Glutamatergic input in the PVN is important in renal nerve response to elevations in osmolality

2003 ◽  
Vol 285 (4) ◽  
pp. F640-F650 ◽  
Author(s):  
Emilio Badoer ◽  
Chi-Wai Ng ◽  
Robert De Matteo
Keyword(s):  
Hypertonic Saline ◽  
Sympathetic Nerve Activity ◽  
Plasma Osmolality ◽  
Neural Responses ◽  
Neuronal Function ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Nerve Response ◽  
Humoral Responses ◽  
Renal Sympathetic

Elevations in plasma osmolality elicit reflex humoral and neural responses. The hypothalamic paraventricular nucleus (PVN) is important in humoral responses. We have investigated whether the PVN contributed to the renal nerve reduction that is normally elicited by increased plasma osmolality in the conscious rabbit. Renal sympathetic nerve activity (RSNA) was monitored after an intravenous infusion of hypertonic saline (1.7 M NaCl, 2 ml/min for 7 min). The responses were examined in animals microinjected with muscimol (10 nmol) into, and outside, the PVN to acutely inhibit neuronal function or with kynurenate (25 nmol) to block glutamate receptors. Compared with vehicle, the maximum reduction in RSNA elicited by hypertonic saline was significantly less with muscimol or kynurenate pretreatment into the PVN. A similar study with kynurenate was also performed in sinoaortically denervated rabbits, and similar effects were observed. The effect was specific to the PVN because microinjections of the drugs outside the PVN had no effect on the response. The findings suggest that excitatory inputs into the PVN may be important in the neural responses elicited by elevations in plasma osmolality.

Partial renal ischemia elicits heterogeneous control of renal sympathetic nerve activity to ischemic and nonischemic regions of the kidney

2006 ◽  
Vol 290 (2) ◽  
pp. R322-R330 ◽  
Author(s):  
Kiyoshi Shimizu ◽  
Kanji Matsukawa ◽  
Jun Murata ◽  
Hirotsugu Tsuchimochi ◽  
Ishio Ninomiya
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Renal Ischemia ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Ischemic Region ◽  
Nerve Bundles ◽  
Renal Sympathetic

We tested the hypothesis that renal sympathetic nerve activity (RSNA) to the ischemic and nonischemic regions responded differently during partial ischemia of the kidney in pentobarbital-anesthetized cats. The renal artery divides into two branches at the front of the renal hilus: one branch perfuses predominantly the dorsal half of the kidney, and the other perfuses its ventral half. We identified the innervated area of a renal nerve bundle by supramaximal electrical stimulation and subsequently determined the changes in RSNA in response to occlusion of either renal arterial branch for 3 min. RSNA to the nonischemic region of the kidney gradually decreased by 23 ± 4% during partial renal ischemia, whereas RSNA to the ischemic region of the same kidney showed no significant change. Crushing either all renal nerve bundles or only the renal nerve bundles terminated to the ischemic region abolished the decrease in RSNA to the nonischemic region. Furthermore, intra-arterial administration of a prostaglandin synthesis inhibitor (meclofenamate, 4 mg/kg) abolished the decrease in RSNA to the nonischemic region of the kidney. Following spinal transection at the level of T7, the inhibitory response in RSNA to the nonischemic region disappeared, whereas the RSNA to the ischemic region was markedly augmented by 47 ± 17%. Thus it is likely that renal chemoreceptors activated during renal partial ischemia elicit heterogeneous control of renal sympathetic outflows to the ischemic and nonischemic regions of the same kidney, which may be determined by a net output between the supraspinal inhibitory and spinal excitatory reflexes.

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.

Effect of muscimol and l-NAME in the PVN on the RSNA response to volume expansion in conscious rabbits

2004 ◽  
Vol 287 (4) ◽  
pp. F739-F746 ◽  
Author(s):  
Chi Wai Ng ◽  
Robert De Matteo ◽  
Emilio Badoer
Keyword(s):  
Nitric Oxide ◽  
Sympathetic Nerve ◽  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Neuronal Function ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Dextran 70 ◽  
Oxide Synthase ◽  
Renal Sympathetic

