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.

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.

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.

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.

Antagonism of vasopressin V1 receptors in NTS attenuates baroreflex control of renal nerve activity

1995 ◽  
Vol 269 (3) ◽  
pp. H1080-H1086 ◽  
Author(s):  
A. A. Hegarty ◽  
R. B. Felder
Keyword(s):  
Arterial Pressure ◽  
Nucleus Tractus Solitarius ◽  
Response Curves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Aortic Depressor Nerve ◽  
Renal Nerve Activity ◽  
Renal Sympathetic

Previous work has shown that arginine vasopressin (AVP) present in the nucleus tractus solitarius (NTS) contributes to the control of peripheral cardiovascular parameters such as arterial pressure, heart rate, and sympathetic activity. In this study, we attempted to elucidate the influence of AVP in the NTS on baroreflex control of mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) in urethan-anesthetized rats. To test the baroreflex, the aortic depressor nerve (ADN) was stimulated over a range of frequencies (1-15 Hz) to produce frequency-response curves for MAP and RSNA. The vasopressin V1-receptor antagonist [d(CH2)5Tyr(Me)]AVP (aAVP) was microinjected bilaterally or unilaterally into the caudal NTS to eliminate the influence of endogenous AVP on decreases in MAP and RSNA elicited by ADN stimulation. Bilateral microinjection of 10 or 100 ng aAVP significantly attenuated the decreases in RSNA elicited by ADN stimulation. Decreases in MAP were only attenuated following bilateral microinjection of 100 ng aAVP. Unilateral microinjection of the same doses of aAVP did not influence baroreflex control of MAP or RSNA. These results indicate that endogenous AVP within the NTS contributes to cardiovascular regulation. They also suggest that AVP within the NTS may specifically influence baroreflex control of RSNA.

Age-dependent changes in afferent renal nerve activity in genetically hypertensive rats

1992 ◽  
Vol 262 (5) ◽  
pp. R834-R841 ◽  
Author(s):  
N. G. Moss ◽  
A. B. Scoltock
Keyword(s):  
Single Unit ◽  
Renal Ischemia ◽  
Renal Nerves ◽  
Hypertensive Rats ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Wky Rats ◽  
Renal Nerve Activity ◽  
Single Unit Recordings ◽  
Wistar Kyoto

Multiunit and single-unit recordings of afferent renal nerve activity (ARNA) were obtained in anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats between 35 and 150 days of age. Intrapelvic backflow of urine at 20 mmHg excited ARNA at all ages in SHR (152 +/- 18% above control) and WKY rats (262 +/- 24%). In SHR, complete renal ischemia was more excitatory in rats older than 120 days (1,233 +/- 103%, n = 8) than in younger SHR (317 +/- 28%, n = 42). Single-unit recordings showed that this was related to the appearance of R1 chemoreceptors in older SHR and coincided with a decline in the proportion of R2 chemoreceptors in the renal nerves. Other chemoreceptive responses were identified in single units that did not show complete R1 or R2 characteristics, some of which showed responses consistent with a transformation process from R2 to R1 receptor type. R1 chemoreceptors were not present in WKY rats studied up to 150 days of age and, unlike SHR, the proportion of R2 chemoreceptors did not decline with age. Accordingly, complete renal ischemia in WKY rats caused a comparable excitation in multiunit ARNA at all ages (285 +/- 33%, n = 43). Oral enalapril from weaning to 100 days of age prevented hypertension in SHR but did not impair the responsiveness of ARNA to any stimulus. In WKY rats, enalapril treatment for the same period resulted in exaggerated ARNA response to renal ischemia (1,250 +/- 377% above control).(ABSTRACT TRUNCATED AT 250 WORDS)

Reflex mechanisms for changes in renal nerve activity during positive end-expiratory pressure

1988 ◽  
Vol 65 (1) ◽  
pp. 109-115 ◽  
Author(s):  
M. Aibiki ◽  
S. Koyama ◽  
K. Ogli ◽  
Y. Shirakawa
Keyword(s):  
Carotid Sinus ◽  
Venous Pressure ◽  
Control Level ◽  
Vagal Afferents ◽  
Positive End Expiratory Pressure ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Anesthetized Dogs ◽  
Cardiopulmonary Receptors

