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PubMed1977

Prostaglandins in adrenergic transmission of isolated perfused rat pancreas.

In the isolated, perfused rat pancreas, prostaglandins (PGs) E1 and E2 1-5 ng/ml, reduced the vasoconstrictor responses to periarterial nerve stimulation and variably affected those to injected norepinephrine. Prostaglandin F2alpha had no consistent effect on the vasoconstrictor responses to both adrenergic stimuli. Stimulation of adrenergic nerves or administration of norepinephrine released a PGE-like substance from the perfused pancreas which was abolished by inhibitors of PG synthesis, acetylsalicylic acid, indomethacin, meclofenamate, and eicosa-5,8,11,14-tetraynoic acid. The latter three agents did not potentiate, but rather reduced the vasoconstrictor responses to both adrenergic stimuli. Arachidonic acid that was converted by the pancreas into PGE2 and PGF2alpha inhibited the vasoconstrictor responses to adrenergic stimuli. The latter effect of arachidonic acid was not altered by the simultaneous infusion of PG synthetase inhibitors. Although these results, which could be attributed to a direct effect of inhibitors of PG synthesis and arachidonic acid on adrenergic neuroeffector junction, fail to establish the role of endogenous PGs in modulating adrenergic responses in rat pancreatic vessels, they emphasize the differences in the effect of PGE1 and PGE2 on adrenergic responses in various vascular beds of the rat.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1993

Free and conjugated catecholamines and serotonin in canine thoracic duct lymph: effects of feeding.

The source and fate of sulfoconjugated catecholamines present in plasma are not known. Sulfated norepinephrine has been shown to overflow together with free norepinephrine from a typical peripheral neuroeffector junction. Some released free norepinephrine is removed via the lymphatic system, but it is not known whether sulfated catecholamines are removed similarly. Serotonin, another biogenic amine, is released from the enterochromaffin cells into portal blood. The aims of the present study were to determine whether conjugated catecholamines and serotonin could be detected in thoracic duct lymph of dogs and to compare concentrations in lymph with those in samples of portal blood collected before and after the dogs were fed. A method is described for the extraction and purification of free and conjugated catecholamines and serotonin from lymph. In lymph and in plasma, there were similar concentrations of free (0.2-0.4 ng/ml) and conjugated (0.1-0.2 ng/ml) norepinephrine and of conjugated dopamine (0.2-1.0 ng/ml). The concentrations of free serotonin were much lower in lymph (0.1-0.2 ng/ml) than in portal blood (100-200 ng/ml). Small amounts of conjugated serotonin (0.1-0.4 ng/ml) were detected in lymph but were not detected in plasma. Feeding caused increases in concentration of conjugated dopamine in lymph and in plasma and small increases in the output of free norepinephrine and free and conjugated serotonin in lymph.

Amines↗
PubMed2000

Enteric locus of action of prokinetics: ABT-229, motilin, and erythromycin.

We investigated the in vivo and in vitro locus of actions of prokinetics: motilin, erythromycin, and ABT-229. The test substances were infused close intra-arterially in short segments of the jejunum in the intact conscious state. Each prokinetic acted on a presynaptic neuron and utilized at least one nicotinic synapse to stimulate circular muscle contractions. The final neurotransmitter at the neuroeffector junction was ACh. Motilin and erythromycin, but not ABT-229, also released nitric oxide. Each prokinetic utilized somewhat different subtypes of muscarinic, serotonergic, tachykininergic, and histaminergic receptors, except for the M(3) receptor, which was common to all of them. In contrast, none of the prokinetics stimulated contractions in mucosa-free or mucosa-attached muscle strips, or rings, even though methacholine or electrical field stimulation induced phasic contractions in all of them. The prokinetics also did not release ACh in longitudinal muscle-myenteric plexus preparations. Each prokinetic, however, decreased the length of enzymatically dispersed single cells. In conclusion, each prokinetic may act on a different subset of presynaptic neurons that converge on the postsynaptic cholinergic and nonadrenergic noncholinergic motoneurons. The presynaptic neurons may be impaired in the muscle bath environment.

Animals↗
PubMed2004

Modulation of neurotransmitter release by NO is altered in mesenteric arterial bed of spontaneously hypertensive rats.

