Vagal C-fiber blockade abolishes sympathetic inhibition by atrial natriuretic factor

1988 ◽  
Vol 255 (1) ◽  
pp. R6-R13 ◽  
Author(s):  
H. D. Schultz ◽  
D. G. Gardner ◽  
C. F. Deschepper ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Atrial Natriuretic Factor ◽  
Splanchnic Nerve ◽  
Nerve Activity ◽  
Renal Nerve ◽  
C Fibers ◽  
Natriuretic Factor ◽  
Anesthetized Rats ◽  
Renal Nerve Activity ◽  
Afferent Vagal ◽  
Atrial Natriuretic

Administration of atrial natriuretic factor (ANF) to anesthetized rats decreases renal nerve activity (RNA), an effect prevented by vagotomy but not by atropine. We sought to determine whether afferent vagal C-fibers mediate the inhibition of sympathetic outflow. ANF (2.5 micrograms/kg iv) decreased mean arterial pressure (MAP) by 25 +/- 2 mmHg, RNA by 11 +/- 5%, and least splanchnic nerve activity (LSNA) by 10 +/- 4% in anesthetized rats with arterial baroreceptors intact, and by 40 +/- 3 mmHg, 28 +/- 7%, and 23 +/- 4%, respectively, in sinoaortic-denervated rats. Inhibition of RNA and LSNA by ANF was reduced slightly by cooling the vagi to 6 or 7 degrees C, a temperature at which conduction in A-fibers was blocked and that in C-fibers attenuated; inhibition was abolished when C-fibers were blocked by cooling to 0 degrees C. We conclude that the inhibition of RNA and LSNA by ANF was mediated by afferent vagal C-fibers. We also obtained evidence that the aortic nerves contribute to ANF-induced inhibition of RNA. Our results support the notion that ANF evokes a generalized decrease in sympathetic tone that contributes to the hypotension, cardiac inhibition, and natriuresis accompanying systemic administration of the peptide.

Neural influences on renal responses to acute volume expansion in rats with heart failure

1996 ◽  
Vol 271 (4) ◽  
pp. H1441-H1448 ◽  
Author(s):  
K. P. Patel ◽  
P. L. Zhang ◽  
P. K. Carmines
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Renal Nerve ◽  
Natriuretic Factor ◽  
Renal Nerve Activity ◽  
Neural Influences ◽  
Renal Responses ◽  
Renal Sympathetic ◽  
Atrial Natriuretic

Experiments were performed to test the postulate that neural influences underlie the suppressed excretory response to acute volume expansion (VE) typically observed 3-4 wk after myocardial infarction to induce chronic heart failure (CHF). Responses to VE were assessed in innervated (intact) and denervated (DNX) kidneys of anesthetized CHF rats and sham-operated controls. CHF rats exhibited blunted natriuretic responses to VE in both intact kidneys (35% of sham response) and DNX kidneys (55% of sham DNX response). CHF rats also displayed suppressed excretory responses to atrial natriuretic factor (0.25 microgram.kg-1.min-1 iv) in both intact kidneys (74% of sham response) and DNX kidneys (63% of sham DNX response). Additional experiments confirmed that the compliance of the venoatrial junction did not differ between sham rats (52 +/- 2 mmHg/microliter) and CHF rats (54-2 mmHg/microliter). The observations support the contention that both tonic renal sympathetic renal nerve activity and suppressed renal atrial natriuretic factor responsiveness likely contribute to the blunted excretory response to VE during CHF.

Central effects of atrial natriuretic factor on renal salt excretion

1991 ◽  
Vol 261 (2) ◽  
pp. F354-F359 ◽  
Author(s):  
P. Rohmeiss ◽  
G. Demmert ◽  
T. Unger
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Renal Nerves ◽  
Urinary Flow ◽  
Renal Nerve ◽  
Ureteral Catheter ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Atrial natriuretic factor (ANF) has been localized in periventricular brain areas involved in cardiovascular and fluid control. We investigated the effect of intracerebroventricular (icv) ANF (alpha-rat atriopeptin III) on renal sodium excretion in unilaterally nephrectomized, conscious unrestrained rats fitted with a chronic ureteral catheter. Isotonic NaCl (1 ml/h) was infused intravenously. ANF injected at doses (icv) of 1 ng (n = 6), 100 ng (n = 7), and 1 microgram (n = 7) reduced urinary sodium excretion (all values mumol/45 min, means +/- SE) from 111.6 +/- 24.4 to 83 +/- 20 (P less than 0.05), from 96.9 +/- 25.2 to 55 +/- 14 (P less than 0.01), and from 90.8 +/- 14.2 to 51 +/- 9 (P less than 0.01), respectively, whereas urinary flow rate did not change. The antinatriuretic effect was immediate in onset and lasted for greater than or equal to 60 min. Blood pressure remained unaltered. ANF (100 ng icv) increased efferent sympathetic renal nerve activity (+36%; n = 6, P less than 0.05), plasma renin activity (4.6 +/- 0.6 to 7.5 +/- 0.5 pmol angiotensin I.ml-1.h-1; n = 9, P less than 0.01), plasma angiotensin II (68.7 +/- 2.5 to 84.7 +/- 3.4 fmol/ml; n = 8, P less than 0.01), and aldosterone (22.3 +/- 3.6 to 37.2 +/- 4.0 ng/ml; n = 9, P less than 0.02). Renal denervation reduced the antinatriuretic effect of ANF by 37%. We conclude that brain ANF has antinatriuretic actions, which may be partly explained by activation of renal nerves.

