Renorenal reflexes in hypertension.
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Afferent Pathways↗
Biomedical subjects
U C Kopp
Publications and source records attributed to U C Kopp.
Effects of the substance P receptor antagonist CP-96,345 on renal sensory receptor activation.
In anesthetized rats, we examined the effects of the substance P (SP) receptor antagonist CP-96,345 on the renorenal reflex responses to renal mechanoreceptor (MR) stimulation produced by increased ureteral pressure. Renal pelvic administration of SP at 0.16, 0.8, 4.0, 20, and 100 micrograms/ml increased ipsilateral afferent renal nerve activity (ARNA) in a concentration-dependent fashion, 45 +/- 28, 134 +/- 26, 185 +/- 24, 185 +/- 25, and 274 +/- 39%, respectively. Renal pelvic perfusion with CP-96,345 at 0.01, 0.1, and 1.0 mg/ml dose-dependently reduced the ARNA response to 4.0 micrograms/ml SP, by 5 +/- 17, 46 +/- 9, and 72 +/- 12%, respectively. Increasing ureteral pressure three times in the presence of renal pelvic perfusion with vehicle, 1 mg/ml CP-96,345, and vehicle, increased ARNA 77 +/- 21, 29 +/- 13, and 101 +/- 36%, respectively. Thus CP-96,345 produced a reversible blockade of the ARNA responses to renal MR stimulation. Increasing ureteral pressure three times in the presence of renal pelvic perfusion with vehicle, CP-96,345 (1 mg/ml), and CP-96,345 + 25-40 micrograms/ml SP, increased ARNA 108 +/- 15, 43 +/- 14, and 153 +/- 63%, respectively. Thus CP-96,345 produced a competitive blockade of the ARNA responses to renal MR stimulation. The contralateral diuretic and natriuretic responses to increased ureteral pressure were also blocked in a reversible and competitive fashion by CP-96,345. The inactive 2R,3R enantiomer of CP-96,345, CP-96,344 (1 mg/ml). had no effect on the ipsilateral ARNA or the contralateral renal excretory responses to increased ureteral pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
Afferent Pathways↗
Role of prostaglandins in renal sensory receptor activation by substance P and bradykinin.
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)
Animals↗
Neural regulation of renin secretion.
In summary, there is now considerable evidence for an interaction between the renal sympathetic nerves and the baroreceptor and macula densa mechanisms in the control of renin secretion rate. Renal sympathetic nerve activity varies from minute to minute throughout the day. At times, increases in renal sympathetic nerve activity sufficient to cause a direct neural release of renin from juxtaglomerular cells may occur. Under other circumstances, changes in renal sympathetic nerve activity may be more modest, but still sufficient to modulate the renin secretion rate responses mediated by other mechanisms. The studies reviewed show that prevailing renal sympathetic nerve activity can modulate the magnitude of the renin secretion rate response to stimulation of the renal vascular baroreceptor and the tubular macula densa receptor mechanisms. The degree of interaction between the neural and non-neural mechanisms is dependent on the level of activation of the non-neural mechanisms and the intensity of renal sympathetic nerve activity.
Animals↗
Renorenal reflexes: interaction between efferent and afferent renal nerve activity.
In rats, stimulation of renal mechanoreceptors by increasing ureteral pressure results in a contralateral inhibitory renorenal reflex response consisting of increases in ipsilateral afferent renal nerve activity, decreases in contralateral efferent renal nerve activity, and increases in contralateral urine flow rate and urinary sodium excretion. Mean arterial pressure is unchanged. To study possible functional central interaction among the afferent renal nerves and the aortic and carotid sinus nerves, the responses to renal mechanoreceptor stimulation were compared in sinoaortic denervated rats and sham-denervated rats before and after vagotomy. In contrast to sham-denervated rats, there was an increase in mean arterial pressure in response to renal mechanoreceptor stimulation in sinoaortic-denervated rats. However, there were no differences in the renorenal reflex responses among the groups. Thus, our data failed to support a functional central interaction among the renal, carotid sinus, and aortic afferent nerves in the renorenal reflex response to renal mechanoreceptor stimulation. Studies to examine peripheral interaction between efferent and afferent renal nerves showed that marked reduction in efferent renal nerve activity produced by spinal cord section at T6, ganglionic blockade, volume expansion, or stretch of the junction of superior vena cava and right atrium abolished the responses in afferent renal nerve activity and contralateral renal function to renal mechanoreceptor stimulation. Conversely, increases in efferent renal nerve activity caused by thermal cutaneous stimulation increased basal afferent renal nerve activity and its responses to renal mechanoreceptor stimulation. These data suggest a facilitatory role of efferent renal nerves on renal sensory receptors.
