Excitation of cardiac sympathetic afferent nerves: effects on renal function

1981 ◽  
Vol 241 (5) ◽  
pp. R267-R270
Author(s):  
R. L. Meckler ◽  
L. J. Macklem ◽  
L. C. Weaver
Keyword(s):  
Renal Function ◽  
Chemical Stimulation ◽  
Afferent Neurons ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Efferent Nerve ◽  
Afferent Nerves ◽  
Renal Nerve Activity ◽  
Anesthetized Dogs ◽  
Stimulation Of

Cardiac sympathetic afferent nerves can reflexly alter renal efferent nerve activity during myocardial ischemia and in response to mechanical or chemical stimulation of cardiac receptors. They also may influence renal excretion of water and electrolytes; however, this potential influence on renal function has not been determined. Therefore, receptors of cardiac sympathetic afferent nerves were chemically stimulated by epicardial application of bradykinin to determine effects on renal function. Experiments were performed in anesthetized dogs in which cervical vagosympathetic trunks were severed and common carotid arteries were tied to diminish influences of arterial baroreceptors and vagal afferent nerves. Chemical stimulation of cardiac afferent neurons excited renal nerve activity and produced decreases in urine flow rate, glomerular filtration rate, and excretion of sodium and potassium. In contrast, no consistent changes in renal function were observed in control dogs, which did not undergo cardiac afferent stimulation. These data provide evidence that activation of cardiac sympathetic afferent neurons can lead to alterations in excretion of water and electrolytes as well as changes in renal nerve activity.

Renal function and renal afferent and efferent nerve activity

1982 ◽  
Vol 243 (5) ◽  
pp. F425-F433 ◽  
Author(s):  
N. G. Moss
Keyword(s):  
Renal Function ◽  
Direct Action ◽  
Renal Nerves ◽  
Renal Tubules ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Efferent Nerve ◽  
Water Excretion ◽  
Renal Nerve Activity ◽  
Stimulation Of

Recent microperfusion studies have fully substantiated the direct action of catecholamines on renal tubular reabsorptive rates. Surprisingly, these techniques have not provided consistent information on the nature of the adrenoceptor responsible for the stimulation of proximal tubular reabsorption. Both alpha- and beta-receptors have been favored for this role. These techniques have confirmed earlier reports that dopamine may have a direct natriuretic action on the renal tubules. The demonstration that renal efferent nerves contain both noradrenergic and dopaminergic fibers lends further support for the participation of dopamine in the regulation of salt and water excretion. Efferent renal nerve activity is modulated by a number of different afferent inputs to the central nervous system. One of these is the renal afferent innervation, which is composed of both chemoreceptor and mechanoreceptor fibers. A number of different reflexes that affect efferent renal nerve activity have been identified by electrical stimulation of renal afferent nerves or by selective stimulation of renal mechanoreceptors and chemoreceptors. These renorenal reflexes may have importance in the coordination of excretory activity between the two kidneys. Studies of these aspects of renal nerve function are reviewed. The importance of the renal nerves in conscious animals is also discussed in the light of evidence that their influence on renal function may be more apparent in abnormal or pathological circumstances.

Contrasting reflex influences of cardiac afferent nerves during coronary occlusion

1981 ◽  
Vol 240 (4) ◽  
pp. H620-H629 ◽  
Author(s):  
L. C. Weaver ◽  
L. M. Danos ◽  
R. S. Oehl ◽  
R. L. Meckler
Keyword(s):  
Blood Pressure ◽  
Myocardial Ischemia ◽  
Coronary Occlusion ◽  
Afferent Neurons ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Arterial Baroreceptors ◽  
Afferent Nerves ◽  
Renal Nerve Activity ◽  
Efferent Neurons

Afferent neurons contained within cardiac sympathetic nerves may have important influences on the circulation when activated during myocardial ischemia. Although such activation is known to reflexly excite upper thoracic sympathetic efferent neurons, effects on other components of sympathetic outflow are unknown. Therefore, cardiac sympathetic afferent nerves were stimulated by occlusion of coronary arteries to investigate their reflex influences on renal sympathetic nerve activity and systemic arterial blood pressure. Responses were observed in anesthetized cats in which sympathetic and/or vagal cardiac afferent nerves remained intact and arterial baroreceptors remained intact or had been denervated. Stimulating sympathetic afferent neurons caused excitation of renal nerve activity, which was accompanied by variable changes in arterial pressure. Stimulation of vagal afferents by coronary occlusion consistently produced inhibition of renal nerve activity and marked depressor responses. When both components of cardiac innervation remained intact, increases or decreases in renal nerve activity and blood pressure were elicited by coronary artery occlusion in the presence or absence of arterial baroreceptors. These results illustrate that cardiac sympathetic afferent nerves can contribute significantly to cardiovascular control during myocardial ischemia.

