Changes in Renal Blood Flow During Renal Nerve Stimulation

Abstract

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...

The renal response to electrical stimulation of renal efferent sympathetic nerves in the anaesthetized greyhound.

“…Higher frequencies were not studied in the present investigation to demonstrate maximum changes in renal blood flow and glomerular filtration rate. Other groups have observed maximal reduction of renal blood flow at 10 Hz (DiSalvo & Fell, 1971;Hermansson, Larson, Kallskog & Wolgast, 1981;Osborn et al 1981).…”

Comparison of the effects of hepatic nerve stimulation on arterial flow, distribution of arterial and portal flows and blood content in the livers of anaesthetized cats and dogs

“…In cats, escape during sympathetic nerve stimulation is marked in the intestine (Folkow et al 1964a, b), intestinal lymph glands (Lundgren & Wallentin, 1964), kidney (Johansson, Sparks & Biber, 1970) and liver, less marked in the spleen (Greenway, Lawson & Stark, 1968) and absent in skeletal muscle (Mellander, 1960) and adipose tissue (Oberg & Rosell, 1967). In dogs, during sympathetic nerve stimulation, it is absent in the liver and appears to be absent in the kidney at low frequencies of stimulation (DiSalvo & Fell, 1971), but it occurs in the intestinal bed (G. Oshiro & C. V. Greenway, unpublished observations). It is not clear C. V. GREEN WAY AND G. OSHIRO whether the mechanism of this escape is the same in all vascular beds in which it occurs, but the reported responses are similar and some common mechanism appears likely.…”

Role of renal sympathetic nerves in mediating hypoperfusion of renal cortical microcirculation in experimental congestive heart failure and acute extracellular fluid volume depletion.

“…These conclusions, however, do not preclude the possibility that when the efferent neural tone is heightened above baseline level, it may profoundly influence renal circulatory dynamics. In fact, direct activation of renal nerves above baseline level induces an increase in renal vascular resistances proportional to the degree of nerve stimulation (4,(9)(10)(11)(12). Recent studies localized the effects of renal nerve stimulation to the pre-and postglomerular arterioles, where they cause constriction, as well as reduction in glomerular capillary ultrafiltration coefficient (4,13,14).…”