Animals↗
Inhibitory renorenal reflexes: a role for substance P or other capsaicin-sensitive neurons.
In anesthetized rats, we examined whether inhibitory renorenal reflex responses to renal pelvic mechanoreceptor (MR) and chemoreceptor (CR) stimulation were mediated by substance P (SP)-containing neurons. Capsaicin (0.5 ng to 5 micrograms) injected into the renal pelvis increased afferent renal nerve activity (ARNA) dose dependently, from 60 +/- 19 to 333 +/- 105%. For a given ARNA response, a 100-fold higher dose was required when capsaicin was injected into the renal interstitium compared with the renal pelvis. Renal pelvic administration of SP (25 ng) increased ipsilateral ARNA by 126 +/- 34% and contralateral urine flow rate and urinary sodium excretion by 21 +/- 4 and 28 +/- 7%, respectively, a response similar to that produced by renal MR and CR stimulation. Mean arterial pressure was unaffected. Ipsilateral renal denervation abolished the contralateral diuresis and natriuresis produced by SP. In rats treated with capsaicin (950 mg/kg subcutaneously over 1 wk) to deplete sensory neurons of SP, renal MR and CR stimulation failed to elicit a renorenal reflex response. The data suggest that the renorenal reflex responses to renal MR and CR stimulation are mediated at least, in part, by SP neurons or other sensory neurons susceptible to depletion by capsaicin.
Animals↗
Inhibitory renorenal reflexes: a role for renal prostaglandins in activation of renal sensory receptors.
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.
Afferent Pathways↗
Novel recordings of renal sympathetic nerve activity in conscious fetal sheep and newborn lambs.
This study describes a technique for measuring efferent renal sympathetic nerve activity (RSNA) during the perinatal period. Experiments were carried out in four chronically instrumented fetal sheep (gestational age, 134-140 days) and 6 newborn lambs (postnatal age, 3-7 days). Surgery, performed under halothane anesthesia, consisted of routine catheter insertions and placement of a Doppler flow probe around the left renal artery. In addition, bipolar platinum electrodes were placed on a branch of the left renal postganglionic nerve. At least 24 h after surgery RSNA was measured in conscious fetal and newborn animals. RSNA was pulse synchronous, reduced with pressor agents, and completely inhibited during ganglionic blockade. Using this method, we have provided direct evidence of efferent renal sympathetic nerve traffic in utero and in the immediate postnatal period. This technique opens new avenues into the investigation of the role of the sympathetic nervous system during the perinatal period.
Animals↗
Renorenal reflexes present in young and captopril-treated adult spontaneously hypertensive rats.
