Renal sympathetic nerve activity modulates afferent renal nerve activity by PGE2-dependent activation of α1- and α2-adrenoceptors on renal sensory nerve fibers

2007 ◽  
Vol 293 (4) ◽  
pp. R1561-R1572 ◽  
Author(s):  
Ulla C. Kopp ◽  
Michael Z. Cicha ◽  
Lori A. Smith ◽  
Jan Mulder ◽  
Tomas Hökfelt
Keyword(s):  
Sensory Nerve ◽  
Nerve Fibers ◽  
Sensory Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Pelvic Wall ◽  
Renal Nerve Activity ◽  
Pelvic Perfusion ◽  
Renal Sympathetic

Increasing efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA). To test whether the ERSNA-induced increases in ARNA involved norepinephrine activating α-adrenoceptors on the renal sensory nerves, we examined the effects of renal pelvic administration of the α1- and α2-adrenoceptor antagonists prazosin and rauwolscine on the ARNA responses to reflex increases in ERSNA (placing the rat's tail in 49°C water) and renal pelvic perfusion with norepinephrine in anesthetized rats. Hot tail increased ERSNA and ARNA, 6,930 ± 900 and 4,870 ± 670%·s (area under the curve ARNA vs. time). Renal pelvic perfusion with norepinephrine increased ARNA 1,870 ± 210%·s. Immunohistochemical studies showed that the sympathetic and sensory nerves were closely related in the pelvic wall. Renal pelvic perfusion with prazosin blocked and rauwolscine enhanced the ARNA responses to reflex increases in ERSNA and norepinephrine. Studies in a denervated renal pelvic wall preparation showed that norepinephrine increased substance P release, from 8 ± 1 to 16 ± 1 pg/min, and PGE2 release, from 77 ± 11 to 161 ± 23 pg/min, suggesting a role for PGE2 in the norepinephrine-induced activation of renal sensory nerves. Prazosin and indomethacin reduced and rauwolscine enhanced the norepinephrine-induced increases in substance P and PGE2. PGE2 enhanced the norepinephrine-induced activation of renal sensory nerves by stimulation of EP4 receptors. Interaction between ERSNA and ARNA is modulated by norepinephrine, which increases and decreases the activation of the renal sensory nerves by stimulating α1- and α2-adrenoceptors, respectively, on the renal pelvic sensory nerve fibers. Norepinephrine-induced activation of the sensory nerves is dependent on renal pelvic synthesis/release of PGE2.

Aging is not accompanied by sympathetic hyperresponsiveness to air-jet stress

1996 ◽  
Vol 271 (2) ◽  
pp. H768-H775 ◽  
Author(s):  
H. M. Stauss ◽  
D. A. Morgan ◽  
K. E. Anderson ◽  
M. P. Massett ◽  
K. C. Kregel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Low Frequency ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Fischer 344 ◽  
Air Jet ◽  
Renal Nerve Activity ◽  
Renal Sympathetic

It has been postulated that sympathetic nervous system reactivity to acutely applied stress is increased with age. We investigated the autonomic and hemodynamic adjustments to air-jet stress in 9 mature (12-mo-old) and 11 senescent (24-mo-old) Fischer 344 rats. Rats were instrumented with arterial and venous catheters, flow probes around the renal artery, and nerve electrodes on the ipsilateral renal nerve. After the rats recovered from surgery, blood pressure, heart rate, renal blood flow, and renal sympathetic nerve activity were recorded during control conditions and during an 8-min continuous air-jet application. Renal resistance and the low (0.01-0.20 Hz)- and mid-frequency (0.20-0.50 Hz) power of blood pressure were computed off-line. The air jet induced an increase in blood pressure, heart rate, renal resistance, renal nerve activity, and blood pressure power in the low- and mid-frequency ranges in both groups. Blood pressure and low-frequency blood pressure power increased less, and the elevations in renal resistance and renal nerve activity were of shorter duration in senescent compared with mature rats. These data suggest that sympathetic responsiveness to air-jet stress is not enhanced with increasing age.

scholarly journals Activation of endothelin A receptors contributes to impaired responsiveness of renal mechanosensory nerves in congestive heart failureThis article is one of a selection of papers published in the two-part special issue entitled 20 Years of Endothelin Research.