Neuronal regulation of renal function: A model system for nervous system interactions

1992 ◽  
Vol 70 (5) ◽  
pp. 733-734 ◽  
Author(s):  
J. Michael Wyss
Keyword(s):  
Nervous System ◽  
Renal Function ◽  
Renal Disease ◽  
Easy Access ◽  
Renal Nerves ◽  
Clinical Consequence ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity

The kidney is the most highly innervated peripheral organ, and both the excretory and endocrine functions of the kidney are regulated by renal nerve activity. The kidney plays a dominant role in body fluid homeostasis, blood ionic concentration, and pH and thereby contributes importantly to systemic blood pressure control. Early studies suggested that the neural-renal interactions were responsible only for short-term adjustments in renal function, but more recent studies indicate that the renal nerves may be a major contributor to chronic renal defects leading to established hypertension and (or) renal disease. The neural-renal interaction is also of considerable interest as a model to elucidate the interplay between the nervous system and peripheral organs, since there is abundant anatomical and physiological information characterizing the renal nerves. The investigator has easy access to the renal nerves and the neural influence on renal function is directly quantifiable both in vivo and in vitro. In this symposium that was presented at the 1990 annual convention of the Society for Neuroscience in St. Louis, Missouri, three prominent researchers evaluate the most recent progress in understanding the interplay between the nervous system and the kidney and explore how the results of these studies relate to the broader questions concerning the nervous system's interactions.First, Luciano Barajas examines the detailed anatomy of the intrarenal distribution of the efferent and afferent renal nerves along the nephron and vasculature, and he evaluates the physiological role of each of the discrete components of the innervation. His basic science orientation combined with his deep appreciation of the clinical consequence of the failure of neural-renal regulation enhances his discussion of the anatomy. Ulla C. Kopp discusses the role of the renorenal reflex, which alters renal responses following stimulation of the contralateral kidney. She also considers her recent findings that efferent renal nerve activity can directly modify sensory feedback to the spinal cord from the kidney. Finally, J. Michael Wyss examines the functional consequences of neural control of the kidney in health and disease. Although the nervous system has often been considered as only an acute regulator of visceral function, current studies into hypertension and renal disease suggest that neural-renal dysfunction may be an important contributor to chronic diseases.Together, these presentations examine most of the recent advances in the area of neural-renal interactions and point out how these data form a basis for future research into neuronal interactions with all visceral organs. The relative simplicity of the neural-renal interaction makes this system an important model with which to elucidate all neural-peripheral and neural-neural interactions.

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.

Factors causing natriuresis after hypothalamic injection of a cholinergic drug in rats

1983 ◽  
Vol 244 (1) ◽  
pp. F64-F69 ◽  
Author(s):  
C. R. Silva-Netto ◽  
R. H. Jackson ◽  
R. E. Colindres
Keyword(s):  
Blood Pressure ◽  
Renal Plasma Flow ◽  
Cholinergic Stimulation ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Conscious Rats ◽  
Clearance Studies ◽  
Renal Nerve Activity ◽  
Stimulation Of ◽  
Cholinergic Drug

We investigated possible mechanisms for the natriuresis seen after injection of the cholinergic drug carbamylcholine chloride (carbachol) into the lateral hypothalamus of conscious rats. In unrestrained rats injection of 1 microgram of carbachol in 1 microliter of 0.15 M NaCl solution through a permanently implanted cannula produced a significant natriuresis and kaliuresis. Injection of vehicle produced no changes. The same animals were then subjected to bilateral renal denervation (n = 13) or sham denervation (n = 13) and injected with the same solutions 1 wk later. Carbachol injection produced a natriuresis (P less than 0.0001) and a kaliuresis (P less than 0.01) in all animals studied. Both responses were of a magnitude similar to the responses seen before denervation. We studied other rats while awake but restrained, which permitted the performance of clearance studies and blood pressure measurements. Injection of carbachol produced diuresis, natriuresis, and kaliuresis in all rats, with no change in p-aminohippurate clearance and only transient change in inulin clearance. An increase in blood pressure occurred in some but not all rats. The response in rats with bilaterally denervated kidneys (n = 7) was similar to that of rats with innervated kidneys (n = 5). The natriuresis seen after cholinergic stimulation of the hypothalamus in conscious rats is not primarily mediated by inhibition of renal nerve activity and can be dissociated from changes in blood pressure, glomerular filtration rate, and renal plasma flow.

