It has been widely known that the stimulation of the proximal end of the vagal nerve is followed by circulatory and respiratory reflexes. On the other hand, it has been suggested that reflexes to the coronary vessels from the visceral organs such as stomach, gallbladder and from the carotid sinus are carried through the cervical vagal nerve. In the persent paper, changes in coronary blood flow by the stimulation of the proximal end of the vagal nerve are reported.Coronary blood flow was measured by rotameter, in anesthetized (with sodium thiopental, 0.03-0.05g/kg intravenously) open-chest dogs weighing 10-15 kg. As shown in Fig. 1 (A), a speically designed cannula (Fig. 1 (B)) was inserted into the ostium of the left coronary artery, thus, a self-perfusing system to the left coronary artery from the right femoral artery was established. A typical calibration curve with rotameter was shown in Fig. 2. The calculated coronary vascular resistance was led from the relationship CVR=(BP)^^^-/CBF, where CVR represents coronary vascular resistance, (BP)^^^-, means blood pressure and CBF, coronary blood flow. The electrical stimulation of the nerve was carried out with spyky wave produced by thyratron. It was continued for 10-15 seconds with frequency of 15-30 cycles per second and intensity of 0.5-30 volts.

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Previous experiments by maekawa and his coworkers showed that "dialyzed Kidney-ATPase" had a marked pressor effect when injected intravenously in rabbits and dogs, and it supported Maekawa's postulation that the disturbance of the ATP-ATPase system is the real cause of hypertension.In this experiment, the pressor effect of repeated intravenous injections of this material and the influence on the kidney and cardiovascular system were further investigated in dogs.Six adult mongrel dogs of 8 to 18 kg. body weight, one male and 5 female, were used. Two of them died after the first injeciton of dialyzed Kidney-ATPase. Remaining 4 dogs were treated daily or every other day with intravenous injection of 20 to 90c.c. dialyzed Kidney-ATPase for 9 to 25 days.Mean blood pressure was occasionally measured by a mercury manometer on the femoral artery immediately before and after injection. In two dogs PAH and sodium thiosulfate clearance were performed before and after injection of this material. In the two died animals, autopsy was performed on the following day. Remaining four dogs were killed by bleeding for autopsy after experiment. The tissues selected for microscopic examination were lung, heart, liver, spleen, kidney and intestine. These tissues were fixed in 10% formalin soluiton, embedded in paraffin and stained with hematoxylin-eosin and, moreover, the heart with Weigert-VanGieson stain.The results were as follows : 1. Blood pressure rose after each injection of dialyzed Kidney-ATPase. Elevation of the mean pressure was 20 to 60 mm.Hg, and it did not decrease by repeated injections so far as the activity of the dialyzed Kidney-ATPase was not abolished.2. RPF and GFR decreased markedly immediately after injection of this material and thereafter improved grdually.3. Two dogs died after the first injection of 25 and 60 cc. of dialyzed Kidney-ATPase showed a conspicuous hemorrhage in the lungs and less severe in the heart muscles and kidneys.4. In four dogs treated with repeated intravenous injections of dialyzed Kidney-ATPase, the most remarkable histological changes were found in the kidney and heart. In the kidney thickened degenerated wall of the arterioles and the small arteries and cell infiltration around the afferent arterioles were most conspicuous. Degeneration of the glomeruli, thickening of the glomerular capsules, inclusion of hyaline substance in the glomerular space and slight degeneration of the tubuli were found occasionally. In the heart thickening and cell infiltration of arteriolar wall, intimal and medial thickening of the arteries with degeneration were observed.It is concluded that repeated injection of dialyzed Kidney-ATPase has a pressor effect in dogs and that they seem to induce the fragility or the degenerative changes of arterial and arteriolar walls.

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It is conceivable that the cardiac nerve has some influence on the metabolism of myocardium. In the study of the nervous control of the coronary circulation, recently it has been stressed that the secondary alteration of the coronary flow due to the change of the metabolism of the myocardium by the cardiac nerve has to be taken into consideration.Using the method of coronary sinus catheterization established by Goodale, the author studied the influence of the stimulation of cardiac nerve on the coronary arteriovenous difference of the concentration of oxygen, carbon dioxide, pyruvic acid, lactic acid and glucose in the naturally pulsating heart of the dog.Method : Coronary sinus catheterization was performed in normal anaesthetized dog. Peripheral part of the cut vagus nerve and stellate ganglion were stimulated electrically for 10 minutes. The blood sample was taken from the coronary sinus and from the femoral artery before and during the stimulation and the arterio-venous difference of the concentartion of each substance was studied.Result : 1) By the stimulation of the vagus nerve, coronary arterio-venous difference of oxygen and lactic acid decreased, that of glucose increase while that of carbon dioxide and pyruvic acid showed no definite tendency.2) By the stimulation of the sympathetic nerve, coronary arterio-venous difference of oxygen, carbon dioxide and lactic acid increased and that of pyruvic acid and glucose showed no tendency.According to Fick's principle, the consumption of the substance by the myoacardium is difined by multipling the coronary arterio-venous difference by coronary flow. It is shown that the coronary flow increases by the sympathetic stimulation and decreases by the vagal stimulation. From the result obtained the author reached the following conclusions.1) By vagal stimulation, the consumption of the oxygen and lactic acid decreses, the utilization of glucose increases and the anaerobic declination of the gaseous metabolism was observed.2) By sympathetic stimulation, the consumption of oxygen and lactic acid increaes and the aerobic declination of the gaseous metabolism was observed.

