Alterations in Renal Hemodynamics and Function in Separate Kidneys During Stimulation of Renal Artery Nerves in Dogs

Houck, C. Riley

doi:10.1152/ajplegacy.1951.167.2.523

Cited by 42 publications

(13 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The sodium and chloride retaining effects of clonidine could be explained on the basis of increased oncotic pressure of the peritubular capillaries as has previously been described (19)(20)(21)(22)(23)(24) or to redistribution of blood flow from the outer salt wasting cortical nephrons into deeper corticomedullary salt retaining nephrons. Similar changes have been described with hemorrhage or stimulation of the renal nerves (25,26). Renal vasodilation leads to opposite effects (27).…”

Section: Bsupporting

confidence: 62%

Water Diuresis from Clonidine (Catapres)

Chrysanthakopoulos¹,

Lavender²

1975

Experimental Biology and Medicine

View full text Add to dashboard Cite

Available clinical and experimental evidence indicates that clonidine 2-2(2,6-di-ch1orophenylamino)-2 imidazoline hydrochloride, has potent hypotensive, bradycardic and bradypneic properties (1-6). It also produces sedation and local anesthesia, inhibits gastric acid secretion, and raises blood sugar (7). Its effect on blood pressure in the anesthetized dog is a bimodal one. An initial short rise is followed by a prolonged decrease. Similar observations have been reported in the rabbit, rat, and cat (8,9). Concerning the actions of clonidine upon renal hemodynamic and excretory functions, it was shown by Onesti et al. (6) that when the drug was given either orally or intravenously to dogs and man, it had no effect on the effective renal plasma flow, glomerular filtration rate, and potassium excretion, while it decreased the excretion of sodium and chloride. The pathophysiologic mechanism by which clonidine exerts its renal effects has not as yet been elucidated. The purpose of this study, therefore, was to attempt to clarify if clonidine has any direct renal effect by infusing the drug in small amounts into the renal artery of one kidney of the anesthetized dog and comparing its effects against the other kidney without disturbing systemic hemodynamics. In a second group of animals the drug was given intravenously in order to study the systemic effects and significance of a different route of administration.Materials and methods. Sixteen well-conditioned dogs of both sexes weighing 22-25 kg were used in this study. The animals were anesthetized with sodium pentobarbital (30 mg/kg) and kept lightly anesthetized for the whole length of the experiments. All the animals were intubated and ventilated with room air. The jugular vein and the external carotid artery were exposed and catheterized with polyethylene tubing for con-tinuous infusion and monitoring of the blood pressure, respectively. The dogs were primed with a solution containing inulin and paraaminohippuric acid (PAH) in isosmotic saline. Thereafter the dogs were maintained with a sustaining solution of similar composition but different concentration administered at a rate of 6.0 ml/min, in order to maintain the dog's blood levels of inulin and PAH at 25-30 mg% and 2-4 mg%, respectively.A mercury manometer was connected to the external carotid artery for continuous monitoring of the blood pressure and blood sampling from a manifold. Both ureters were exposed through a midline incision and catheterized with polyethylene tubing for continuous urine collection into graduated cylinders. In 10 dogs (Group 1) the right renal artery was exposed through a left flank incision and cannulated through the abdominal aorta with an 18-gauge Rochester needle for infusion of the drug. In six dogs (Group 2) the drug was given intravenously. The experiments in both groups were divided into a control and experimental period. The control period consisted of four urine collections 20 min each and the experimental period of six collections 20 min each also. Blood for clearances of...

show abstract

Section: Bsupporting

confidence: 62%

Water Diuresis from Clonidine (Catapres)

Chrysanthakopoulos¹,

Lavender²

1975

Experimental Biology and Medicine

View full text Add to dashboard Cite

show abstract

“…Therefore, the action of the reflexly activated renal sympathetic fibres remains obscure. There are no reports of renal vasodilator fibres; in fact, electrical stimulation of renal nerves is reported to produce vasoconstriction (Houck, 1951;Block, Wakim & Mann, 1952). It is possible that the sympathetic fibres excited by this reflex subserve other renal mechanisms concerned with secretion, or absorption, both of which are reported to be modified by electrical stimulation of renal nerves (Houck, 1951;Block et al 1952;Study & Shipley, 1950).…”