Facilitatory role of efferent renal nerve activity on renal sensory receptors

1987 ◽  
Vol 253 (4) ◽  
pp. F767-F777 ◽  
Author(s):  
U. C. Kopp ◽  
L. A. Smith ◽  
G. F. DiBona
Keyword(s):  
Superior Vena ◽  
Isotonic Saline ◽  
Vena Cava ◽  
Urinary Sodium Excretion ◽  
Nerve Fibers ◽  
Facilitatory Effect ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Stimulation Of

The effects of decreasing and increasing efferent renal nerve activity (ERNA) on the renorenal reflex responses to stimulation of renal mechanoreceptors (MR) (increased ureteral pressure) or renal chemoreceptors (CR) (retrograde ureteropelvic perfusion with 0.9 M NaCl) were examined in anesthetized rats. During prevailing ERNA, renal MR stimulation increased ipsilateral afferent renal nerve activity (ARNA) from 6 to 41 counts/s (spike counter) (n = 37) and from 2 to 6 resets/min, (voltage integrator) (n = 23), contralateral urine flow rate from 5.3 to 7.4 microliters . min-1 . g-1 (n = 38) and urinary sodium excretion from 0.7 to 1.1 mumol . min-1 . g-1 (n = 38) (all P less than 0.01), without affecting mean arterial pressure or contralateral glomerular filtration rate. Similar results were obtained with renal CR stimulation. Decreasing ERNA 74+/- 4% by hexamethonium, 10% body weight isotonic saline volume expansion, or inflation of a balloon at the junction of right atria and superior vena cava abolished the increase in ipsilateral ARNA and the contralateral diuresis and natriuresis produced by stimulation of renal MR or CR. Increasing ERNA 254+/- 120% (peak response, n = 15, P less than 0.01) by placing the rat's tail in 53 degrees C water increased basal ARNA 249+/- 80% (n = 6, P less than 0.05) and enhanced the ipsilateral ARNA response 202+/- 78% (n = 9, P less than 0.01) to renal MR stimulation. These results indicate that ERNA exerts a facilitatory effect on renal MR and CR and their afferent renal nerve fibers in the renorenal reflexes.

Effect of sympathetic sensitization of baroreceptors on renal nerve activity

1987 ◽  
Vol 252 (2) ◽  
pp. R328-R335 ◽  
Author(s):  
J. L. Seagard ◽  
F. A. Hopp ◽  
J. P. Kampine
Keyword(s):  
Sympathetic Activity ◽  
Carotid Sinus ◽  
Baroreceptor Sensitivity ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Efferent Nerve ◽  
Before And After ◽  
Renal Nerve Activity ◽  
Sinus Pressure ◽  
Renal Sympathetic

The role of sympathetic efferent innervation of the carotid sinus on the regulation of baroreceptor sensitivity was examined in thiopental-sodium anesthetized dogs (5 mg X kg-1 X h-1 infusion). Baroreflex sensitivity was defined as the slope of renal sympathetic efferent nerve activity vs. carotid sinus pressure in an isolated, perfused carotid sinus. Slopes were obtained before and after sinus sympathectomy performed by section of the cervical sympathetic trunk. There was no significant differences between baroreflex decreases in renal sympathetic activity due to increases in carotid sinus pressure before and after sympathectomy, but the responses to decreases in carotid sinus pressure after sympathectomy were significantly greater than control. Base-line level of renal sympathetic activity, obtained at a constant perfusion pressure of 115 mmHg, abruptly increased by 11% in response to sinus sympathectomy. The response of baroreceptors to sympathomimetic stimulation was examined by recording carotid baroreceptor afferent nerve activity during ramp changes in carotid sinus pressure after addition of epinephrine (10(-8) to 10(-6) M) to the perfusate of the sympathetically denervated sinus. The slopes of the sinus nerve activity vs. carotid sinus pressure were used as direct indexes of baroreceptor sensitivity. Lower levels of epinephrine (10(-8), 10(-7) M) increased the sensitivity of the baroreceptors and reduced renal nerve activity back toward presympathectomy levels. A higher dose of epinephrine (10(-6) M) did not significantly increase baroreceptor sensitivity. The results of this study suggest that sinus sympathetic fibers produce a tonic sensitization of the baroreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Pressoreceptor modulation of renal but not splenic sympathetic reflexes