In the present study, we have investigated whether the hypothalamic paraventricular nucleus (PVN) contributed to the reflex reduction in renal sympathetic nerve activity (RSNA) normally elicited by volume expansion in the conscious rabbit. RSNA was monitored after volume expansion (Dextran 70, 2 ml/min for 30 min) in animals microinjected into, and outside, the PVN with muscimol (10 nmol), to acutely inhibit neuronal function. Because nitric oxide within the PVN inhibits RSNA, we also examined the effect of NG-nitro-l-arginine methyl ester (l-NAME; 20 nmol) to block nitric oxide synthase. Compared with vehicle, the reduction in RSNA elicited by volume expansion was abolished by injection of muscimol into the PVN. The effect was specific to the PVN because microinjections of muscimol outside the PVN had no effect on the response. l-NAME microinjected into or outside the PVN had no effect on the RSNA response. The findings suggest that the PVN is essential in the central pathways mediating the renal sympathetic nerve response elicited by elevations in plasma volume but that nitric oxide does not play a major role.

Hypertonic sodium resuscitation after hemorrhage improves hemodynamic function by stimulating cardiac, but not renal, sympathetic nerve activity

2011 ◽  
Vol 300 (2) ◽  
pp. H685-H692 ◽  
Author(s):  
Robert Frithiof ◽  
Rohit Ramchandra ◽  
Sally G. Hood ◽  
Clive N. May
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hypertonic Saline ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

Small volume hypertonic saline resuscitation can be beneficial for treating hemorrhagic shock, but the mechanism remains poorly defined. We investigated the effects of hemorrhagic resuscitation with hypertonic saline on cardiac (CSNA) and renal sympathetic nerve activity (RSNA) and the resulting cardiovascular consequences. Studies were performed on conscious sheep instrumented with cardiac ( n = 7) and renal ( n = 6) sympathetic nerve recording electrodes and a pulmonary artery flow probe. Hemorrhage (20 ml/kg over 20 min) caused hypotension and tachycardia followed by bradycardia, reduced cardiac output, and abolition of CSNA and RSNA. Resuscitation with intravenous hypertonic saline (1.2 mol/l at 2 ml/kg) caused rapid, dramatic increases in mean arterial pressure, heart rate, and CSNA, but had no effect on RSNA. In contrast, isotonic saline resuscitation (12 ml/kg) had a much delayed and smaller effect on CSNA, less effect on mean arterial pressure, no effect on heart rate, but stimulated RSNA, although the plasma volume expansion was similar. Intracarotid infusion of hypertonic saline (1 ml/min bilaterally, n = 5) caused similar changes to intravenous administration, indicating a cerebral component to the effects of hypertonic saline. In further experiments, contractility (maximum change in pressure over time), heart rate, and cardiac output increased significantly more with intravenous hypertonic saline (2 ml/kg) than with Gelofusine (6 ml/kg) after hemorrhage; the effects of hypertonic saline were attenuated by the β-receptor antagonist propranolol ( n = 6). These results demonstrate a novel neural mechanism for the effects of hypertonic saline resuscitation, comprising cerebral stimulation of CSNA by sodium chloride to improve cardiac output by increasing cardiac contractility and rate and inhibition of RSNA.

Increased renal nerve activity in cardiac failure: arterial vs. cardiac baroreflex impairment

1995 ◽  
Vol 268 (1) ◽  
pp. R112-R116 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin
Keyword(s):  
Normal Control ◽  
Cardiac Failure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Baroreceptor Reflex ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Cardiac failure is characterized by increased renal sympathetic nerve activity that is associated with an impairment of both arterial and cardiac baroreceptor reflex function. These reflex dysfunctions are in the afferent limb at the level of the peripheral baroreceptors. This study sought to define the relative quantitative magnitude of the defects in arterial and cardiac baroreceptor function in cardiac failure. Renal sympathetic nerve activity was measured in anesthetized normal control rats and rats with cardiac failure (left coronary ligation) during sequential random order sinoaortic denervation and vagotomy to interrupt afferent input from the arterial and cardiac baroreceptors, respectively. Increases in renal sympathetic nerve activity after individual or combined sinoaortic denervation and vagotomy were less (P < 0.05 for both) in cardiac failure than in normal control rats in both order sequences (42 +/- 5 vs. 87 +/- 8%; 44 +/- 5 vs. 108 +/- 7%). In cardiac failure rats, vagotomy produced lesser increases (P < 0.05 for both) in renal sympathetic nerve activity than sinoaortic denervation in both order sequences (10 +/- 4 vs. 32 +/- 5%; 13 +/- 2 vs. 30 +/- 5%). The relative magnitude of impaired cardiac baroreceptor reflex function that is associated with the increased renal sympathetic nerve activity of cardiac failure is greater than that of impaired arterial baroreceptor reflex function.