This study was designed to investigate the interaction between carotid sinus baroreceptors and cardiopulmonary receptors in the reflex control of renal nerve activity (RNA) during positive end-expiratory pressure (PEEP) in anesthetized dogs. PEEP at two different levels (10 and 20 cmH2O) was applied to the following groups: animals with neuraxis intact (I group, n = 12); vagal and aortic nerve denervated animals with carotid sinus nerves intact (V group, n = 6); carotid sinus denervated animals with vagal and aortic nerves intact (SD group, n = 6); and carotid sinus denervated animals also having severed vagal and aortic nerves (SAV group, n = 12). Mean blood pressure (MBP), central venous pressure, and mean airway pressure were also simultaneously measured. In the I group, no significant alterations in RNA occurred during PEEP at both levels, even when MBP fell significantly. Although the drop in MBP in the SD group was similar to that in the I group, RNA decreased significantly 10 s after intervention at both PEEP levels, followed by a recovery of RNA toward the control level. In contrast, a significant increase in RNA, which continued until the end of PEEP, appeared in the V group immediately after each intervention. In the SAV group, RNA responses to PEEP, which were observed in the other groups, were abolished. These results provide evidence that during PEEP, renal nerve activity is modified by an interaction between carotid sinus baroreceptors and cardiopulmonary receptors; excitatory effects occur via carotid sinus nerves and inhibitory effects occur via vagal afferents.

Renal nerve responses to cardiac receptor stimulation with bradykinin in monkeys

1983 ◽  
Vol 244 (6) ◽  
pp. F659-F665 ◽  
Author(s):  
A. J. Gorman ◽  
I. H. Zucker ◽  
J. P. Gilmore
Keyword(s):  
Nonhuman Primate ◽  
Chemical Activation ◽  
Species Difference ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Depressor Response ◽  
Arterial Blood ◽  
Renal Nerve Activity ◽  
Cardiac Afferents

Previous data from our laboratory demonstrated a species difference between the cat and dog in the arterial blood pressure (ABP) and renal nerve activity (RNA) responses to epicardial bradykinin (BK) applications. The present study was carried out to determine the ABP and renal nerve responses to chemical activation of cardiac afferents by BK in the intact and sinoaortic-denervated and vagotomized (SAD + VX) nonhuman primate. Seven Macaque monkeys (fascicularis and nemestrina) anesthetized with pentobarbital or chloralose were used in this study. The heart was exposed and suspended in a pericardial cradle. A left atrial (LA) catheter was inserted through the appendage. Changes in ABP and RNA (percent change from control) were determined when 1 and 10 micrograms/ml BK (in 1-ml volume) were applied to the anterior surface of the left ventricle or injected into the LA (0.3 and 3.0 micrograms/kg BK) in the intact and SAD + VX state. In both the intact and SAD + VX monkeys, ABP and RNA were significantly reduced with epicardial BK. In the intact state, LA injections of BK produced a significant decrease in the % delta of RNA and a depressor response. In the SAD + VX monkey, significant hypotensive responses were also observed with LA injections of BK concomitant with significant reductions in RNA. These results show the existence of a depressor response and inhibition of renal sympathetic nerve activity in the nonhuman primate mediated by the action of bradykinin on cardiac sympathetic afferents.

Saline diuresis and natriuresis in unanesthetized dogs: a missing atrial factor?

1992 ◽  
Vol 263 (3) ◽  
pp. H792-H797
Author(s):  
A. W. Cowley ◽  
A. G. Brice ◽  
M. M. Skelton
Keyword(s):  
Plasma Renin ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Cardiac Denervation ◽  
Volume Load ◽  
Before And After ◽  
Intravenous Saline ◽  
Renal Nerve Activity ◽  
The Central Nervous System

Recent studies in our laboratory indicated that a blunted (40–50%) renal excretory response to isotonic intravenous saline loads occurred in conscious, renal-denervated dogs after 70% of the atrial mass was removed. The blunted responses could not be explained by differences in the responses of arterial pressure, renal nerve activity, or by measured changes of plasma immunoreactive atrial natriuretic peptide (iANP), arginine vasopressin (AVP), plasma renin activity (PRA), or aldosterone (Aldo). The present study was designed to determine whether the central nervous system (CNS) was the source of an unidentified substance, which could account for the blunting of the urine excretory response seen in the atrial-resected dogs. Renal denervation was performed in all dogs to eliminate alterations in efferent renal sympathetic nerve activity derived from reflexes activated during volume expansion. Cardiac denervation (CDX) was used to eliminate sensory cardiac afferent nerve activity to the CNS. A group of five renal-denervated dogs was given an isotonic volume load (400 ml/30 min) before and after complete CDX. Plasma AVP was fixed at normal plasma levels of 3 pg/ml by continuous intravenous infusion. Na and H2O excretion were not different in renal-denervated dogs compared with combined renal and cardiac denervation during the 5 h after the saline load. Plasma AVP and Aldo were unchanged with the volume loads, although PRA rose gradually over the 5 h after the saline loads. Plasma iANP increased transiently in the combined renal and cardiac-denervated state rising from a control of 65–120 pg/ml at the end of the load period.(ABSTRACT TRUNCATED AT 250 WORDS)

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