Journal of Okayama Medical Association
Published by Okayama Medical Association

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腎性高血圧症に関する研究 第1編 実験的研究

河原 徹 岡山大学医学部砂田外科教室
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Experimental studies on renovascular hypertension were made on dogs. Hypertension was successfully produced by constriting left renal artery with concomitant right nephrectomy. Left femoral-renal artery anastomosis was made with an given interval after hypertension was stabilized. Changes in blood pressure, renal clearance, serum natrium and potassium, blood nonprotein nitrogen, and urinary excretion of aldosterone were followed through the course of experiment. In addition to, effects of intravenous drip infusion of Angiotensin Ⅱ on those elements were studied on normal dogs. The following results were obtained. 1) Blood pressure was measured on right carotid artery which was displaced superficially and wrapped with skin flap in this series. Normal systolic pressure was in the range from 111 mmHg to 140 mmHg. 2) Persistent hypertension was successfully produced by constricting left renal artery with concomitant right nephrectomy and it was relieved with increase of renal blood flow by left femoral-renal artery anastomosis. 3) Renal plasma and blood flow, and glomerular filtration rate were decreased, although decrease of the last one was slight compared to that of the former two, resulting increase of filtration rate. They retruned to pre-experimental values after successful left renal artery reconstruction. 4) No marked changes were found in serum natrium, potassium, and nonprotein nitrogen. 5) Urinary excretion of aldosterone was definitely increased when hypertension was produced compared to before experiment and after revascularization of left kidney. 6) Blood pressure was elevated from ten to fifteen minutes later after beginning of drip infusion on Angiotensin Ⅱ. It was kept constantly in high level during infusion and returned to the preexperimental level after discontinuation of infusion. 7) Renal plasma and blood flow, and glomerular filtration rate decreased during Angiotensin Ⅱ infusion, although decrease of the last one was slight compared to that of the former two, resulting decrease of filtration rate. These values returned to the preexperimental level after discontinuation of infusion. 8) No marked changes were found in serum natrinm, potassium and nonprotein nitrogen was inclined to decrease during Angiotensin Ⅱ infusion, showing increase of potassium-natrium ratio which did not return to normal after discontinuation of infusion, too. 9) Urinary excretion of natrium and potassium was inclined to decrease during Angiotensin Ⅱ infusion, showing increase of potassium-natrium ratio which did not return to normal after discontinuiation of infusion, too. 10) Urinary output decreased slightly during Angiotensin Ⅱ infusion and showed some increase after discontinuation of infusion. 11) Urinary excretion of aldosterone increased definitely during 24 hours after Angiotensin Ⅱ infusion, compared to before experiment and on the 3rd day after infusion. 12) It was confirmed from the above data that mechanism of renal hypertension and stimulating factor of aldosterone excretion are due to Renin-Angictensin Ⅱ system.
ISSN
0030-1558
NCID
AN00032489