2010 ◽  
Vol 88 (6) ◽  
pp. 622-629 ◽  
Author(s):  
Ulla C. Kopp ◽  
Michael Z. Cicha ◽  
Susan Y. Jones
Keyword(s):  
Substance P ◽  
Sensory Nerve ◽  
Reflex Response ◽  
Nerve Activity ◽  
Renal Nerve ◽  
P Release ◽  
Renal Nerve Activity ◽  
Pelvic Perfusion ◽  
Substance P Release ◽  
Pelvic Pressure

Increasing renal pelvic pressure results in PGE2-mediated release of substance P, leading to increases in afferent renal nerve activity (ARNA) and natriuresis, that is, a renorenal reflex response. The renorenal reflexes are impaired in congestive heart failure (CHF). Impairment of the renorenal reflexes may contribute to the increased renal sympathetic nerve activity and sodium retention in CHF. Endothelin (ET)-1 contributes to the pathological changes in cardiac and renal function in CHF. Therefore, we examined whether the ETA receptor antagonist BQ123 altered the responsiveness of renal mechanosensory nerves in CHF. The ARNA responses to increasing renal pelvic pressure were suppressed in CHF but not in sham-CHF rats. In CHF, increasing renal pelvic pressure by 7.5 mm Hg before and during renal pelvic perfusion with BQ123 increased ARNA 12% ± 3% and 21% ± 3% (p < 0.05 vs. vehicle). In isolated renal pelvises from CHF rats, PGE2 increased substance P release from 5 ± 0 to 7 ± 1 pg/min without BQ123 and from 4 ± 1 to 9 ± 1 pg/min with BQ123 in the bath (p < 0.01 vs. vehicle). BQ123 had no effect on the ARNA responses or substance P release in sham-CHF. In conclusion, activation of ETA receptors contributes to the impaired responsiveness of renal mechanosensory nerves in CHF rats by a mechanism(s) at the renal sensory nerve endings.

Somatosensory influences on renal sympathetic nerve activity in anesthetized Wistar and hypertensive rats

1997 ◽  
Vol 272 (3) ◽  
pp. R982-R990 ◽  
Author(s):  
T. Zhang ◽  
E. J. Johns
Keyword(s):  
Power Spectra ◽  
Total Power ◽  
Hypertensive Rats ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Somatosensory Stimulation ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Nerve Activity ◽  
Cardiopulmonary Receptors ◽  
Renal Sympathetic

This study compared the cardiovascular and renal nerve activity responses to somatosensory stimulation with capsaicin in normotensive and hypertensive rats. The importance of the cardiopulmonary receptors in these two states was examined with the use of phenylbiguanide (PBG) infusion. Subcutaneous capsaicin increased blood pressure (BP), heart rate (HR), and renal nerve activity (RNA) 6-35% (P < 0.01), and total power (TP) and %power at HR (%PHR) rose two- to threefold (P < 0.001). PBG reduced basal RNA, TP, and %PHR (20-70%, P < 0.05). PBG did not change the cardiovascular, but attenuated the TP and %PHR increases due to capsaicin (P < 0.001-0.01). PBG given to vagotomized normotensive rats normalized the cardiovascular and RNA responses to capsaicin. In hypertensive rats, capsaicin increased BP, HR, RNA(10-20%), TP, and %PHR (50-70%, P < 0.001). PBG infusion into hypertensive rats decreased RNA (20%, P < 0.01) and the capsaicin-dependent rise in RNA was smaller (P < 0.05). TP and %PHR were unchanged, except in vagotomized hypertensive rats given PBG, in which these responses were minimally affected. Somatosensory modulation of RNA power spectra was suppressed by the cardiopulmonary receptors in normotensive rats, but in hypertensive rats their impact was much smaller.