Acute responses of renal nerve activity to microgravity induced by free drop in anesthetized rats

2000 ◽  
Vol 37 (3) ◽  
pp. 221-226 ◽  
Author(s):  
Hironobu Morita ◽  
Nobuhiro Fujiki ◽  
Masanobu Hagiike ◽  
You Tsuchiya ◽  
Taro Miyahara ◽  
...  
Keyword(s):  
Nerve Activity ◽  
Renal Nerve ◽  
Anesthetized Rats ◽  
Acute Responses ◽  
Renal Nerve Activity ◽  
Free Drop

Effects of Adenosine Receptor Agonists on Efferent Renal Nerve Activity in Anesthetized Rats

2000 ◽  
Vol 35 (2) ◽  
pp. 189-194
Author(s):  
Simonetta Genovesi ◽  
Federico Pieruzzi ◽  
Paola Camisasca ◽  
Giudy Ragonesi ◽  
Giuseppe Protasoni ◽  
...  
Keyword(s):  
Adenosine Receptor ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Adenosine Receptor Agonists ◽  
Receptor Agonists ◽  
Anesthetized Rats ◽  
Renal Nerve Activity

Effects of 17β-estradiol on sympathetic activity and pressor response to phenylephrine in ovariectomized rats

1998 ◽  
Vol 275 (4) ◽  
pp. R1202-R1208 ◽  
Author(s):  
Xiao-Rui He ◽  
Weihua Wang ◽  
Joan T. Crofton ◽  
Leonard Share
Keyword(s):  
Sympathetic Activity ◽  
Baroreflex Sensitivity ◽  
Pressor Response ◽  
Splanchnic Nerve ◽  
Ovariectomized Rats ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Sympathetic Function ◽  
Renal Nerve Activity ◽  
17Β Estradiol

The effects of 17β-estradiol (E2) on sympathetic activity were examined in conscious unrestrained ovariectomized rats, instrumented under methohexital anesthesia to record mean arterial pressure (MABP), heart rate (HR), renal nerve activity (RNA), and splanchnic nerve activity (SNA) 1 day before the experiment. Injection of E2 (150 μg/kg iv) caused reductions ( P < 0.01) in RNA (29 ± 6%), SNA (25 ± 2%), and HR (26 ± 5 beats/min) within 20 min, but MABP remained unchanged. Ninety minutes after intravenous injection of E2 or vehicle, intravenous infusion of phenylephrine (PE; 6.2 μg ⋅ min−1 ⋅ kg−1) induced similar increases in MABP and decreases in HR, RNA, and SNA in both groups. By contrast, in rats chronically treated with E2, the pressor response to PE was smaller ( P < 0.01; 22 ± 5 mmHg) than in vehicle-treated rats (40 ± 4 mmHg). The changes in HR, RNA, and SNA were similar in both groups, but the ratios of changes in HR and SNA to MABP, an index of baroreflex sensitivity, were greater in the E2-treated rats. These findings suggest that E2 can act centrally to modulate sympathetic function and thereby participate in cardiovascular regulation.

Mechanism of inhibition of renin response to hypotension by atrial natriuretic factor

1989 ◽  
Vol 257 (1) ◽  
pp. R194-R203 ◽  
Author(s):  
D. A. Scheuer ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Atrial Natriuretic Factor ◽  
Neural Control ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Neural Stimulation ◽  
Renin Release ◽  
Renal Nerve ◽  
Natriuretic Factor ◽  
Stimulation Of ◽  
Atrial Natriuretic

We have reported that infusion of atrial natriuretic factor (ANF) inhibited the rise in plasma renin activity (PRA) in response to constriction of the abdominal aorta to cause a reduction in renal perfusion pressure (RPP). To evaluate the effect of ANF on neural control of renin release, acute thoracic inferior vena caval constriction (TIVCC) was performed in conscious dogs to reduce arterial pressure by 25% of control and stimulate PRA by a reflex increase in renal nerve activity and a reduction in RPP. Propranolol was used to block neural stimulation of renin release. TIVCC caused significant increases in PRA, plasma aldosterone, arginine vasopressin (AVP), and adrenocorticotropic hormone (ACTH) concentrations. The increase in PRA was significantly reduced by the infusion of either ANF at 20 ng.kg-1.min-1 or propranolol. The combined infusion of ANF and propranolol produced an additive and complete inhibition of the renin response to TIVCC; therefore the effect of ANF is independent of neural stimulation of renin release. ANF at 20 ng.kg-1.min-1 also inhibited increases in aldosterone, AVP, and ACTH, but ANF at 5 ng.kg-1.min-1 only affected the aldosterone response to TIVCC. Therefore ANF inhibits angiotensin II-stimulated aldosterone synthesis and/or secretion at very low doses and at higher doses attenuates reflex increases in AVP and ACTH caused by hypotension.

