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.

Lack of effect of chronic renal denervation on altered sodium reabsorption during increased ureteral pressure

1980 ◽  
Vol 58 (5) ◽  
pp. 477-483 ◽  
Author(s):  
D. R. Wilson ◽  
M. Cusimano ◽  
U. Honrath
Keyword(s):  
Isotonic Saline ◽  
Urine Osmolality ◽  
Tubular Reabsorption ◽  
Renal Nerves ◽  
Sodium Reabsorption ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Water Excretion ◽  
Renal Nerve Activity

The role of the renal nerves in the altered sodium reabsorption which occurs during increased ureteral pressure was studied using clearance techniques in anaesthetized rats undergoing diuresis induced by isotonic saline infusion. In rats with a sham denervated kidney, an ipsilateral increase in ureteral pressure to 20 cm H2O resulted in a marked and significant decrease in sodium and water excretion, increased fractional sodium reabsorption, and increased urine osmolality with no significant change in glomerular filtration rate. A similar significant ipsilateral increase in tubular reabsorption of sodium occurred in rats with chronically denervated kidneys during increased ureteral pressure. The changes in tubular reabsorption were rapidly reversible after return of ureteral pressure to normal. These experiments indicate that enhanced tubular reabsorption of sodium during an ipsilateral increase in ureteral pressure is not mediated by increased renal nerve activity. During the antinatriuresis of increased ureteral pressure there was a decrease in the fractional reabsorption of sodium from the opposite normal kidney. The role of the renal nerves in this compensatory change in function in the opposite kidney was studied in two further groups of animals. The renal response to a contralateral increase in ureteral pressure was similar in denervated and sham-denervated kidneys. The results indicate that altered renal nerve activity, through ipsilateral or contralateral renorenal reflexes, is not responsible for the changes in tubular reabsorption of sodium which occur during increased ureteral pressure induced by partial ureteral obstruction.

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.

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.

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.

Selective enhancement in SHR of hypotension and bradycardia caused by NTS-injected serotonin

1994 ◽  
Vol 266 (2) ◽  
pp. R599-R605 ◽  
Author(s):  
M. Okada ◽  
R. D. Bunag
Keyword(s):  
Cerebrospinal Fluid ◽  
Spontaneously Hypertensive Rats ◽  
Nucleus Tractus Solitarius ◽  
Isotonic Saline ◽  
Hypertensive Rats ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Spontaneously Hypertensive ◽  
Artificial Cerebrospinal Fluid ◽  
Renal Nerve Activity

To examine whether serotonergic mechanisms in the nucleus tractus solitarius (NTS) become altered by hypertension, responses to serotonin (5-HT) or L-glutamate injected into the NTS were compared in anesthetized rats. Because isotonic saline had appreciable effects whereas artificial cerebrospinal fluid did not, artificial cerebrospinal fluid was routinely used as the vehicle. Microinjections of 5-HT or L-glutamate always reduced mean pressure, heart rate, and renal nerve activity. Depressor and bradycardic responses to 5-HT were consistently more pronounced in spontaneously hypertensive rats than in either regular Wistar or Wistar-Kyoto rats, but similar responses elicited with L-glutamate did not differ between rat groups. By contrast, attendant inhibition of renal nerve activity was the same in all rats, thereby suggesting that it either is not a good indicator of sympathetic activity or does not contribute to the hypotensive effects of 5-HT. Our results are compatible with the interpretation that hypotensive responses to 5-HT were enhanced because serotonergic mechanisms for cardiovascular regulation in the NTS were sensitized in spontaneously hypertensive rats.

Renorenal reflexes: neural components of ipsilateral and contralateral renal responses

1985 ◽  
Vol 249 (4) ◽  
pp. F507-F517 ◽  
Author(s):  
U. C. Kopp ◽  
L. A. Smith ◽  
G. F. DiBona
Keyword(s):  
Spinal Cord ◽  
Venous Pressure ◽  
Urinary Sodium Excretion ◽  
Reflex Response ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Electrophysiological Responses ◽  
Renal Nerve Activity ◽  
Renal Vascular ◽  
Renal Responses

In anesthetized rats, stimulating renal mechanoreceptors (MR) by increasing renal venous pressure (RVP) 22 mmHg increased ipsilateral (ipsi) renal vascular resistance (RVR) from 23.5 to 31.3 mmHg/(ml X min-1 X g-1), ipsi urinary sodium excretion (UNaV) from 0.26 to 0.49 mumol X min-1 X g-1, contralateral (contra) urine flow rate (V) from 3.13 to 4.43 microliter X min-1 X g-1, and UNaV from 0.30 to 0.46 mumol X min-1 X g-1. Ipsi renal denervation (DNX) did not affect the increase in ipsi RVR but reduced the increase in ipsi UNaV. The increases in contra V and UNaV were abolished by either ipsi or contra renal DNX. Increases RVP increased ipsi afferent renal nerve activity (ARNA) 288 counts/10 s and decreased ipsi and contra efferent renal nerve activity (ERNA) 242 and 490 counts/10 s, respectively. Renal pelvic instillation of lidocaine (5 micrograms/ml) did not affect the renal functional or electrophysiological responses to increases RVP but abolished the increase in ipsi ARNA, the decrease in contra ERNA, and the increases in contra V and UNaV produced by increasing ureteral pressure (UP) or retrograde ureteropelvic perfusion with 0.9 M NaCl [chemoreceptor (CR) stimulation]. Chronic T6 spinal cord section abolished the increase in ipsi ARNA, the decrease in contra ERNA, and the increases in contra V and UNaV produced by renal MR (increases RVP, increases UP) and CR stimulation. We conclude increases that RVP results in an ipsi and contra inhibitory renorenal reflex. Differential blockade with pelvic lidocaine suggests that the sensory receptors activated by increases RVP are located in an anatomically different area than those activated by increases UP or retrograde ureteropelvic perfusion with 0.9 M NaCl. An intact spinal cord is required for the normal responsiveness of renal sensory neuroreceptor complexes to specific stimuli in the context of the complete renorenal reflex response.