Pulmonary serotonin 5-HT3-sensitive afferent fibers modulate renal sympathetic nerve activity in rats

1997 ◽  
Vol 272 (2) ◽  
pp. H979-H986 ◽  
Author(s):  
R. Veelken ◽  
M. Leonard ◽  
A. Stetter ◽  
K. F. Hilgers ◽  
J. F. Mann ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Vagal Afferents ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Afferent Fibers ◽  
Renal Nerve Activity ◽  
Cardiac Afferents ◽  
Renal Sympathetic

Cardiopulmonary reflexes with vagal afferents may control volume homeostasis by influencing renal nerve activity. Such reflexes can be stimulated mechanically and chemically, e.g., by serotonin 5-HT). We have demonstrated that stimulation of epicardial 5-HT3 receptors inhibits renal sympathetic nerve activity (RSNA) by a cardiorenal reflex. We now tested the hypothesis that pulmonary 5-HT3-sensitive vagal afferent fibers participate in the control of renal nerve activity. Two sets of experiments were performed. First, the responses of multifiber RSNA, heart rate (HR), and blood pressure (BP) to the 5-HT3-receptor agonist phenylbiguanide (PBG; 10 microg iv) were recorded in the presence of intact pulmonary afferents. Abdominal afferents were removed by subdiaphragmatic vagotomy. Cardiac afferents were blocked by intrapericardial injection of 10% procaine. Second, the responses of 25 single vagal pulmonary afferent C fibers to PBG were assessed. PBG decreased BP, HR, and RSNA (-90 +/- 8%). When cardiac afferents were blocked by procaine, BP and HR failed to decrease in response to PBG; however, the RSNA decrease was still -48 +/- 8%. Single fibers generally responded to PBG by a slight increase in firing rate. A distinct subset of fibers (5 of 25) showed an activity increase of >15 Hz that preceded changes in BP and HR. The decreased RSNA in the absence of cardiac and abdominal vagal afferents and the strong response of 20% of pulmonary single fibers to intravenous PBG suggest that pulmonary fibers play a role in a 5-HT3 serotenergic reflex. Thus pulmonary serotonin could influence the neural control of renal function.

scholarly journals Dietary sodium modulates the interaction between efferent renal sympathetic nerve activity and afferent renal nerve activity: role of endothelin

2009 ◽  
Vol 297 (2) ◽  
pp. R337-R351 ◽  
Author(s):  
Ulla C. Kopp ◽  
Olaf Grisk ◽  
Michael Z. Cicha ◽  
Lori A. Smith ◽  
Antje Steinbach ◽  
...  
Keyword(s):  
Substance P ◽  
Dietary Sodium ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
P Release ◽  
Pelvic Wall ◽  
Renal Nerve Activity ◽  
Substance P Release

Increasing efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), which in turn decreases ERSNA via activation of the renorenal reflexes in the overall goal of maintaining low ERSNA. We now examined whether the ERSNA-induced increases in ARNA are modulated by dietary sodium and the role of endothelin (ET). The ARNA response to reflex increases in ERSNA was enhanced in high (HNa)- vs. low-sodium (LNa) diet rats, 7,560 ± 1,470 vs. 900 ± 390%·s. The norepinephrine (NE) concentration required to increase PGE2 and substance P release from isolated renal pelvises was 10 pM in HNa and 6,250 pM in LNa diet rats. In HNa diet pelvises 10 pM NE increased PGE2 release from 67 ± 6 to 150 ± 13 pg/min and substance P release from 6.7 ± 0.8 to 12.3 ± 1.8 pg/min. In LNa diet pelvises 6,250 pM NE increased PGE2 release from 64 ± 5 to 129 ± 22 pg/min and substance P release from 4.5 ± 0.4 to 6.6 ± 0.7 pg/min. In the renal pelvic wall, ETB-R are present on unmyelinated Schwann cells close to the afferent nerves and ETA-R on smooth muscle cells. ETA-receptor (R) protein expression in the renal pelvic wall is increased in LNa diet. In HNa diet, renal pelvic administration of the ETB-R antagonist BQ788 reduced ERSNA-induced increases in ARNA and NE-induced release of PGE2 and substance P. In LNa diet, the ETA-R antagonist BQ123 enhanced ERSNA-induced increases in ARNA and NE-induced release of substance P without altering PGE2 release. In conclusion, activation of ETB-R and ETA-R contributes to the enhanced and suppressed interaction between ERSNA and ARNA in conditions of HNa and LNa diet, respectively, suggesting a role for ET in the renal control of ERSNA that is dependent on dietary sodium.