In normotensive Sprague-Dawley rats and Wistar-Kyoto (WKY) rats stimulation of renal mechanoreceptors or chemoreceptors by increasing ureteral pressure or renal pelvic perfusion with 0.9 M NaCl results in a contralateral inhibitory renorenal reflex response with contralateral diuresis and natriuresis. However, in 14-15-week-old spontaneously hypertensive rats (SHR) renal sensory receptor stimulation failed to elicit a contralateral inhibitory renorenal reflex response. The present study was performed to examine whether the lack of a renorenal reflex response in SHR was related to elevated arterial pressure by studying the responses to renal sensory receptor stimulation in 5-6-week-old SHR and in 12-16-week-old SHR that had been treated with captopril from 3 weeks of age to prevent the development of hypertension. In 5-6-week-old SHR, mean arterial pressure was 113 +/- 3 mm Hg. Graded increases of ureteral pressure of 15 and 29 mm Hg resulted in graded increases in ipsilateral afferent renal nerve activity of 57 +/- 22% and 120 +/- 38%. Contralateral urinary sodium excretion increased from 0.26 +/- 0.06 to 0.35 +/- 0.07 mumol/min/g and from 0.36 +/- 0.08 to 0.46 +/- 0.11 mumol/min/g, respectively. In captopril-treated SHR, mean arterial pressure was 109 +/- 3 mm Hg. Increasing ureteral pressure by 34 mm Hg increased ipsilateral afferent renal nerve activity 65 +/- 21% and contralateral urinary sodium excretion from 1.28 +/- 0.24 to 1.53 +/- 0.30 mumol/min/g. Similar results were produced by renal chemoreceptor stimulation. It is concluded that renal sensory receptor stimulation results in a contralateral inhibitory renorenal reflex response in 5-6-week-old SHR and in SHR treated with captopril to prevent the development of hypertension. These results suggest that the previously demonstrated lack of a renorenal reflex response to renal sensory receptor stimulation in hypertensive SHR is related to the maintenance of hypertension.
Animals↗
Impaired renorenal reflexes in two-kidney, one clip hypertensive rats.
In normotensive rats, stimulation of renal mechanoreceptors by an increase in ureteral pressure results in a contralateral inhibitory renorenal reflex response with contralateral natriuresis. Similar effects are produced by stimulation of renal chemoreceptors by renal pelvic perfusion with 0.9 M NaCl. However, in spontaneously hypertensive rats the renorenal reflex responses to renal mechanoreceptor and chemoreceptor stimulation are impaired. The present study was performed to examine whether the renorenal reflexes were altered in two-kidney, one clip hypertensive rats, a model of hypertension in which it has been suggested that the afferent renal nerves contribute to the enhanced peripheral sympathetic nervous activity. A 0.2 mm silver clip was placed around one renal artery 4 weeks before the study. At the time of study, mean arterial pressure was 156 +/- 4 mm Hg. Renal mechanoreceptor and chemoreceptor stimulation of either the nonclipped or clipped kidney failed to affect ipsilateral afferent renal nerve activity, contralateral efferent renal nerve activity, and contralateral urine flow rate and urinary sodium excretion. Renal denervation of the nonclipped kidney increased ipsilateral urinary sodium excretion from 0.65 +/- 0.13 to 1.50 +/- 0.42 mumol/min/g and decreased contralateral urinary sodium excretion from 0.18 +/- 0.03 to 0.13 +/- 0.03 mumol/min/g (p less than 0.05). Thus, denervation of the nonclipped kidney resulted in a similar contralateral excitatory renorenal reflex response as in normotensive rats. However, denervation of the clipped kidney increased both ipsilateral and contralateral urinary sodium excretion, from 0.14 +/- 0.04 to 0.27 +/- 0.5 mumol/min/g and from 1.29 +/- 0.33 to 2.09 +/- 0.59 mumol/min/g (p less than 0.01), respectively. Taken together these data suggest that the lack of inhibitory renorenal reflexes from the clipped kidney may enhance efferent sympathetic nervous activity and thereby contribute to the hypertension in two-kidney, one clip hypertensive rats.
Animals↗
Renorenal reflexes in normotension and hypertension.
The renorenal reflex responses to physiological stimulation of the afferent renal nerves are species-dependent. In dogs, renal mechanoreceptor (MR) stimulation results in a contralateral excitatory renorenal reflex response with a fall in contralateral renal blood flow and urinary sodium excretion at unchanged mean arterial pressure. In cats, renal MR stimulation increases mean arterial pressure and produces variable effects on contralateral renal excretion. In rats, renal MR stimulation results in a contralateral inhibitory renorenal reflex response with contralateral diuresis and natriuresis at unchanged systemic and contralateral renal hemodynamics. Renal chemoreceptor (CR) stimulation produces similar results. In spontaneously hypertensive rats renal MR and CR stimulation fails to produce a renorenal reflex response.
Afferent Pathways↗
Role of renal nerves in excretory responses to exogenous and endogenous opioid peptides.