1987 ◽  
Vol 252 (1) ◽  
pp. R26-R33
Author(s):  
J. C. Tobey ◽  
L. C. Weaver
Keyword(s):  
Sympathetic Nerve Activity ◽  
Apparent Effect ◽  
Nerve Activity ◽  
Receptor Stimulation ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Sympathetic Reflexes ◽  
Sympathetic Responses ◽  
Renal Sympathetic ◽  
Stimulation Of

Influences of sinoaortic and vagally innervated vascular pressoreceptors on excitatory splenic and renal sympathetic responses to splenic receptor stimulation were investigated in anesthetized cats. These experiments demonstrated that these pressoreceptors have little apparent effect on the magnitude of splenic nerve responses to splenic receptor stimulation by capsaicin, bradykinin, or congestion. In contrast, activation of these pressoreceptors attenuated renal nerve responses to splenic receptor stimulation. Influences of sinoaortic and vagally innervated receptors on tonic sympathetic nerve activity also were evaluated. Stimulation of these receptors by small increases in arterial pressure (15–21 mmHg) caused equivalent inhibition of splenic and renal nerve activity; large increases (50–66 mmHg) caused significantly greater inhibition of renal than splenic nerve activity. These results illustrate that excitatory renal and splenic sympathetic responses to splenic receptor stimulation are not suppressed equally by pressoreceptor activation, vascular pressoreceptors can have greater inhibitory influences on tonic renal than splenic nerve activity, and vascular pressoreceptor influences on sympathetic reflexes are similar to those on tonic nerve activity.

Inhibitory effect of renal nerve activity during canine anaphylactic hypotension

1990 ◽  
Vol 258 (2) ◽  
pp. R383-R387 ◽  
Author(s):  
S. Koyama ◽  
T. Fujita ◽  
H. Uematsu ◽  
T. Shibamoto ◽  
M. Aibiki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systemic Blood Pressure ◽  
Inhibitory Effect ◽  
Baroreceptor Reflex ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Vagal Nerves ◽  
Renal Nerve Activity ◽  
Anesthetized Dogs ◽  
Reflex Control

We have examined baroreceptor regulation of renal nerve activity (RNA) during anaphylactic hypotension that affects renal nerve activity. In anesthetized dogs, mean blood pressure (MBP), heart rate (HR), and RNA were simultaneously measured. To test for a normally functioning baroreceptor reflex in each animal, a transient hypotension was induced by an intravenous injection of sodium nitroprusside (4 micrograms/kg). Nitroprusside produced a reflex increase in RNA (+63 +/- 12% at -20 mmHg and +139 +/- 8% at -40 mmHg) and HR (+13 +/- 1 beats/min at -20 mmHg and +21 +/- 2 beats/min at -40 mmHg). However, intravenous administration of Ascaris suum antigen in animals with an intact neuraxis caused a decrease in RNA (-15 +/- 14% at -20 mmHg and -42 +/- 11% at -40 mmHg blood pressure during the antigen-induced hypotension) in parallel with a fall in systemic blood pressure. HR responses were -5 +/- 2 beats/min at -20 mmHg and -10 +/- 1 beats/min at -40 mmHg during the hypotension induced by the antigen. In animals with combined denervation of the carotid sinus and vagal nerves, HR did not change significantly during anaphylactic hypotension. However, a decrease in RNA remained (-60 +/- 4% at -20 mmHg and -72 +/- 4% at -40 mmHg of hypotension). The decrease in RNA after antigen administration was significantly greater after denervation than in animals with an intact neuraxis. These results indicate that systemic baroreceptor reflex control of RNA is reduced during anaphylactic hypotension. Impaired reflex control of sympathetic nerve activity may result from an impairment of sympathetic outflow through the central nervous system.

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