Vasopressin facilitates inhibition of renal nerve activity mediated through vagal afferents

1987 ◽  
Vol 253 (1) ◽  
pp. H1-H7
Author(s):  
B. N. Gupta ◽  
A. L. Abboud ◽  
J. S. Floras ◽  
P. E. Aylward ◽  
F. M. Abboud
Keyword(s):  
Sympathetic Nerve ◽  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Vagal Afferents ◽  
Reflex Inhibition ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Nerve Activity ◽  
Renal Sympathetic

We measured the effect of vasopressin (8 mU X kg-1 X min-1) on reflex inhibition of renal sympathetic nerve activity induced by volume expansion in 13 sinoaortic-denervated anesthetized rabbits. Volume expansion increased left ventricular end-diastolic pressure (LVEDP) from 5.1 +/- 0.7 to 14.1 +/- 1.4 mmHg and decreased renal nerve activity (RNA) from 57.4 +/- 6.9 to 30.2 +/- 5.6 impulses/s. Infusion of vasopressin elevated LVEDP from 6.0 +/- 1.0 to 7.3 +/- 1.1 mmHg and decreased RNA from 61.8 +/- 7.2 to 47.1 +/- 6.3 impulses/s. Heart rate fell from 243 +/- 7 to 231 +/- 9 beats/min; no other significant hemodynamic changes were seen. During the infusion of vasopressin, volume expansion increased LVEDP to 13.7 +/- 1.2 mmHg and decreased RNA to 17.0 +/- 4.2 impulses/s. The slopes relating the percent decrease in RNA to the rise in LVEDP were calculated from values of RNA recorded at several levels of LVEDP. The slope averaged -6.2 +/- 1.1%/mmHg before vasopressin and nearly doubled (-11.9 +/- 1.8%/mmHg) during vasopressin. Infusion of placebo (saline) instead of vasopressin did not alter the reflex inhibition of nerve activity. Bilateral vagotomy abolished the decrease in resting nerve activity that occurred during infusion of vasopressin as well as the reflex inhibition of RNA. These data demonstrate that vasopressin facilitates the reflex inhibition of renal sympathetic nerve activity associated with increases in LVEDP and mediated through vagal afferents.

Mechanism of biphasic response of renal nerve activity during acute cardiac tamponade in conscious rabbits

1999 ◽  
Vol 276 (5) ◽  
pp. R1232-R1240
Author(s):  
Masanobu Hagiike ◽  
Hajime Maeta ◽  
Hiroshi Murakami ◽  
Kenji Okada ◽  
Hironobu Morita
Keyword(s):  
Cardiac Tamponade ◽  
Endogenous Opioid ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Nerve Activity ◽  
The Mean ◽  
Conscious Rabbits ◽  
Cardiac Receptors ◽  
Renal Sympathetic

