Intravesical pressure is considered an important factor in the formation of urine. It seems logical to believe that the back pressure can reduce urinary output by physical means, e.g. an increase of the intravesical pressure resulting in increased ureteral, intrapelvic and subsequently, intranephric pressure. However, in dogs with ureteral fistulas in which there was no mechanical connection between the bladder and the kidney. Lawson and Tomlinson (1951) observed the suppression of urine formation following bladder distension. Therefore, they suggested that some
other mechanism was involved, namely, a reflex oliguria due to increased vesical pressure. Tolls and Dille (1955) again clearly confirmed this phenomenon in dogs with no hydraulic connection between the kidney and bladder through which back pressure might be exerted. However, the relation between bladder pressure and urine formation has not been investigated. This investigation is undertaken to determine the reflex pathways from bladder to kidney and also the possibility of antidiuretic hormone involvement in this phenomenon.
A modification of the procedure of Tolls and Dille (1955) was used. Female dogs and male rabbits varying in body weight were weight were used. Aesthesia was induced by pentobarbital sodium. The trachea was cannulated and the carotid blood pressure recorded. The jugular vein was cannulated for continuous intravenous infusion of saline to maintain an adequate and constant urine flow. Both ureters were ligated near their entrance into the bladder and the proximal ureters were cannulated with polyethylene tubes inserted into either the ureters or the renal pelvis. The free ends of the tubing were exteriorized through stab wounds in each lower quadrant. The output of each kidney was recorded in drops per minute and
expressed as per cent change relative to those prior to bladder distension. The bladder was cannulated with a Foley catheter which was connected by a T-tube to an overhead reservoir containing warmed physiologic saline for changing the intravesical pressure. The side arm of the T-tube was connected to a mercury manometer of recording the intravesical pressure.
Left celiac ganglionectomy or denervation of the renal artery was performed in several animals. The celiac ganglion in the dog is paired. The left celiac ganglion was found on the ventral surface of the left renal artery. The renal minute blood volume was directly measured in syringes attached by way of a 3-way stopcock to a plastic tube which joined the renal to the femoral veins. The assay of antidiuretic hormone was performed by injecting blood or urine of the animal undergoing bladder distension into rabbits or puppies having ureteral cannulation. Indigo carmine was injected into the jugular vein and the color change of the kidney surface was compared by visual observation and color photography before and after distension of bladder. Various autonomic drugs and other agents which might affect to either bladder of kidney were applied. In five human volunteers both ureters were catheterized cystoscopically and the urine flow was measured before and after changing bladder pressure.
The reduction in urine flow commenced immediately after bladder distension and occurred only while the bladder was full. When the bladder was emptied the urine flow quickly increased and returned to its original level. The intravesical pressure was always fluctuant when bladder filling was stopped and the bladder was
kept distended at a level of 30mm,Hg. In sixteen animals with the renal pelvises cannulated the urine flow from the right and left was reduced to an average of 38.7% and 35.9% below control, respectively, when the urinary bladder was destended to a pressure level of 30mm Hg. This finding indicates that the rate of urine flow in both kidneys was fairly constant and the mean rate of reduction was 37.3%. It was found that more uniform rates of urinary reduction following distenssion of bladder could be obtained if the cannulas for collectiong urine were placed in the
renal pelvis. Distension of the bladder in two dogs with extraperitoneally exposed bladders also resulted in a similar suppression of urine flow. The blood pressure in these animals showed no change or a slight fall during bladder distension. In
five volunteers the urine flow after distending the bladder at a level of 25mm,Hg. was markedly reduced to an average of 87.0% and the blood pressure showed a slight increase during distension in these subjects.
Denervation of left artery completely abolished the response of urinary output due to bladder distension. However, the intact right kidney was not effected. The rate of urine flow from the denervated kidney was little or not changed by bladder distenstion whereas in the intact kidney it was reduced to on the average 48% of the control.
Similarily, left celiac ganglionectony again completely abolished the urinary response to bladder distension, namely, no urine suppression at all in comparison with an average reduction rate of 33 per cent prior to ganglionectomy. The urine flow was however seppressed to a much greater extent than normal in the intact right kidney following left ganhlionectomy, namely, from an average rate of 29.6 per cent to 66 per cent following bladder distension.
The renal blood flow measured directly from renal vein, which had been connected to femoral vein, showed a significant reduction on bladder distension, i.e. and average 44.7 per cent reduction from normal flow rate in normally innervated kidneys.
Again, the denervation of the renal artery of celiac ganglionectomy completely abolished the responses of both urinary output and renal blood flow to bladder distension.
When indigo carmine was injected into the jugular vein, the coloring of the cortical surface of the kidneys did not appear in animals with distended bladders while the dye stained the cortical surface diffusely in dogs and rabbits with undistended bladders while the dye .
The injection of 1 ml of either blood or urine, obtained from animals with distended bladders resulted in significant reduction of urinary output in the rabbit or puppy used to assay ADH activity.
When artopine, adrenaline, dibenzyline or serotonin were injection into the animals, the urinary reduction due to bladder distention was significantly enhaced. On the other hand, when pilocarpine or histamine were injected intravemously, there was no significant change in the urinary response following the distension of bladder. Neither the local application of 0.5% tetracaine to the bladder mucosa nor the intravenous administration of Hexamethonium had any effect in dogs on the
urinary response to bladder distension.
The above results lead us to the conclusion that the intravesical pressure may regulate the formation of urine through either short vesico-renal reflex, which has a major role, mediated by celiac ganglionic synapses and in part by the long
vesico-hypothalamic reflex which releases the antidiuretic hormone.