The present study was designed to investigate opioid peptide-mediated changes in renal function in conscious Sprague-Dawley rats after administration of the native opioid agonist methionine enkephalin (ME), its synthetic analog D-Ala2-methionine enkephalinamide (DALA) and the opioid antagonist naloxone. Intravenous infusion of DALA (25 micrograms/kg/min) and ME (75 micrograms/kg/min) produced no changes in mean arterial pressure, heart rate, glomerular filtration rate or effective renal plasma flow in rats with intact or bilaterally denervated kidneys. In contrast, i.v. infusion of these opioid agonists produced differing effects on the renal excretion of water and sodium; DALA produced an increase in urinary flow rate and sodium excretion and ME produced a decrease in these parameters. Changes in renal sympathetic nerve activity were not involved in producing these effects as supported by measurements of renal sympathetic nerve activity and the finding that prior bilateral renal denervation did not alter the renal responses to either agonist. The renal excretory responses to both DALA and ME infusion were prevented by pretreatment with the opioid receptor antagonist naloxone, thus suggesting an opioid receptor-mediated effect of both agonists. Intravenous bolus injections of naloxone alone produced a dose-dependent diuresis and natriuresis without producing changes in systemic or renal hemodynamics or renal sympathetic nerve activity. These studies, therefore, provide evidence that the administration of opioid receptor agonists and antagonists produce changes in the renal excretion of water and sodium via an action on renal tubular reabsorptive mechanisms which are independent of changes in systemic or renal hemodynamics or renal sympathetic nerve activity.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Facilitatory role of efferent renal nerve activity on renal sensory receptors.
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.
Animals↗
Impaired renorenal reflexes in spontaneously hypertensive rats.
In normotensive Sprague-Dawley rats stimulation of renal mechanoreceptors and chemoreceptors by increasing ureteral pressure and retrograde ureteropelvic perfusion with 0.9 M NaCl results in a contralateral inhibitory renorenal reflex response with contralateral diuresis and natriuresis. Since efferent renal nerve activity is increased in spontaneously hypertensive rats (SHR) and renal denervation delays the onset of hypertension in SHR in association with increased diuresis and natriuresis, the present study was undertaken to examine whether renorenal reflexes were altered in SHR compared with normotensive Wistar-Kyoto rats (WKY). In WKY mean arterial pressure was 113 +/- 2 mm Hg and remained unchanged during renal mechanoreceptor and chemoreceptor stimulation. Increasing ureteral pressure 35 mm Hg increased ipsilateral afferent renal nerve activity 4.5 +/- 1.7 resets/min, decreased contralateral efferent renal nerve activity 3.2 +/- 0.8 resets/min, and increased contralateral urine flow rate 33 +/- 4% and urinary sodium excretion 49 +/- 8%. Similarly, retrograde ureteropelvic perfusion with 0.9 M NaCl increased ipsilateral afferent renal nerve activity 2.5 +/- 0.6 resets/min, decreased contralateral efferent renal nerve activity 2.4 +/- 1.1 resets/min, and increased contralateral urine flow rate 39 +/- 5% and urinary sodium excretion 38 +/- 8%. Stimulating renal mechanoreceptors and chemoreceptors to the same extent in SHR failed to increase ipsilateral afferent renal nerve activity, decrease contralateral efferent renal nerve activity, and produce a contralateral diuresis and natriuresis. It is concluded that renorenal reflexes are impaired in SHR. Failure of ipsilateral afferent renal nerve activity to increase during renal mechanoreceptor and chemoreceptor stimulation indicates a peripheral defect at the level of the renal sensory receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Renorenal reflex responses to renal sensory receptor stimulation in normotension and hypertension.