Sensitization of cardiac receptors (vagal afferents) by intracoronary acetylstrophanthidin

1980 ◽  
Vol 239 (5) ◽  
pp. H628-H635 ◽  
Author(s):  
M. D. Thames ◽  
L. A. Waickman ◽  
F. M. Abboud
Keyword(s):  
Coronary Artery ◽  
Left Atrial ◽  
Volume Expansion ◽  
Coronary Occlusion ◽  
Left Atrial Pressure ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Afferent Vagal ◽  
Cardiac Receptors

The purpose of this study was to determine if sensitization of cardiac receptors with acetylstrophanthidin augments the inhibition of renal nerve activity resulting from expansion of the blood volume or from coronary artery occlusion. Ten chloralose-anesthetized dogs with sinoaortic baroreceptor denervation were subjected to volume expansion with dextran in saline. Under control conditions, volume expansion resulted in decreases in renal nerve activity (% or control) that were inversely related to left atrial pressure (-13.0%/mmHg left atrial pressure). After intracoronary acetylstrophanthidin, volume expansion resulted in a significantly greater suppression of renal nerve activity (-20.6%/mmHg). Occlusion of the circumflex coronary artery in 19 dogs with carotid baroreceptor denervation resulted in a 29 +/- 5% (SE) reduction in renal nerve activity. After intracoronary acetylstrophanthidin, circumflex occlusion resulted in a significantly greater decrease in renal nerve activity (45 +/- 4%). Vagotomy abolished the decreases in renal nerve activity, which resulted from volume expansion and from circumflex coronary occlusion. These data show that volume expansion and coronary occlusion reflexly decrease renal nerve activity via cardiac afferent vagal endings. These reflex inhibitory influences are augmented after intracoronary acetylstrophanthidin. The results are consistent with the view that intracoronary acetylstrophanthidin sensitizes cardiac afferent vagal endings.

Atrial natriuretic factor reduces renin release by opposing alpha-adrenoceptor activity

1991 ◽  
Vol 261 (2) ◽  
pp. E240-E245
Author(s):  
P. A. Naess ◽  
G. Christensen ◽  
F. Kiil
Keyword(s):  
Nerve Stimulation ◽  
Atrial Natriuretic Factor ◽  
Renin Release ◽  
Renal Nerve ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Natriuretic Factor ◽  
Stimulation Experiments ◽  
Ureteral Occlusion ◽  
Atrial Natriuretic

To examine how atrial natriuretic factor (ANF) inhibits renin release during renal sympathetic nerve stimulation, experiments were performed in barbiturate-anesthetized dogs. In five dogs, intravenous ANF infusion (50 ng.min-1.kg body wt-1) reduced renin release induced by renal nerve stimulation (1 Hz) from 16.8 +/- 8.4 to 3.5 +/- 2.1 micrograms angiotensin I (ANG I)/min. In two groups, renin release was raised by ureteral occlusion, which enhances the effects of beta-adrenoceptor stimulation and increased prostaglandin synthesis. During ureteral occlusion, intrarenal infusion of isoproterenol (0.2 micrograms.min-1.kg body wt-1) increased renin release in eight dogs to 82.6 +/- 10.9 micrograms ANG I/min, which was not significantly reduced by ANF infusion (81.1 +/- 10.1 micrograms ANG I/min). Similarly, intrarenal infusion of arachidonic acid (80 micrograms.min-1.kg body wt-1) during ureteral occlusion increased renin release in five dogs to 22.2 +/- 3.0 micrograms ANG I/min, which was not significantly reduced by ANF infusion (22.5 +/- 3.5 micrograms ANG I/min). Finally, in six dogs examined at free urine flow, intrarenal infusion of phenylephrine, an alpha-adrenergic agonist, raised renin release from 0.5 +/- 0.3 to 20.1 +/- 6.8 micrograms ANG I/min, which was reduced to 10.6 +/- 3.9 micrograms ANG I/min by intravenous ANF infusion (100 ng.min-1.kg body wt-1). These results indicate that ANF does not counteract stimulation of renin release by beta-adrenoceptors and prostaglandins but reduces nerve-stimulated renin release by opposing alpha-adrenoceptor activity.

Sign in / Sign up

Export Citation Format

Share Document