Continuous measurement of renal blood flow changes to renal nerve stimulation and intra-arterial drug administration in the rat

1978 ◽  
Vol 234 (2) ◽  
pp. H219-H222 ◽  
Author(s):  
G. D. Fink ◽  
M. J. Brody
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Renal Artery ◽  
Nerve Stimulation ◽  
Continuous Measurement ◽  
Renal Nerve ◽  
Renal Nerve Stimulation ◽  
Renal Vascular ◽  
Flow Circuit ◽  
Stimulation Of

A method is described for continuous measurement of renal blood flow in the anesthetized rat without dissection of the renal artery. Blood flow and arterial pressure were measured in an extracorporeal flow circuit between the carotid artery and an aortic pouch from which the left renal artery was the only outlet. Injection into the flow circuit allowed delivery of drugs directly into the arterial blood supply of the kidney. Electrical stimulation of undamaged periarterial renal kidney. Electrical stimulation of undamaged periarterial renal nerves was possible since the renal artery remained undisturbed. Extracorporeal autoperfusion of the rat kidney produced renal flow and resistance measurements that did not differ from those obtained with a flow probe placed directly on the renal artery. Renal nerve stimulation was found to cause renal vasoconstriction due to activation of alpha-adrenergic receptors by norepinephrine released from postganglionic sympathetic neurons. Renal vascular responses to a variety of intra-arterial vasoactive agents were also determined. The method described here allows the evaluation of renal vascular control in the variety of disease states for which suitable rat models have been developed.

Differentiated sympathetic neural control of the kidney

1996 ◽  
Vol 271 (1) ◽  
pp. R84-R90 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin ◽  
S. Y. Jones
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Nerve Stimulation ◽  
Nerve Fibers ◽  
Urinary Flow ◽  
Renal Nerve ◽  
Renal Vasoconstriction ◽  
Central Chemoreceptors ◽  
Renal Nerve Stimulation ◽  
Stimulation Of

Anatomic and neurophysiological methods were used to identify functionally specific subgroups of renal sympathetic nerve fibers. The distribution of diameters of the predominating unmyelinated fibers showed a major mode at 1.1 microns and a minor mode at 1.6 microns. The conduction velocity was 2.10 +/- 0.10 m/s, consistent with unmyelinated C fibers. Analysis of strength-duration relationships during renal nerve stimulation showed that both rheobase and chronaxie values for renal blood flow were greater than those for urinary flow rate and were independent of stimulation frequency. This difference suggests a higher stimulation threshold (smaller diameter) for those renal nerve fibers involved in the renal blood flow response (renal vasoconstriction) compared with those for the urinary flow rate response (antidiuresis) to renal nerve stimulation. Single renal units that responded to preganglionic splanchnic nerve stimulation were studied. Those with spontaneous activity (88%) responded to stimulation of arterial baroreceptors, arterial and central chemoreceptors, and peripheral thermoreceptors, whereas those that lacked spontaneous activity (12%) responded only to stimulation of peripheral thermoreceptors (known to produce renal vasoconstriction). A minority population of single renal units has been identified that, although renal vasoconstrictor, does not exhibit other characteristic features of vasoconstrictor neurons (i.e., responsiveness to stimulation of arterial baroreceptors and arterial and central chemoreceptors). These findings suggest the existence of functionally specific subgroups of renal nerve fibers.

Attenuation by prostaglandins of adrenergically induced renal vasoconstriction in anesthetized rats

1984 ◽  
Vol 246 (2) ◽  
pp. R228-R235
Author(s):  
K. Inokuchi ◽  
K. U. Malik
Keyword(s):  
Arachidonic Acid ◽  
Renal Artery ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Renal Vascular Resistance ◽  
Cyclooxygenase Inhibitor ◽  
Renal Nerve ◽  
Vasoconstrictor Response ◽  
Renal Nerve Stimulation ◽  
Renal Vascular

We have investigated the role of prostaglandins (PG) in the modulation of adrenergic neuroeffector events by examining the effect of PGI2 and PGE2 and their precursor, arachidonic acid, on the decrease in renal blood flow elicited by renal nerve stimulation or by injected norepinephrine in pentobarbital-anesthetized rats, with or without pretreatment with the cyclooxygenase inhibitor, sodium meclofenamate. Administration of PGI2 or PGE2 (0.4 micrograms X kg-1 X min-1) or arachidonic acid (5 micrograms X kg-1 X min-1) into the renal artery reduced vascular resistance and inhibited the vasoconstrictor response elicited by renal nerve stimulation or by injected norepinephrine. In contrast, administration of sodium meclofenamate (10 mg/kg iv + 30 micrograms X kg-1 X min-1) into the renal artery increased renal vascular resistance and enhanced the renal vasoconstrictor response to both adrenergic stimuli. In animals pretreated with the cyclooxygenase inhibitor, the ability of arachidonic acid, but not that of either PGE2 or PGI2, to reduce renal vascular resistance and the vasoconstrictor response to either nerve stimulation or injected norepinephrine was abolished. These data indicate that one or more prostaglandins, probably PGE2 or PGI2, formed in the kidney reduce renal vascular tone by their direct action on the vascular smooth muscle and by attenuating the influence of adrenergic stimuli on renal vasculature.