Nitric oxide (NO) reacts with catecholamines resulting in their deactivation. In the present study with the use of the perfused mesenteric arterial bed as a model of the sympathetic neuroeffector junction, the NO synthase (NOS) inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME) resulted in the enhancement of the periarterial nerve stimulation-induced increase in perfusion pressure and norepinephrine overflow while decreasing neuropeptide Y (NPY) overflow. These changes were prevented by l-arginine, demonstrating that the effects of l-NAME were specific to the inhibition of NOS. From the fact that norepinephrine acts on prejunctional alpha(2)-adrenoceptors to inhibit the evoked release of sympathetic cotransmitters, we carried out experiments in the presence of the alpha(2)-adrenergic receptor antagonist yohimbine to investigate the possibility that the decrease in NPY observed in the presence of l-NAME was due to the increase in bioactive norepinephrine acting on its autoreceptor. Periarterial nerve stimulation in the presence of both l-NAME and yohimbine prevented the previously observed decrease in NPY, indicating that the cause of this decrease was, as predicted, due to alpha(2)-adrenoceptor activation. The periarterial nerve stimulation-induced increase of norepinephrine overflow was greater in the spontaneously hypertensive rat compared with normotensive rats. In contrast to what was observed in the isolated perfused mesenteric arterial bed obtained from normotensive animals, inhibition of NOS did not result in a further increase in the overflow of norepinephrine or in a subsequent decrease in NPY. These results demonstrate that, in addition to being a direct vasodilator, NO, by deactivating norepinephrine, can modulate sympathetic neurotransmission and that this modulation is altered in the spontaneously hypertensive rat.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed2002

Endothelin-induced modulation of neuropeptide Y and norepinephrine release from the rat mesenteric bed.

The effect of three endothelin (ET) agonists [ET-1, ET-3, and sarafotoxin (STX6C)] on the nerve stimulation-induced release of norepinephrine (NE) and neuropeptide Y-immunoreactive compounds (NPY-ir) from the perfused mesenteric arterial bed of the rat as well as the effect on perfusion pressure were examined. ET-1, ET-3, and STX6C all produced a significant, concentration-dependent decrease in the evoked release of NPY-ir but had no effect on the release of NE. In contrast, all three ETs potentiated the nerve stimulation-induced increase in perfusion pressure. The inhibition of nerve stimulation-induced NPY-ir release by ET-1 was significantly blocked by the ET(A)/ET(B) antagonist PD-142893 and the ET(B) antagonist RES-701-1 but not by the ET(A) antagonist BQ-123. The potentiation of the nerve stimulation-induced increase in perfusion pressure by ET-1 was significantly blocked by PD-142893 and BQ-123 and attenuated by RES-701-1. Prior exposure of the preparation to indomethacin or meclofenamate failed to alter the attenuation of the evoked release of NPY-ir or the potentiation of the increase in perfusion pressure produced by ET-1 or ET-3. These results are consistent with the idea that sympathetic cotransmitters can be preferentially modulated by paracrine mediators at the vascular neuroeffector junction.

Animals↗
PubMed1981

Release of acetylcholine in the isolated heart.

This article summarizes methods for studying release of acetylcholine (ACh) in the heart and reviews the literature on release, synthesis, and inactivation of ACh. Cholinergic mechanisms involved in cardiac neuroeffector transmission are, in principle, the same as in ganglia and motor endplates, but their relative functional significance exhibits unique features. First, release of ACh evoked by nerve stimulation is maintained at a high level due to rapid formation of free extracellular choline from phospholipids. Choline derived from ACh hydrolysis plays a minor role in ACh synthesis. The constant efflux of choline allows continuous monitoring of changes in formation and removal of extracellular choline, e.g., by activation of neuronal uptake during nerve stimulation. Second, ACh released from terminal nerve fibers is rapidly washed into the circulation and thereby escapes hydrolysis by cholinesterase activity to a functionally significant extent. Hydrolysis and diffusion appear as equally important mechanisms of transmitter inactivation in the heart. The cardiac neuroeffector junction is not a morphological or functional entity restricted to adjacent pre- and postsynaptic elements.

Acetylcholine↗
PubMed1985

Uptake and metabolism of norepinephrine by endothelium of dog pulmonary artery.