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The relationship of the adrenal cortex to hypertension has been the subject of a great amount of works and speculations experimentaly and clinically. In spite of an enormous maount of data that have accumulated, this relationship is by no means clear at the present time. From such a point of view, the author has attempted experiments to investigate the relationship between hypertension and adrenal cortex. The present study is to describe the histologic and histochemical responses occurring in the adrenal cortex of animals with hypertension which was produced by various kinds of method as follows : 1) section of the buffer nerves, 2) constriction of renal arteries or encapsulation of the kidney, 3) administration of salt, and 4) injection of desoxy-corticosterone acetate. The determination of 17-ketosteroids in urine was also performed in all experimental hypertensive animals.THE HISTOCHEMICAL METHOD OF STUDY ON THE ADRENAL CORTICAL FUNCTIONS The author applied H. W. Deane's method to detect ketosteroids in the adrenal cortex (Sudan III staining, Schiff's reaction, Schultz reaction, birefringence and aceton solubility).EXPERIMENTAL HYPERTENSION DUE TO DENERATION OF PRESSORECEPTORS The author performed the histologic and histochemical study of the adrenal cortex, determination of 17-ketosteroids in urine to investigate the relationship between experimental hypertension due to denervation of pressoreceptors and the drenal cortex. Ten adult dogs 8.0-16.0 kg. weight, were used in this experiment, and hypertension were produced by cutting the both sides of aortic and carotid sinus nerves according to Hering's method. In the course of experiment, the author clinically investigated body weight, urive volume, blood pressure, histamine test, blood sugar and 17-ketosteroids excretion in urine.After the animals were sacrificed, the author performed the histologic and histochemical examinations of the adrenal cortex. The summary and conclusion of this study are as follows : Section of buffer nerves was followed by hypertrophy and hyperplasia of cells and an appearance of small ketosteroid droplets in zona glomerulosa of the adrenal cortex except one case, namely the signs of hyperfunciton of this zone were observed. But marked changes were not observed in zona fasciculata.There was no relationship between funcitons of zona glomerulosa and elevation of blood pressure. Also an intimate relationship was not found between urinary excretion of 17-ketosteroids and elevation of blood pressure.It is suggested that hypertension produced by section of buffer nerves may develop through the intermediate of adrenaline and/or noradrenaline. But from above results, the author could find no evidence that this hypertension is produced by activation of the pitutitary-adrenal system.

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The author performed the histologic and histochemical study of the adrenal cortex, determination of 17-ketosteroids in urine and caluclation of eosinophil count in blood ot investigate the relationship between experimental renal hypertension and adrenal cortex.Twenty adult dogs, 7.0-17.2 kg. weight, were uesd in this experiment, and hypertension produced by application of Goldblatt's clamp and by Page's cellophane perinephritis. They were divided into two groups. The first group consists of 12 dogs whose renal arteries were constricted by Goldblatt's clamp, and the second group consists of 8 dogs whose kidneys were wrapped by cellophane.In the course of experiment, the author performed the clinical examinations including the measurement of body weight, urinary volume, blood pressure, urinary 17-ketosteroids excretion and eosinophil count. After the animals were sacrificed, the author performed the histologic and histochemical examination of the adrenal cortex.The summary and conclusion of this study are as follows : Adrenal cortical changes occured in experimental renal hypertensive dogs due to application of Goldblatt's clamp and Page's cellophaneperinephritis were hypertrophy and hyperplasia of cells and an appearance of small ketosteroid droplets in zona glomerulosa of the adrenal cortex. These changes which are considered the sign of hyperfunction are almost proportional to the degree of the elevation of blood pressure and its duration. The sign of slight stress was observed in zona faciculata, but not marked in degree.There was no relations between urinary 17-ketosteroids excretion, eosinophil count and elevation of blood pressure.The changes of zona glomerulosa suggest that the hypersecretion of mineralocorticoids is concerned with the elevation of blood pressur in experimental renal hypertension.

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