Specificity of Blockade of Renal Renin Release by Propranolol in the Cat

1974 ◽  
Vol 47 (4) ◽  
pp. 331-343
Author(s):  
E. J. Johns ◽  
Bertha Singer
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Nerve Stimulation ◽  
Direct Action ◽  
Renin Release ◽  
Racemic Mixture ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Renal Nerve Stimulation ◽  
Renal Artery Constriction

1. The anaesthetized cat, unilaterally nephrectomized and with renal nerves sectioned, has been used in a study of the specificity of the inhibitory effect of propranolol on renin release. 2. The effect of (+)-propranolol on the rise in plasma renin activity (PRA) induced by renal nerve stimulation has been examined. When administered at approximately the same dose as the racemic mixture which blocks renin release in response to this stimulus, (+)-propranolol did not significantly reduce the magnitude of the response. Therefore the action of racemic propranolol in blocking the response to neural stimulation can be attributed to the (−)-isomer. 3. Renal artery constriction, producing blood flow changes similar to those resulting from renal nerve stimulation, also induces a rise in PRA. (±)-Propranolol, in amounts which block the rise in PRA observed with renal nerve stimulation, did not prevent the increase seen with renal artery constriction. 4. Reduction of renal perfusion pressure within the autoregulatory range for 20 min resulted in a rise in PRA in all experiments. (±)-Propranolol did not significantly affect the response. 5. It is concluded that the release of renin in response to renal nerve stimulation cannot be attributed to associated changes in renal blood flow. The evidence is compatible with a direct action of the neurotransmitter on renin-containing cells via a β-adrenergic receptor. When renin release is induced by non-adrenergic mechanisms propranolol blockade has no significant effect on the response.

Renal afferent input to the ventrolateral medulla of the cat

1992 ◽  
Vol 263 (2) ◽  
pp. R412-R422 ◽  
Author(s):  
M. A. Vizzard ◽  
A. Standish ◽  
W. S. Ammons
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Conditioning Stimulus ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Renal Nerves ◽  
Renal Nerve ◽  
C Fibers ◽  
Renal Nerve Stimulation ◽  
Stimulation Of

Experiments were performed to determine if information from the kidneys projects to the rostral ventrolateral medulla. Extracellular action potentials were recorded from 148 cells within the rostral ventrolateral medulla of alpha-chloralose-anesthetized cats. Cells within the rostral ventrolateral medulla were tested for responses to electrical stimulation of both left and right renal nerves. Electrical stimulation of renal nerves excited 144 cells (97.3%) and inhibited 4. The majority of cells received either bilateral or contralateral renal nerve input. Cells with bilateral renal nerve input responded to contralateral renal nerve stimulation with a significantly greater number of impulses compared with ipsilateral renal nerve stimulation (P less than 0.05). All cells but one responding to renal nerve stimulation had convergent somatic input. Comparisons between thresholds for cell responses and activation thresholds for the A and C volleys of the compound action potential recorded in the least splanchnic nerve revealed that 44 cells required activation of A delta-fibers, and 12 cells required activation of both A delta- and C-fibers. A conditioning stimulus applied to renal nerves on one side significantly decreased the response elicited by a test stimulus applied to the renal nerves on the opposite side for at least 300 ms (P less than 0.05). The demonstration that an afferent connection exists between the kidneys and the ventrolateral medulla suggests that the rostral ventrolateral medulla may play a role in mediating supraspinal reflexes of renal origin.

Inhibition by bradykinin of renal adrenergic effects in anesthetized rats

1984 ◽  
Vol 246 (4) ◽  
pp. F387-F394
Author(s):  
K. Inokuchi ◽  
K. U. Malik
Keyword(s):  
Arachidonic Acid ◽  
Renal Artery ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Rat Kidney ◽  
Renal Vascular Resistance ◽  
Cyclooxygenase Inhibitors ◽  
Renal Nerve ◽  
Anesthetized Rats ◽  
Renal Vascular

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.