The contribution of endothelium of dog pulmonary artery to the extraneuronal metabolism of norepinephrine was determined. Pulmonary artery was cut into helical strips; the endothelium was removed from half of the strips by gently stroking them with a wooden applicator stick. All strips were immersed in l-[3H]norepinephrine (2 X 10(-7) M) and mounted for superfusion. Superfusate was collected continuously before, during, and after electrical stimulation (10 V, 2 ms, 2 Hz). Column chromatography was used to separate [3H]norepinephrine and its radiolabeled metabolites in superfusate. Quantitation was by liquid scintillation spectrometry. Previous studies have established that 3,4-dihydroxyphenylglycol is of neuronal origin and that O-methylated metabolites are of extraneuronal origin. Since cocaine prevented neuronal uptake of norepinephrine, the reduction in metabolites of norepinephrine of extraneuronal origin in arteries with endothelium removed represented the contribution of endothelium to extraneuronal metabolism. O-Methylated metabolites were decreased from 3.50 to 2.17 X 10(3) dpm/2 ml of superfusate during basal conditions preceding electrical stimulation and from 11.16 to 6.94 X 10(3) dpm/2 ml of superfusate during electrical stimulation when endothelium had been removed. Decreases in extraneuronal metabolite production continued throughout the basal periods following stimulation. These studies suggest that in small pulmonary artery a substantial amount of the total norepinephrine that is released at the neuroeffector junction may be metabolized following uptake into endothelium.

Animals↗
PubMed1990

Adrenergic denervation in rabbits with diabetes mellitus.

The influence of alloxan-induced diabetes mellitus on the sympathetic neuroeffector junction of the rabbit carotid artery denuded of endothelium was studied. Six weeks of diabetes resulted in a neuropathy characterized by a 38% reduction in the arterial content of norepinephrine. Norepinephrine release from the nerves measured from electrically stimulated superfused arterial segments was decreased. The cocaine-sensitive accumulation of [3H]-norepinephrine (NE) was also reduced, reflecting decreased neuronal uptake. The consequences of these prejunctional changes were studied by measuring isometric contractions of arterial rings caused by electrical nerve stimulation or by exogenous norepinephrine. Despite the reduced release of norepinephrine, neurogenic contractions were normal, suggesting an increased sensitivity of the smooth muscle. After neuronal uptake was blocked, the neurogenic contractions of diabetic arteries were less than normal, reflecting the reduction in transmitter release. The sensitivity of diabetic arteries to exogenous norepinephrine was increased under control conditions; maximal contractions were unchanged. Blockade of norepinephrine uptake increased norepinephrine sensitivity more in normal than in diabetic arteries, and there was no longer a significant difference in sensitivity. Thus, under control conditions, neurogenic contractions of the partially denervated diabetic rabbit carotid artery are paradoxically normalized by increased alpha-adrenergic sensitivity of the smooth muscle. The increased sensitivity caused by reduced neuronal uptake can thus preserve neurogenic vasoconstriction and cause supersensitivity to exogenous catecholamines in the sympathetic neuropathy caused by diabetes mellitus.

Adrenergic Fibers↗
PubMed1981

Bradykinin effects on adrenergic transmission in the canine kidney: relation to prostaglandins.

We studied the action(s) of bradykinin at the renal vascular neuroeffector junction, and its relation to prostaglandin synthesis, by investigating the effect of the peptide on the renal venous output of the neurotransmitter and on the renal vasoconstrictor responses elicited by sympathetic nerve stimulation and by norepinephrine in pentobarbital-anesthetized dogs. Renal arterial infusion of bradykinin at 10 ng . kg-1 . min-1 increased blood flow to the kidney and inhibited the vasoconstrictor effect of renal nerve stimulation (1-8 Hz) and injected norepinephrine (0.06-0.5 micrograms). However, bradykinin did not alter the rise in venous output of norepinephrine elicited by nerve stimulation. Infusion of another vasodilatory peptide, substance P (2 ng . kg-1 . min-1) into the renal artery also increased blood flow to the kidney but failed to alter the vasoconstriction produced by either adrenergic stimulus. Pretreatment of dogs with an inhibitor of prostaglandin synthesis, either sodium meclofenamate or indomethacin (5 mg/kg), abolished the inhibitory effect of the kinin on renal vasoconstriction produced by adrenergic stimuli. These data suggest that bradykinin acts on postjunctional sites to reduce adrenergically induced vasoconstriction in the canine kidney by a mechanism dependent on prostaglandin synthesis.