Renal neurohormonal and vascular responses to dynamic exercise in humans

1991 ◽  
Vol 70 (5) ◽  
pp. 2279-2286 ◽  
Author(s):  
B. Tidgren ◽  
P. Hjemdahl ◽  
E. Theodorsson ◽  
J. Nussberger
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Plasma Concentrations ◽  
Dynamic Exercise ◽  
Ang Ii ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Effects of graded supine dynamic exercise (30, 60, and 80-90% of maximal physical capacity, i.e., work loads of 69, 132, and 188 W) on renal vascular resistance (RVR); renal sympathetic nerve activity [assessed by the renal venous overflow of norepinephrine (NE)]; renal overflows of dopamine (DA), immunoreactive neuropeptide Y (NPY-LI), and renin; as well as plasma concentrations of angiotensin-(1-8)-octapeptide (ANG II) were evaluated in eight healthy male volunteers. Exercise evoked stimulus-dependent and marked elevations of RVR, arterial NE, epinephrine (Epi), and DA. RVR increased by 140% and the renal overflows of NE and DA increased by 1,331 and 179%, respectively, at 188 W. A net removal of NPY-LI at rest turned into a small net renal overflow, which correlated with increases in RVR at 188 W. Increases in renin release (+1,200% at 188 W) correlated with increases in renal NE and DA overflows and with arterial Epi levels. Arterial ANG II levels increased stimulus dependently (by 264% at 188 W) and correlated more closely with increases in RVR than did other variables. Thus dynamic exercise is a potent stimulus for renal nerve activation in humans, and renal sympathetic nerve activity may contribute to increased RVR both directly (NE and, at exhaustive work loads, possibly NPY) and indirectly (via renin-mediated ANG II formation).

Is osmolality a long-term regulator of renal sympathetic nerve activity in conscious water-deprived rats?

2002 ◽  
Vol 282 (2) ◽  
pp. R560-R568 ◽  
Author(s):  
Karie E. Scrogin ◽  
Donogh F. McKeogh ◽  
Virginia L. Brooks
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Water Deprivation ◽  
Sympathetic Nerve Activity ◽  
Plasma Osmolality ◽  
Vasopressin Receptor ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Acute increases in osmolality suppress renal sympathetic nerve activity (RSNA). However, it is not known whether prolonged physiological increases in plasma osmolality chronically inhibit RSNA. To address this hypothesis, mean arterial blood pressure (MAP), heart rate (HR), and RSNA were measured during acute normalization of plasma osmolality in conscious rats made hyperosmotic by 48 h of water deprivation. Water deprivation significantly elevated MAP (120 ± 1 vs. 114 ± 3 mmHg, P < 0.05) and plasma osmolality (306 ± 1 vs. 293 ± 1 mosmol/kgH20, P < 0.01). When plasma osmolality was subsequently lowered to normal (−17 ± 1 mosmol/kgH20) with a 2-h (0.12 ml/min) infusion of 5% dextrose in water (5DW), MAP decreased (−11 ± 1 mmHg), and RSNA increased (25 ± 10% baseline). To assess the role of circulating vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist before infusion of 5DW. The antagonist lowered MAP (−4 ± 1 mmHg) and raised RSNA (31 ± 3% baseline) and HR (25 ± 5 beats/min) in water-deprived rats (all changes P < 0.05). However, V1-vasopressin receptor blockade did not increase RSNA or HR independently of baroreflex responses to decreases in arterial pressure. After V1 blockade, infusion of 5DW lowered blood pressure (−8 ± 1 mmHg) but did not further affect HR or RSNA. An isotonic saline infusion that produced the same volume expansion as 5DW lowered MAP (−5 ± 2 mmHg) and HR (−68 ± 2 beats/min) but had no effect on osmolality or RSNA in water-deprived rats. Finally, 5DW infusion had negligible effects in water-replete animals. In conclusion, these results fail to support the hypothesis that sustained increases in plasma osmolality, either directly or via increased vasopressin, tonically suppress RSNA.

Sign in / Sign up

Export Citation Format

Share Document