Renal sympathetic nerve activity (RSNA) responses to acute cardiac tamponade were studied in conscious rabbits with all reflexes intact (Int) or after either surgical sinoaortic denervation (SAD) or administration of intrapericardial procaine (ip-Pro) or intravenous procaine (iv-Pro). In Int rabbits, the mean arterial pressure (MAP) remained relatively constant until the pericardial volume reached 7.7 ml, whereas the RSNA increased to 226% [compensated cardiac tamponade (CCT)], then, at a pericardial volume of 9.3 ml, the MAP fell sharply and RSNA decreased to 34% [decompensated cardiac tamponade (DCT)]; 1 min after cessation of pericardial infusion, an intravenous injection of naloxone resulted in increases in both MAP and RSNA. In SAD rabbits, RSNA did not alter throughout CCT and DCT, but increased on injection of naloxone. In ip-Pro rabbits, RSNA increased during CCT but did not decrease during DCT, whereas, in iv-Pro rabbits, the RSNA response was similar to that in Int rabbits. These results indicate that RSNA responses to cardiac tamponade are biphasic, with an increase during CCT and a decrease during DCT. Sinoaortic baroreceptors are involved in mediating the increase in RSNA, whereas cardiac receptors may be involved in mediating the decrease in RSNA. An endogenous opioid may be responsible for the decrease in RSNA seen during DCT.

PGE2 increases release of substance P from renal sensory nerves by activating the cAMP-PKA transduction cascade

2002 ◽  
Vol 282 (6) ◽  
pp. R1618-R1627 ◽  
Author(s):  
Ulla C. Kopp ◽  
Michael Z. Cicha ◽  
Lori A. Smith
Keyword(s):  
Substance P ◽  
Area Under The Curve ◽  
Nerve Fibers ◽  
Sensory Nerves ◽  
Renal Nerve ◽  
Pelvic Wall ◽  
Pelvic Nerves ◽  
Renal Nerve Activity ◽  
Pka Pathway ◽  
Pelvic Pressure

Increasing renal pelvic pressure increases afferent renal nerve activity (ARNA) by a PGE2-mediated release of substance P (SP) from renal pelvic nerves. The role of cAMP activation in the PGE2-mediated release of SP was studied by examining the effects of the adenylyl cyclase (AC) activator forskolin and AC inhibitor dideoxyadenosine (DDA). Forskolin enhanced the bradykinin-mediated release of SP from an isolated rat renal pelvic wall preparation, from 7.3 ± 1.3 to 15.6 ± 3.0 pg/min. PGE2 at a subthreshold concentration for SP release mimicked the effects of forskolin. The EP2 receptor agonist butaprost, 15 μM, and PGE2, 0.14 μM, produced similar increases in SP release, from 5.8 ± 0.8 to 17.0 ± 2.3 pg/min and from 8.0 ± 1.3 to 21.6 ± 2.7 pg/min. DDA blocked the SP release produced by butaprost and PGE2. The PGE2-induced release of SP was also blocked by the PKA inhibitors PKI14–22 and H-89. Studies in anesthetized rats showed that renal pelvic administration of butaprost, 10 μM, and PGE2, 0.14 μM, resulted in similar ARNA responses, 1,520 ± 390 and 1,170 ± 270% · s (area under the curve of ARNA vs. time) that were blocked by DDA. Likewise, the ARNA response to increased renal pelvic pressure, 7,180 ± 710% · s, was blocked by DDA. In conclusion, PGE2activates the cAMP-PKA pathway leading to a release of SP and activation of renal pelvic mechanosensory nerve fibers.

scholarly journals Does glucagon-like peptide-1 induce diuresis and natriuresis by modulating afferent renal nerve activity?

