽  
Vol 91 (6) ◽  
pp. 2413-2421 ◽  
Author(s):  
Yu-Zhen Pan ◽  
Hui-Lin Pan
Keyword(s):  
Quantitative Difference ◽  
Peak Amplitude ◽  
Primary Afferent ◽  
Afferent Stimulation ◽  
Synaptic Inputs ◽  
Postsynaptic Currents ◽  
Afferent Nerves ◽  
Primary Afferent Nerves ◽  
Spinal Lamina ◽  
Stimulation Of

Spinal lamina II (substantia gelatinosa) neurons play an important role in processing of nociceptive information from primary afferent nerves. Anatomical studies suggest that neurons in the outer (lamina IIo) and inner (lamina IIi) zone of lamina II receive distinct afferent inputs. The functional significance of this preferential afferent termination in lamina II remains unclear. In this study, we examined the differential synaptic inputs to neurons in lamina IIo and IIi in response to primary afferent stimulation. Whole cell voltage-clamp recordings were performed on neurons in lamina IIo and IIi of the rat spinal cord slice under visual guidance. Capsaicin (1 μM) significantly increased the frequency of glutamatergic miniature excitatory postsynaptic currents (mEPSCs) in all 27 lamina IIo neurons and significantly increased the amplitude of mEPSCs in 12 of 27 lamina IIo neurons. However, capsaicin only significantly increased the frequency of mEPSCs in 9 of 22 (40.9%) lamina IIi neurons and increased the amplitude of mEPSCs in 6 of these 9 neurons. Furthermore, the peak amplitude of EPSCs, evoked by electrical stimulation of the attached dorsal root, in 40 lamina IIo neurons was significantly greater than that [160.5 ± 16.7 vs. 87.0 ± 10.4 (SE) pA] in 37 lamina IIi neurons. On the other hand, the peak amplitude of evoked inhibitory postsynaptic currents (IPSCs) in 40 lamina IIo neurons was significantly smaller than that (103.1 ± 11.6 vs. 258.4 ± 24.4 pA) in 37 lamina IIi neurons. In addition, the peak amplitudes of both EPSCs and IPSCs, evoked by direct stimulation of lamina II, were similar in lamina IIo and IIi neurons. This study provides new information that stimulation of primary afferents differentially potentiates synaptic inputs to neurons in lamina IIo and IIi. The quantitative difference in excitatory and inhibitory synaptic inputs to lamina IIo and IIi neurons may be important for integration of sensory information from primary afferent nerves.

Contrasting reflexes evoked by chemical activation of cardiac afferent nerves

1980 ◽  
Vol 239 (3) ◽  
pp. H316-H325 ◽  
Author(s):  
K. A. Reimann ◽  
L. C. Weaver
Keyword(s):  
Potassium Chloride ◽  
Chemical Activation ◽  
Sympathetic Nerves ◽  
Sympathetic Outflow ◽  
Afferent Neurons ◽  
Renal Nerve ◽  
Afferent Nerves ◽  
Excitatory Responses ◽  
Upper Thoracic ◽  
Arterial Baroreceptor

Afferent neurons within cardiac sympathetic nerves can reflexly excite central sympathetic outflow. However, their contribution to cardiovascular control remains unclear because they are potentially opposed by inhibitory reflexes of cardiac vagal or arterial baroreceptor afferent origin. It was considered that sympathetically mediated, excitatory responses might be more prominent when initiated by chemical stimulation. In chloralose-anesthetized, vagotomized, sinoaortic-denervated cats, epicardial or intracoronary administration of bradykinin or potassium chloride evoked renal nerve excitation and pressor responses mediated by cardiac sympathetic afferent nerves. When upper thoracic sympathetic nerves were severed, and vagal afferent nerves remained intact, bradykinin and potassium chloride produced inhibition of renal nerve activity and depressor responses. When sympathetic and vagal components of cardiac innervation remained intact, these substances produced excitation, inhibition, or no change in sympathetic outflow. Excitation occurred as often as inhibition. A similar pattern was observed when arterial baroreceptor nerves remained intact. These data illustrate that cardiac sympathetic afferent neurons can have significant excitatory influences on the cardiovascular system in spite of opposition by inhibitory afferent groups.

Excitation of cardiac sympathetic afferent nerves: effects on renal function

1981 ◽  
Vol 241 (5) ◽  
pp. R267-R270
Author(s):  
R. L. Meckler ◽  
L. J. Macklem ◽  
L. C. Weaver
Keyword(s):  
Renal Function ◽  
Chemical Stimulation ◽  
Afferent Neurons ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Efferent Nerve ◽  
Afferent Nerves ◽  
Renal Nerve Activity ◽  
Anesthetized Dogs ◽  
Stimulation Of

Cardiac sympathetic afferent nerves can reflexly alter renal efferent nerve activity during myocardial ischemia and in response to mechanical or chemical stimulation of cardiac receptors. They also may influence renal excretion of water and electrolytes; however, this potential influence on renal function has not been determined. Therefore, receptors of cardiac sympathetic afferent nerves were chemically stimulated by epicardial application of bradykinin to determine effects on renal function. Experiments were performed in anesthetized dogs in which cervical vagosympathetic trunks were severed and common carotid arteries were tied to diminish influences of arterial baroreceptors and vagal afferent nerves. Chemical stimulation of cardiac afferent neurons excited renal nerve activity and produced decreases in urine flow rate, glomerular filtration rate, and excretion of sodium and potassium. In contrast, no consistent changes in renal function were observed in control dogs, which did not undergo cardiac afferent stimulation. These data provide evidence that activation of cardiac sympathetic afferent neurons can lead to alterations in excretion of water and electrolytes as well as changes in renal nerve activity.