Animals↗
PubMed1990

Acetylcholinesterase inhibitor, pyridostigmine bromide, reduces skin blood flow in humans.

Five subjects exercised on a cycle ergometer for 30 min at 55% peak oxygen consumption on two occasions in an environmental test chamber (ambient temperature = 29 degrees C; dew point temperature = 10 degrees C). Pyridostigmine bromide (PYR), an acetylcholinesterase (AChE) inhibitor, was ingested (30 mg) approximately 150 min before one experiment, and no drug was administered during the other experiment (control). Red blood cell AChE inhibition averaged 40 (+/- 7)% during PYR treatment. Esophageal temperature (Tes), an eight site-derived mean skin temperature, forearm blood flow (FBF; venous occlusion plethysmography), skin blood flow (SkBF; laser-Doppler velocimetry), and metabolic rate (indirect calorimetry) were measured. SkBF decreased 37% after PYR treatment compared with control (P less than or equal to 0.05). The Tes threshold for initiation of cutaneous vasodilation was 36.8 (+/- 0.3) degrees C for the control treatment and 37.0 (+/- 0.3) degrees C for the PYR treatment (P less than or equal to 0.01). FBF was not significantly different between treatments, whereas heart rate was reduced by 7 and 9 beats/min during rest and exercise, respectively (P less than or equal to 0.01). The increased threshold for initiation of cutaneous vasodilation with AChE inhibition by PYR is compatible with nonthermal modulation of the control of thermoregulation through increased acetylcholine (ACh) accumulation. This could potentiate preganglionic transmission to enhance adrenergic vasoconstrictor tone. One suggested mechanism possible at the neuroeffector junction of the sweat gland may be that accumulated ACh diffusion across the adventitia of adjacent arterioles to muscarinic receptors initiates contraction of the smooth muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Relation of plasma norepinephrine and sympathetic traffic during hypotension in humans.

We compared changes in antecubital venous plasma levels of norepinephrine (NE) and peroneal nerve muscle sympathetic activity (MSA) during and after nitroprusside (NP)-induced hypotension in nine healthy volunteers. During NP, MSA increased at 98.7%/min, peaked at 4 min at 399 +/- 77% (SE) of base line, and then decreased, so that at the end of the infusion MSA was 298 +/- 39% of base line. NE increased at 9.2%/min and peaked at 14.5 min at 231 +/- 31% of base line just before the end of the infusion. Percent increases of MSA and NE near the end of NP were not significantly different. The time-to-peak NE lagged the time-to-peak MSA by nearly 10 min. These results suggest that during increases of sympathetic outflow diffusion and washout of NE from neuroeffector junctions result in delayed increases in NE in the venous drainage; percent changes in MSA and NE during prolonged stable mild hypotension are similar. The findings provide conditional support for the use of changes in NE to indicate changes in sympathetic traffic.

Adult↗
PubMed1995

Sympathetic vasoconstrictive responses to high- and low-sodium diets in diabetic and normal subjects.

Uncomplicated insulin-dependent diabetes mellitus (IDDM) is associated with a suppressed reflex response to sympathetic nervous system (SNS) stimulation and an enhanced pressor response to catecholamines. This study examined the SNS in subjects with IDDM (duration < 5 yr, n = 9) to determine the responsible mechanism within the cardiopulmonary baroreflex arc and the role played by extracellular fluid volume (ECFV) expansion. The reflex arc was tested by examining the plasma norepinephrine (PNE) and forearm vascular (FVR) responses to 60 min of cardiopulmonary baroreceptor unloading by lower body negative pressure (LBNP) at -15 mmHg. The effector limb was tested by measuring the PNE, FVR, and mean arterial pressure (MAP) response to the cold pressor test (CPT). The postganglionic neuroeffector junction was tested by measuring the venoconstrictive response to local norepinephrine infusion. ECFV was varied by altering dietary sodium. In IDDM subjects on a 250 mmol sodium diet, PNE and FVR responses to LBNP (delta PNE = 0.15 +/- 0.05; delta FVR = 4.3 +/- 1.2) were attenuated compared with controls (delta PNE = 0.36 +/- 0.23; delta FVR = 11.56 +/- 2.72). MAP and FVR responses to the CPT were intact (delta MAP = 9.74 +/- 1.9; delta FVR = 7.02 +/- 3.11) compared with controls (delta MAP = 10.74 +/- 2.69; delta FVR = 8.26 +/- 2.94), but the PNE response was attenuated. The peripheral vasculature was hyperresponsive to norepinephrine infusion in IDDM subjects [mean effective dose (ED50) = 57 +/- 10 ng/min] compared with controls (ED50 = 133 +/- 30 ng/min). Sodium restriction (20 mmol/day) normalized the FVR response to LBNP and the venous response to norepinephrine infusion. The PNE response both to LBNP and the CPT remained attenuated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Cholinesterase affects dynamic transduction properties from vagal stimulation to heart rate.