2019 ◽  
Vol 317 (4) ◽  
pp. F1010-F1021 ◽  
Author(s):  
Kenichi Katsurada ◽  
Shyam S. Nandi ◽  
Neeru M. Sharma ◽  
Hong Zheng ◽  
Xuefei Liu ◽  
...  
Keyword(s):  
Intravenous Infusion ◽  
Sensory Nerve ◽  
Nerve Fibers ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Underlying Mechanisms

Glucagon-like peptide-1 (GLP-1), an incretin hormone, has diuretic and natriuretic effects. The present study was designed to explore the possible underlying mechanisms for the diuretic and natriuretic effects of GLP-1 via renal nerves in rats. Immunohistochemistry revealed that GLP-1 receptors were avidly expressed in the pelvic wall, the wall being adjacent to afferent renal nerves immunoreactive to calcitonin gene-related peptide, which is the dominant neurotransmitter for renal afferents. GLP-1 (3 μM) infused into the left renal pelvis increased ipsilateral afferent renal nerve activity (110.0 ± 15.6% of basal value). Intravenous infusion of GLP-1 (1 µg·kg−1·min−1) for 30 min increased renal sympathetic nerve activity (RSNA). After the distal end of the renal nerve was cut to eliminate the afferent signal, the increase in efferent renal nerve activity during intravenous infusion of GLP-1 was diminished compared with the increase in total RSNA (17.0 ± 9.0% vs. 68.1 ± 20.0% of the basal value). Diuretic and natriuretic responses to intravenous infusion of GLP-1 were enhanced by total renal denervation (T-RDN) with acute surgical cutting of the renal nerves. Selective afferent renal nerve denervation (A-RDN) was performed by bilateral perivascular application of capsaicin on the renal nerves. Similar to T-RDN, A-RDN enhanced diuretic and natriuretic responses to GLP-1. Urine flow and Na+ excretion responses to GLP-1 were not significantly different between T-RDN and A-RDN groups. These results indicate that the diuretic and natriuretic effects of GLP-1 are partly governed via activation of afferent renal nerves by GLP-1 acting on sensory nerve fibers within the pelvis of the kidney.

Nitric oxide modulates renal sensory nerve fibers by mechanisms related to substance P receptor activation

2001 ◽  
Vol 281 (1) ◽  
pp. R279-R290 ◽  
Author(s):  
Ulla C. Kopp ◽  
Michael Z. Cicha ◽  
Lori A. Smith ◽  
Tomas Hökfelt
Keyword(s):  
Nitric Oxide ◽  
Substance P ◽  
Sensory Nerve ◽  
Receptor Activation ◽  
Nerve Fibers ◽  
Sensory Nerves ◽  
Renal Nerve ◽  
Inhibitory Neurotransmitter ◽  
Pelvic Perfusion ◽  
Pelvic Pressure

Nerve terminals containing neuronal nitric oxide synthase (nNOS) are localized in the renal pelvic wall where the sensory nerves containing substance P and calcitonin gene-related peptide (CGRP) are found. We examined whether nNOS is colocalized with substance P and CGRP. All renal pelvic nerve fibers that contained nNOS-like immunoreactivity (-LI) also contained substance P-LI and CGRP-LI. In anesthetized rats, renal pelvic perfusion with the nNOS inhibitor S-methyl-l-thiocitrulline (l-SMTC, 20 μM) prolonged the afferent renal nerve activity (ARNA) response to a 3-min period of increased renal pelvic pressure from 5 ± 0.4 to 21 ± 2 min ( P < 0.01, n = 14). The magnitude of the ARNA response was unaffected byl-SMTC. Similar effects were produced by N ω-nitro-l-arginine methyl ester (l-NAME) but not d-NAME. Increasing renal pelvic pressure produced similar increases in renal pelvic release of substance P before and during l-SMTC, from 5.9 ± 1.4 to 13.6 ± 4.2 pg/min before and from 4.9 ± to 12.6 ± 2.7 pg/min during l-SMTC. l-SMTC also prolonged the ARNA response to renal pelvic perfusion with substance P (3 μM) from 1.2 ± 0.2 to 5.6 ± 1.1 min ( P < 0.01, n = 9) without affecting the magnitude of the ARNA response. In conclusion: activation of NO may function as an inhibitory neurotransmitter regulating the activation of renal mechanosensory nerve fibers by mechanisms related to activation of substance P receptors.

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