Differential Efect of Noradrenaline and Renal Nerve Stimulation on Vascular Resistance in the Dog Kidney and the Release of a Prostaglandin E-Like Substance

1972 ◽  
Vol 42 (2) ◽  
pp. 223-233 ◽  
Author(s):  
J. C. McGiff ◽  
K. Crowshaw ◽  
N. A. Terragno ◽  
K. U. Malik ◽  
A. J. Lonigro
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Nerve Stimulation ◽  
Venous Blood ◽  
Urine Flow ◽  
Rapid Recovery ◽  
Prostaglandin E ◽  
Early Recovery ◽  
Renal Nerve ◽  
Renal Nerve Stimulation

1. The concentrations of prostaglandin E(PGE)- and prostaglandin F(PGF)-like substances in renal venous blood were determined by parallel bioassay of extracts of renal venous effluent before and during adrenergic stimulation of the kidney and were related to simultaneous measurements of renal blood flow and urine flow. 2. When noradrenaline was infused continuously into the renal artery, its initial vasoconstrictor and antidiuretic effects diminished on seven of eight occasions in six dogs. Rapid recovery of renal blood flow and urine flow was invariably associated with increasing concentration in renal venous blood of a substance having the physicochemical, chromatographic and biological properties of a prostaglandin of the E series. In the one instance when rapid early recovery of renal blood flow was not observed the concentration of PGE-like substance was not increased. 3. In contrast, during renal nerve stimulation early rapid recovery of renal blood flow and urine flow did not occur and the concentration of a PGE-like substance in renal venous blood did not increase. The concentration of a PGF-like substance in renal venous effluent did not increase in response to either stimulus. 4. Since PGE2, unlike PGF2α, is a potent renal vasodilator and diuretic, the intrarenal release of this substance by noradrenaline in concentrations similar to those determined for a PGE-like substance (>0·50 ng/ml assayed as PGE2 equivalents) would account for the changes in renal blood flow and urine flow in these experiments when the renal actions of noradrenaline were attenuated. 5. These results support the proposal that renal prostaglandins function in an intrarenal negative feedback control system which regulates antidiuretic and vasoconstrictor systems.

Electrophysiological characteristics of primate spinothalamic neurons with renal and somatic inputs

1989 ◽  
Vol 61 (6) ◽  
pp. 1121-1130 ◽  
Author(s):  
W. S. Ammons
Keyword(s):  
Nerve Stimulation ◽  
Receptive Fields ◽  
High Threshold ◽  
Spinothalamic Tract ◽  
Renal Nerve ◽  
C Fibers ◽  
Afferent Fibers ◽  
Renal Nerve Stimulation ◽  
Somatic Receptive Fields ◽  
Stimulation Of

1. Spinothalamic tract (STT) neurons in the T10-L3 segments were studied for responses to renal and somatic stimuli. A total of 90 neurons was studied in 25 alpha-chloralose anesthetized monkeys (Macaca fascicularis). All neurons were antidromically activated from the ventral posterior lateral nucleus of the thalamus. 2. Sixty-two cells were excited by renal nerve stimulation and six inhibited. Probability of locating cells with renal input was greatest in T11-L1. Cells were located in laminae I and IV-VII; however, most were located in laminae V-VII. Antidromic latencies averaged 4.61 +/- 0.32 (SE) ms, whereas antidromic conduction velocities averaged 43.23 +/- 9.03 m/s. 3. Cells with excitatory renal input received A delta input only (36 cells) or A delta- and C-fiber inputs (26 cells). Stimulation of A delta renal afferent fibers evoked bursts of 1-10 spikes/stimulus [mean 3.6 +/- 0.9 spikes/stimulus] with onset latencies of 10.7 +/- 0.5 ms. Stimulation of C-fibers evoked 1.3 +/- 0.5 spikes/stimulus with onset latencies of 61.7 +/- 11.1 ms. Magnitude of responses to A delta-fiber stimulation was greatest in T12 and decreased both rostrally and caudally. Inhibitory responses to renal nerve stimulation required activation of renal C-fibers. 4. All cells that responded to stimulation of renal afferent fibers received convergent inputs from somatic structures. Forty-four cells were classified as wide dynamic range, 10 were high threshold, 12 were high-threshold cells with inhibitory input from hair, 2 were deep, and 2 were low threshold. Somatic receptive fields were large and located on the flank and abdomen and/or the upper hindlimb. Fourteen cells had inhibitory receptive fields located on the contralateral hindlimb or one of the forearms. 5. It is concluded that T11-L1 STT cells in the monkey respond reliably to renal nerve stimulation. Thoracolumbar STT cells may thus play a role in pain that results from renal disease. The locations of the somatic receptive fields of the cells suggest that they are responsible for the referral of renal pain to the flank and abdomen.

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