Recent investigations in our laboratory using a Gaussian white noise technique showed that the transfer function representing the dynamic properties of transduction from vagus nerve activity to heart rate had characteristics of a first-order low-pass filter. However, the physiological determinants of those characteristics remain to be elucidated. In this study, we stimulated the vagus nerve according to a Gaussian white noise pattern to estimate the transfer function from vagal stimulation to the heart rate response in anesthetized rabbits and examined how changes in acetylcholine kinetics affected the transfer function. We found that although increases in the mean frequency of vagal stimulation from 5 to 10 Hz did not change the characteristics of the transfer function, administration of neostigmine (30 microg . kg-1 . h-1 iv), a cholinesterase inhibitor, increased the dynamic gain from 8.19 +/- 3.66 to 11.7 +/- 4.88 beats . min-1 . Hz-1 (P < 0.05), decreased the corner frequency from 0.12 +/- 0.05 to 0.04 +/- 0.01 Hz (P < 0.01), and increased the lag time from 0.17 +/- 0.12 to 0.27 +/- 0.08 s (P < 0.05). These results suggest that the rate of acetylcholine degradation at the neuroeffector junction, rather than the amount of available acetylcholine, plays a key role in determining the dynamic properties of transduction from vagus nerve activity to heart rate.

Acetylcholine↗
PubMed1999

Neuronal uptake affects dynamic characteristics of heart rate response to sympathetic stimulation.

Recently, studies in our laboratory involving the use of a Gaussian white noise technique demonstrated that the transfer function from sympathetic stimulation frequency to heart rate (HR) response showed dynamic characteristics of a second-order low-pass filter. However, determinants for the characteristics remain to be established. We examined the effect of an increase in mean sympathetic stimulation frequency and that of a blockade of the neuronal uptake mechanism on the transfer function in anesthetized rabbits. We found that increasing mean sympathetic stimulation frequency from 1 to 4 Hz significantly (P < 0.01) decreased the dynamic gain of the transfer function without affecting other parameters, such as the natural frequency, lag time, or damping coefficient. In contrast, the administration of desipramine (0.3 mg/kg iv), a neuronal uptake blocking agent, significantly (P < 0.01) decreased both the dynamic gain and the natural frequency and prolonged the lag time. These results suggest that the removal rate of norepinephrine at the neuroeffector junction, rather than the amount of available norepinephrine, plays an important role in determining the low-pass filter characteristics of the HR response to sympathetic stimulation.

Adrenergic Uptake Inhibitors↗
PubMed2000

Norepinephrine reuptake, baroreflex dynamics, and arterial pressure variability in rats.

This study examined the effect of norepinephrine reuptake blockade with desipramine (DMI) on the spontaneous variability of the simultaneously recorded arterial pressure (AP) and renal sympathetic nerve activity (SNA) in conscious rats. Acute DMI administration (2 mg/kg iv) depressed AP Mayer waves ( approximately 0.4 Hz) and increased low-frequency (<0.2 Hz) components of AP variability. DMI decreased renal SNA variability, especially due to the abolition of oscillations related to Mayer waves. To examine whether DMI-induced changes in AP and renal SNA variabilities could be explained by alterations in the dynamic characteristics of the baroreceptor reflex loop, the frequency responses of mean AP to aortic depressor nerve stimulation were studied in urethan-anesthetized rats. DMI accentuated the low-pass filter properties of the transfer function without significantly altering the fixed time delay. The frequency responses of iliac vascular conductance to stimulation of the lumbar sympathetic chain were studied in an additional group of anesthetized rats. DMI did not markedly alter the low-pass filter properties of the transfer function and slightly increased the fixed time delay. These results suggest that the DMI-induced decrease in the dynamic gain of the baroreceptor reflex is responsible for the decreased spontaneous renal SNA variability and the accompanying increased AP variability. The "slowing down" of baroreflex responses cannot be attributed to an effect of DMI at the vascular neuroeffector junction.