The renorenal reflex responses to renal mechano-(MR) and chemoreceptor (CR) stimulation have been examined in anesthetized dogs, cats, and rats. Renal MR were stimulated by increased ureteral pressure and renal CR by retrograde ureteropelvic perfusion with 0.9 M NaCl at unchanged ureteral pressure. In the dog, renal MR stimulation results in an increase in ipsilateral afferent renal nerve activity (ARNA) and contralateral efferent RNA (ERNA) and a contralateral renal vasoconstriction. Mean arterial pressure (MAP) is unchanged. Renal CR stimulation is without effect. In the cat, renal MR and CR stimulation increases MAP and either increases or decreases contralateral urine flow rate and urinary sodium excretion at unchanged renal perfusion pressure. In the rat, renal MR and CR stimulation increases ipsilateral ARNA, decreases contralateral ERNA and increases contralateral urine flow rate and urinary sodium excretion. The magnitude of the renorenal reflex responses is related to the magnitude of the stimulation. Furthermore the renorenal reflex responses are attenuated in spontaneously hypertensive rats (SHR). We conclude that there is a species difference in the nature of the renorenal reflex responses to renal MR and CR stimulation. The attenuated renorenal reflexes in SHR might contribute to their hypertension by promoting increased ERNA and sodium retention.
Animals↗
Interaction between epinephrine and renal nerves in control of renin secretion rate.
To determine whether the increase in renin secretion rate (RSR) produced by the beta 2-adrenoceptor agonist epinephrine was dependent on intact renal innervation, epinephrine (10 ng X kg-1 X min-1) was infused bilaterally into an innervated and a denervated kidney (ira) of the same anesthetized dog at spontaneous and reduced renal arterial pressure (decreases RAP, 100 mmHg). Epinephrine ira did not affect mean arterial pressure, renal hemodynamics, or urinary sodium excretion of either kidney. At spontaneous RAP epinephrine ira increased RSR from 633 +/- 134 to 926 +/- 137 ng/min in innervated kidneys but did not change RSR in denervated kidneys. decreases RAP in the presence of epinephrine ira resulted in an increase in RSR from 969 +/- 248 to 2,564 +/- 630 ng/min in innervated kidneys, which was greater than that produced in the absence of epinephrine, from 741 +/- 244 to 1,606 +/- 431 ng/min. In denervated kidneys decreases RAP resulted in similar increases in RSR in the absence and presence of epinephrine ira from 41 +/- 15 to 166 +/- 60 ng/min and from 59 +/- 210 to 235 +/- 78 ng/min, respectively. These results demonstrate that the increase in RSR produced by epinephrine is dependent on intact renal innervation at spontaneous and decreases RAP and suggest that epinephrine increases RSR by a prejunctional mechanism. The beta 1-adrenoceptor antagonist metoprolol (0.3-0.5 microgram X kg-1 X min-1 ira) abolished the enhanced RSR response to decreases RAP produced by epinephrine ira. Similarly, the beta 2-adrenoceptor antagonist ICI 118551 (0.005-0.25 microgram X kg-1 X min-1 ira) abolished the enhanced RSR response to decreases RAP produced by epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Renorenal reflexes: neural components of ipsilateral and contralateral 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.
Afferent Pathways↗
Renorenal reflexes: neural and functional responses.
Evidence supporting the existence of renorenal reflexes is reviewed. Renal mechanoreceptors (MR) and afferent renal nerve fibers are localized in the corticomedullary region and in the wall of the renal pelvis. Stimulating renal MR by increased ureteral pressure (increases UP) or increased renal venous pressure (increases RVP) and renal chemoreceptors (CR) by retrograde ureteropelvic perfusion with 0.9 M NaCl results in increased ipsilateral afferent renal nerve activity (ARNA) in a variety of species. However, renorenal reflex responses to renal MR and CR differ among species. In the dog, stimulating renal MR results in a modest contralateral excitatory renorenal reflex response with contralateral renal vasoconstriction that is integrated at the supraspinal level. Renal CR stimulation is without effect on systemic and renal function. However, in the rat the responses to renal MR and CR stimulation are opposite to those of the dog. Increased ureteral pressure, renal venous pressure, or retrograde ureteropelvic perfusion with 0.9 M NaCl each results in a receptor-specific contralateral inhibitory renorenal reflex response. The afferent limb consists of increased ipsilateral ARNA and the efferent limb of decreased contralateral efferent RNA with contralateral diuresis and natriuresis. The renorenal reflex responses to MR and CR stimulation are integrated at the supraspinal level.
Afferent Pathways↗