Inhibitory renorenal reflexes: a role for renal prostaglandins in activation of renal sensory receptors

1991 ◽  
Vol 261 (6) ◽  
pp. R1513-R1521 ◽  
Author(s):  
U. C. Kopp ◽  
L. A. Smith
Keyword(s):  
Chemical Activation ◽  
Urinary Sodium Excretion ◽  
Reflex Response ◽  
Sensory Receptor ◽  
Chemical Stimulus ◽  
Sensory Receptors ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Pelvic Perfusion

In anesthetized rats, activation of renal sensory receptors with a mechanical stimulus (increased ureteral pressure) and a chemical stimulus (renal pelvic perfusion with 0.9 M NaCl) results in an increase in ipsilateral afferent renal nerve activity and a reflex increase in contralateral urine flow rate and urinary sodium excretion, i.e., a contralateral inhibitory renorenal reflex. Because both interventions are known to increase renal prostaglandin (PG) synthesis, we examined whether renal PGs were involved in the renorenal reflex response to renal sensory receptor stimulation. In the first part, mechanical and chemical activation of renal sensory receptors was performed in the absence and presence of renal pelvic perfusion with indomethacin or meclofenamate (0.2 micrograms/min). Indomethacin inhibited the ipsilateral afferent renal nerve activity response to increased ureteral pressure (7 +/- 2 vs. 38 +/- 10%, P less than 0.01) and renal pelvic perfusion with 0.9 M NaCl (3 +/- 3 vs. 28 +/- 5%, P less than 0.01) and the contralateral diuretic and natriuretic responses in the absence of any renal hemodynamic changes. Similar effects were produced by meclofenamate. In the second part, mechanical and chemical activation of renal sensory receptors was performed in the presence of renal pelvic perfusion with vehicle, indomethacin, and indomethacin plus PGE2 (20 micrograms/min). Addition of PGE2 to the renal pelvic perfusate in indomethacin-treated kidneys restored the responses to mechanical and chemical activation of renal sensory receptors to levels not different from their pre-indomethacin control values. We conclude that PGs in the renal pelvic area are involved in inhibitory renorenal reflex responses to mechanical and chemical activation of renal sensory receptors.

Role of prostaglandins in renal sensory receptor activation by substance P and bradykinin

1993 ◽  
Vol 265 (3) ◽  
pp. R544-R551 ◽  
Author(s):  
U. C. Kopp ◽  
L. A. Smith
Keyword(s):  
Substance P ◽  
Urinary Sodium Excretion ◽  
Receptor Activation ◽  
Prostaglandin Synthesis ◽  
Sensory Receptor ◽  
Sensory Receptors ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Pelvic Perfusion

In anesthetized rats increasing ureteral pressure results in an increase in ipsilateral afferent renal nerve activity and a reflex increase in contralateral urine flow rate and urinary sodium excretion that is dependent on intact prostaglandin synthesis. Activation of renal pelvic substance P receptors contributes to the renorenal reflex responses to increased ureteral pressure. Because these data suggested that renal sensory receptors could be activated by both prostaglandins and substance P we examined whether activation of renal sensory receptors by substance P was dependent on intact prostaglandin synthesis. The renal pelvis was perfused with capsaicin, 2.5 micrograms/ml, or substance P, 4 micrograms/ml, before and during renal pelvic perfusion with the prostaglandin synthesis inhibitor indomethacin, 50 micrograms/ml. Indomethacin reduced the peak ipsilateral afferent renal nerve activity responses to capsaicin and substance P by 83 +/- 15% and 81 +/- 8%, respectively, as well as the contralateral diuretic and natriuretic responses. We also examined the effects of renal pelvic administration of indomethacin on the responses to renal pelvic perfusion with bradykinin. Bradykinin, 20 micrograms/ml, increased peak ipsilateral afferent renal nerve activity by 197 +/- 47% and contralateral urine flow rate and urinary sodium excretion by 31 +/- 6 and 20 +/- 6%, respectively. Indomethacin reduced the ipsilateral afferent renal nerve activity response by 76 +/- 9% and abolished the contralateral diuretic and natriuretic responses to bradykinin. We conclude that renal sensory receptor activation by capsaicin, substance P, and bradykinin is dependent on intact renal prostaglandin synthesis.(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.

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