Animals↗
PubMed1979

Anatomy of the juxtaglomerular apparatus.

The juxtaglomerular apparatus, located in the glomerular hilum, consists of a vascular component (afferent and efferent arterioles and extraglomerular mesangium) and a tubular component (macula densa). Two types of contact between vascular and tubular components are observed: a) a complex type, involving distal tubule, extraglomerular mesangium, and proximal efferent arteriole, and b) a simple type, consisting of apposition of the basement membranes of the vascular and tubular components. Juxtaglomerular granular cells, the source of renin, are present throughout the vascular component but are more numerous in the afferent arteriole. They can be considered as "myoendocrine" cells, since they contain myofibrils and attachment bodies, together with secretory granules and crystalline protogranules. Macula densa cells differ from those elsewhere in the distal tubule in that their nuclei are closer to each other, the Golgi apparatus is basally located, and their basal membrane infoldings are less prominent. Adrenergic nerves are demonstrable by fluorescence histochemistry in the juxtaglomerular region. Electron microscopy reveals unmyelinated nerve fibers containing small dense-cored vesicles and capable, as shown by ultrastructural autoradiography, of incorporating exogenous tritiated norepinephrine. Neuroeffector junctions occur between nerves and cells of the vascular and, less frequently, the tubular component. In addition, adrenergic axons are observed in a juxtaglomerular cell tumor. Nerve terminals are seen in direct contact with the tumor cells.

Acetylcholinesterase↗
PubMed1984

Inhibition by bradykinin of renal adrenergic effects in anesthetized rats.

We studied the contribution of prostaglandins to the actions of bradykinin at the renal vascular adrenergic neuroeffector junction by examining the effect of the peptide on the decrease in renal blood flow elicited by renal nerve stimulation and injected norepinephrine in pentobarbital-anesthetized rats with or without pretreatment with the cyclooxygenase inhibitors sodium meclofenamate or indomethacin. Infusion of bradykinin, 10 ng X kg-1 X min-1, into the renal artery reduced both the basal and the rise in renal vascular resistance produced by nerve stimulation or norepinephrine. The prostaglandin precursor arachidonic acid, 5 micrograms X kg-1 X min-1, infused into the renal artery, also reduced renal vascular resistance and the vasoconstrictor response elicited by either adrenergic stimulus. In animals pretreated with either sodium meclofenamate or indomethacin, the effect of arachidonic acid, but not that of bradykinin, to produce renal vasodilation and to attenuate adrenergically induced renal vasoconstriction was abolished. These data suggest that bradykinin produces renal vasodilation and inhibits the renal vasoconstrictor effect of adrenergic stimuli in the rat kidney in vivo by a mechanism unrelated to prostaglandin synthesis.

Acetylcholine↗
PubMed1997

Neural control of renal function.

The renal nerves are the communication link between the central nervous system and the kidney. In response to multiple peripheral and central inputs, efferent renal sympathetic nerve activity is altered so as to convey information to the major structural and functional components of the kidney, the vessels, glomeruli, and tubules, each of which is innervated. At the level of each of these individual components, information transfer occurs via interaction of the neurotransmitter released at the sympathetic nerve terminal-neuroeffector junction with specific postjunctional receptors coupled to defined intracellular signaling and effector systems. In response to normal physiological stimuli, changes in efferent renal sympathetic nerve activity contribute importantly to homeostatic regulation of renal blood flow, glomerular filtration rate, renal tubular epithelial cell solute and water transport, and hormonal release. Afferent input from sensory receptors located in the kidney participates in this reflex control system via renorenal reflexes that enable total renal function to be self-regulated and balanced between the two kidneys. In pathophysiological conditions, abnormal regulation of efferent renal sympathetic nerve activity contributes significantly to the associated abnormalities of renal function which, in turn, are of importance in the pathogenesis of the disease.

Animals↗