Section: Discussionmentioning

confidence: 99%

Renal receptors evoking a spinal vasometer reflex

Beacham¹,

Kunze²

1969

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. Certain afferent fibres in the renal nerves show an increased rate of discharge in response to small increases in renal vein pressure and to substantial increases of ureteral pressure. Such fibres enter the spinal cord largely through the upper lumbar dorsal roots.2. In spinal cats, stimuli exciting these afferent fibres evoke a reflex discharge in sympathetic nerves to the kidney and a fall in systemic arterial pressure. Change in flow or peripheral resistance, independent of arterial pressure, could not be demonstrated for the renal vascular bed. In spite of a lack of evidence for a renal vasomotor effect, the existence of the reflex fall in arterial pressure following excitation of receptors sensitive to venous pressure strongly implies that there is a form of circulatory regulation at the spinal cord level.

show abstract

“…The effects of direct renal nerve stimulation (RNS) on renal tilood flow (RBF) have been studied by a number of investigators (1)(2)(3). However, most studies involved indirect measurements of RBF by clearance techniques which (a) limit measurements to steady state conditions, and (b) require arterial and renal venous blood samples so that repeated measurements in the same animal could result in modest decreases of circulating blood volume.…”

mentioning

confidence: 99%

Changes in Renal Blood Flow During Renal Nerve Stimulation

DiSalvo

Fell

1971

Experimental Biology and Medicine

View full text Add to dashboard Cite

The effects of direct renal nerve stimulation (RNS) on renal tilood flow (RBF) have been studied by a number of investigators (1-3). However, most studies involved indirect measurements of RBF by clearance techniques which (a) limit measurements to steady state conditions, and (b) require arterial and renal venous blood samples so that repeated measurements in the same animal could result in modest decreases of circulating blood volume. Although excellent direct methods for measuring RBF are available (4), such procedures do not permit facile and accurate examination of RBF changes during commencement, maintenance, and cessation of RNS.In the present study, RBF changes during direct RNS were measured with an electromagnetic flowmeter. This technique permits examination of transient and sustained flow changes during RNS over a wide range of frequencies in the presence and absence of autonomic blocking drugs. The results show that extent of renal vasoconstriction is directly proportional to frequency of RNS a t frequencies between 1 and 10 cycles per second (cps), maximal a t 10 cps, and inversely proportional to frequency at frequencies greater than 10 cps. They also show that RBF returns to control flow levels during continued RNS at frequencies above 10 cps. Renal vasoconstrictor responses during RNS appear to be due to activation of alpha-adrenergic receptors, while beta-adrenergic and cholenergic receptors do not seem to be involved. NO evidence for extrinsic renal vasodilator innervation was obtained. Methods.Experiments were performed in 20 mongrel dogs (15-20 kg), of either sex, anesthetized with sodium pentobarbital (30 mg/kg, iv 30-60 min. following subcutaneous injection of morphine sulfate (3 mg/kg). Each animal breathed spontaneously throughout the experiment. Central arterial and venous pressures were continuously monitored through catheters inserted into the right femoral artery and vein and advanced centrally until their tips were close to the heart. The catheters were attached to Statham P23AC pressure transducers which were connected to a Grass Model 5 polygraph.The left renal artery was exposed through a retroperitoneal incision. RBF was measured with a noncannulating electromagnetic flow sensor (Statham-Medicon) of the gated sine wave type. Zero flow base line was determined at the beginning of each experiment and checked at the termination of the experiment by occluding the artery distal to the flow sensor.The renal nerves were isolated and tied with two silk ligatures. The nerve bundle was severed between the ligatures, kept warm and moist, and the peripheral end was stimulated with platinum electrodes. Square wave stimuli of 2-msec duration and variable frequencies (1-200 cps) were delivered from a Grass SD 5 stimulator. In each experiment, voltage (15-30 V ) was adjusted until a maximal response occurred at 10 cps. The duration of each stimulus trial (20-30 sec), and elapsed time between trials (1-2 min) was constant in each experiment.Autonomic blocking drugs, dissolved in saline, were inje...

show abstract

Alterations in Renal Hemodynamics and Function in Separate Kidneys During Stimulation of Renal Artery Nerves in Dogs

Cited by 42 publications

References 0 publications

Water Diuresis from Clonidine (Catapres)

Water Diuresis from Clonidine (Catapres)

Renal receptors evoking a spinal vasometer reflex

Changes in Renal Blood Flow During Renal Nerve Stimulation

Contact Info

Product

Resources

About