Renal nerves in exaggerated water and sodium excretion by hypertrophied kidney of anesthetized rats

1988 ◽  
Vol 254 (1) ◽  
pp. F32-F37 ◽  
Author(s):  
G. Szenasi ◽  
G. Kottra ◽  
P. Bencsath ◽  
L. Takacs
Keyword(s):  
Thiobarbituric Acid ◽  
Male Rats ◽  
Renal Nerves ◽  
Sham Operation ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Before And After ◽  
Renal Nerve Activity ◽  
And Control ◽  
Water And Sodium Excretion

The effect of acute renal denervation (RD) on water (V), sodium (UNaV), and potassium excretion (UKV) from the hypertrophied and control kidney was studied in 5-sec-butyl-5-ethyl-2-thiobarbituric acid (Inactin)-anesthetized male rats 7 days after unilateral nephrectomy (Nx) or sham operation (SNx). V, UNaV, and UKV from the hypertrophied kidney were similar before and after RD or sham RD. In contrast, in SNx rats, left RD resulted in an ipsilateral increase in V (from 2.76 +/- 0.39 to 5.31 +/- 0.99 microliters.min-1.g-1), UNaV (from 109 +/- 36 to 857 +/- 331 nmol.min-1.g-1), and UKV (from 144 +/- 44 to 807 +/- 130 nmol.min-1.g-1; P less than 0.05 in all cases). Moreover, renal parameters from the hypertrophied kidney, subjected to either RD or sham RD, were not different from values after RD in SNx rats (V: Nx, sham RD = 5.72 +/- 1.10; Nx, RD = 5.23 +/- 0.66; SNx, RD = 5.31 +/- 0.99 microliters.min-1.g-1; UNaV: Nx, sham RD = 896 +/- 319; Nx, RD = 821 +/- 262; SNx, RD = 857 +/- 331 nmol.min-1.g-1; UKV: Nx, sham RD = 782 +/- 127; Nx, RD = 860 +/- 82; SNx, RD = 807 +/- 130 nmol.min-1.g-1). In additional experiments, integrated renal nerve activity (RNA) to the kidney in Nx and SNx rats was 4.0 +/- 0.3 and 10.7 +/- 0.9 microV (P less than 0.05), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal prostanoids after unclipping the denervated one-kidney, one-clip hypertensive rat

1985 ◽  
Vol 249 (4) ◽  
pp. F542-F545 ◽  
Author(s):  
R. Vandongen ◽  
H. McGowan ◽  
H. Anderson ◽  
A. Barden
Keyword(s):  
Blood Pressure ◽  
Neural Mechanisms ◽  
Renal Nerves ◽  
Minor Role ◽  
Similar Extent ◽  
Before And After ◽  
Blood Pressures ◽  
A Minor ◽  
Prostanoid Synthesis ◽  
Stimulation Of

The contribution of the renal nerves in maintaining blood pressure and modulating renal prostanoid synthesis was examined in established (less than 8 wk in duration) one-kidney, one-clip (1K,1C) hypertension in the rat. Systolic blood pressure was measured for 7 days after renal denervation, at which time the renal artery clip was removed. Twenty-four-hour urinary excretion of PGE2 and 6-keto-PGF1 alpha (stable degradation product of PGI2) was determined before and after denervation and unclipping. Compared with sham-denervated rats, denervation (n = 15) resulted in a small but significant fall in blood pressure (from 216 +/- 4 to 182 +/- 4 mmHg after 48 h) and an increase in urinary 6-keto-PGF1 alpha (from 31 +/- 4 to 43 +/- 5 ng/24 h after 24 h). There was no change in PGE2 excretion. Seven days after surgery, blood pressures were similar in denervated (202 +/- 4 mmHg) and sham-denervated (211 +/- 5 mmHg) rats and fell to a similar extent 24 h after unclipping (142 +/- 3 and 147 +/- 4 mmHg, respectively). Urinary 6-keto-PGF1 alpha increased from 25 +/- 5 to 74 +/- 11 in denervated and 21 +/- 2 to 72 +/- 9 ng/24 h in sham-denervated rats in the 24 h after unclipping. PGE2 excretion increased approximately twofold over this period. These findings indicate that the renal nerves have only a minor role in established hypertension in the 1K,1C rat and that the reversal of hypertension and stimulation of renal prostanoid synthesis following unclipping is not dependent on neural mechanisms.

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