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.

Basal norepinephrine overflow into the renal vein: effect of renal nerve stimulation

1980 ◽  
Vol 239 (4) ◽  
pp. F371-F377 ◽  
Author(s):  
Juan A. Oliver ◽  
John Pinto ◽  
Robert R. Sciacca ◽  
Paul J. Cannon
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Nerve Stimulation ◽  
Renal Vein ◽  
Renal Nerves ◽  
Plasma Norepinephrine ◽  
Renal Nerve ◽  
Sympathetic Nervous ◽  
Renal Nerve Stimulation ◽  
Renal Sympathetic

In order to determine whether the fraction of norepinephrine released from the renal nerves that escapes into the circulation can be used an an index of renal sympathetic nervous activity, arterial and renal vein plasma norepinephrine concentrations were measured by a radioenzymatic technique along with renal blood flow in anesthetized dogs under control conditions and during electrical renal nerve stimulation. In 25 animais studied under conditions of normal sodium balance, plasma norepinephrine in the renal vein, 198 ± 26 pg/ml, was significantly higher than in arterial blood, 102 ± 10 pg/ml (P < 0.001). In five dogs, electrical stimulation of the renal nerves (12 V, 3 ms) at frequencies of 0.5, 2,6, 12, and 18 Hz for 1 min was associated with increased norepinephrine concentration in renal venous plasma and an increase in the calculated renal norepinephrine overflow. There was a significant linear relationship between the frequency of stimulation and norepinephrine overflow into the renal vein in each animal, but there was also a significant interanimal variation in the slope of this relationship (P <0.01). Electrical stimulation at a frequency of 2 Hz significantly decreased renal blood flow (-24 ± 7 ml/min, P < 0.01). The maximal effect was achieved at 6 Hz (-66 ± 11 ml/min). The data indicate that there is a base-line overflow of norepinephrine into the renal venous blood of the dog that increases with increasing frequency of electrical nerve stimulation. They suggest that measurements of norepinephrine overflow into the renal vein may be used to assess the activity of the renal sympathetic nervous system. renal blood flow; catecholamines; renin; dog Submitted on January 10, 1980 Accepted on April 29, 1980

Influence of sodium intake on catecholamine release by angiotensin and renal nerve stimulation in dogs

1980 ◽  
Vol 58 (9) ◽  
pp. 1092-1101 ◽  
Author(s):  
Serge Carrière ◽  
Jean Cardinal ◽  
Christian Le Grimellec
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Nerve Stimulation ◽  
Sodium Intake ◽  
Regional Blood Flow ◽  
Blood Flow Rate ◽  
Renal Nerve ◽  
Salt Diet ◽  
Renal Nerve Stimulation ◽  
Total Renal Blood Flow

For 10 days, dogs were fed a normal salt diet containing 70 mequiv. Na+/day (NSD) followed by a high salt diet containing 170 mequiv. Na+/day (HSD) or 240 mequiv. Na+/day (VHSD), or the order was reversed. K+ in these diets was fixed at 40 mequiv./day. The different diets did not influence the basal level of serum catecholamines (CA). Intravenous angiotensin II (ATII) in subpressor doses produced, under NSD and HSD, an increase in serum CA accompanied by reductions in total renal blood flow as well as regional blood flow rates (microspheres), mostly in the deeper regions of the cortex. Under VHSD, ATII did not affect serum CA and barely decreased total renal blood flow, reducing regional blood flow rate in C3 and C4 only. The increase in renal vein serum CA produced by renal nerve stimulation was potentiated by ATII but under constant plasma levels of the latter, progressive increments of Na+ in the diet markedly exaggerated the liberation of CA following renal nerve stimulation and the hemodynamic response of the kidney. We conclude that the Na+ content in the diet markedly influences the increase in serum CA after renal nerve stimulation and greatly influences the response of that organ to renal nerve stimulation.

Renal neuroadrenergic transmission

1975 ◽  
Vol 229 (1) ◽  
pp. 60-65 ◽  
Author(s):  
GL Slick ◽  
AJ Aguilera ◽  
EJ Zambraski ◽  
GF DiBona ◽  
GJ Kaloyanides
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Nerve Stimulation ◽  
Sodium Excretion ◽  
Sympathetic Nerves ◽  
Adrenergic Blockade ◽  
Renal Nerve ◽  
Group I ◽  
Renal Nerve Stimulation ◽  
Renal Sympathetic

To study the role of the renal sympathetic nerves in the regulation of sodium excretion, we examined the renal functional response to left renal nerve stimulation before (group I) and after (group II) left renal adrenergic blockade with guanethidine. In group I dogs, absolute sodium excretion from the left kidney fell markedly after left renal nerve stimulation; the decreases in glomerular filtration rate and renal blood flow were of a similar magnitude. Using the radiolabeled microsphere technique, distribution of renal blood flow to the outer cortex was diminished after left renal nerve stimulation. In group II dogs, guanethidine blocked all of these effects of left renal nerve stimulation. In group iii studies, a low level of left renal nerve stimulation was used which resulted in a decrease in sodium excretion in the absence of changes in glomerular filtration rate, renal blood flow, or intrarenal distribution of blood flow; this effect was blocked by renal adrenergic blockade with guanethidine in group iv studies. These data support a role for the renal sympathetic nerves to directly influence renal tubular sodium transport in the absence of alterations in renal hemodynamics.

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