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.

Cardiac afferents play the dominant role in renal nerve inhibition elicited by volume expansion in the rabbit

1998 ◽  
Vol 274 (2) ◽  
pp. R383-R388 ◽  
Author(s):  
Emilio Badoer ◽  
Viatcheslav Moguilevski ◽  
Barry P. McGrath
Keyword(s):  
Sympathetic Nerve ◽  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Dominant Role ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Conscious Rabbit ◽  
Renal Sympathetic Nerve ◽  
Cardiac Afferents ◽  
Renal Sympathetic

In the rabbit, vagotomy combined with arterial baroreceptor denervation abolishes the renal sympathoinhibition elicited by volume expansion. However, the effect of removing cardiopulmonary afferents alone has not been investigated. The aim of the present study was to determine the role of the cardiac afferents in the renal sympathetic response elicited by volume expansion in the normal conscious rabbit. Four experimental groups were used in which rabbits were administered 1) volume expansion (Haemaccel, 1.9 ml/min for 60 min), 2) volume expansion + bolus intrapericardial procaine (20 mg) to block cardiac afferents, 3) volume expansion + intravenous procaine (20 mg bolus), and 4) intrapericardial procaine alone (20 mg bolus). Volume expansion did not significantly affect mean arterial pressure or heart rate but produced a profound fall in renal sympathetic nerve activity (∼50%). Intrapericardial procaine administered 30 min after the start of volume expansion markedly reversed the renal sympathoinhibition to within 20% of the pre-volume expansion level, an effect that wore off over 25 min. In contrast, intravenous procaine lowered renal sympathetic nerve activity slightly further. The results suggest that cardiac afferents play the dominant role in the renal sympathoinhibition in response to volume expansion in the normal conscious rabbit.

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.

Augmented renal sympathetic nerve activity by central command during overground locomotion in decerebrate cats

1998 ◽  
Vol 275 (4) ◽  
pp. H1115-H1121 ◽  
Author(s):  
Kanji Matsukawa ◽  
Jun Murata ◽  
Tetsuya Wada
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Vagal Afferents ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Freely Moving ◽  
Decerebrate Cats ◽  
Rostral Part ◽  
Renal Sympathetic

We examined whether the cerebrum is essential for producing the rapid autonomic adjustment at the onset of spontaneous overground locomotion. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), heart rate (HR), and electromyogram of the forelimb triceps brachialis were measured when freely moving, decerebrate cats spontaneously produced overground locomotion, supporting body weight. Decerebration was performed at the level of the precollicular-premammillary body. RSNA increased 95 ± 14 impulses/s (68 ± 10% of baseline value) at the onset of spontaneous locomotion, which was followed by rises in MAP and HR (7 ± 1 mmHg and 18 ± 2 beats/min, respectively). Concomitantly with the MAP rise, RSNA declined toward control values and then increased again during the subsequent period of locomotion. The same rapid increase in RSNA at the onset of locomotion was observed after sinoaortic denervation and vagotomy. It is concluded that some central site(s), other than the cerebrum and the rostral part of the diencephalon, can generate the centrally induced autonomic adjustment at the onset of spontaneous overground locomotion, which is independent of arterial baroreceptor and vagal afferents.

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).

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