Atrial natriuretic peptide (ANP)의 혈압조절에 대한 효과를 구명하기 위하여 2-kidney, 1-clip 흰쥐의 고혈압 발생에 미치는 ANP의 영향을 조사하였다. 실험군은 왼쪽 신동맥에 clip을 끼우고 경정맥내에 지속적으로 ANP를 주입한(atriopeptin III, 500 ng/h) 군으로 하였으며, 대조군은 clip을 끼웠으나 ANP를 주입하지 않은 군으로 하였다. Clip을 끼우기 전과 clip을 끼운 제 4,7,10일에 꼬리동맥으로부터 혈압을 측정한 후 단두하여 혈액을 채취하고 양측 신장을 떼어내어 renin 치를 구하였다. ANP 주입군은 대조군에 비하여 고혈압의 발생이 약화되었고 혈장 renin활성도가 유의하게 낮았으나 신피질 renin함량은 양군간에 유의한 차이가 없었다. 한편 clip을 끼우지 않은 흰쥐에서는 ANP 주입군과 비주입군간에 혈압, 혈장 renin 활성도와 신피질 renin 함량 등이 모두 서로 유의한 차이를 보이지 않았다. 이상의 실험결과는 지속적 ANP 주입이 2-K, 1-C 흰쥐의 고혈압 발생을 방지하지는 못하였으나 약화시켰음을 보여주었으며, ANP는 적어도 부분적으로는 renin-angiotensin계를 길항하므로써 장기적 혈압 조절에 관여하는 것이 시사되었다.
Effects of atrial natriuretic peptide (ANP) on the development of hypertension in 2-kidney, 1-clip (2-K, 1-C) rats were examined. In one group of rats, ANP infusion (500 ng/hr, iv) started immediately after clipping the renal artery. Another group of rats with one kidney-clipped was without ANP infusion and served as a control. Blood pressure was measured on days 4, 7, and 10 following clipping the renal artery. Upon the last blood pressure measurement finished, blood sample was collected by decapitation to measure plasma renin activity (PRA), and both kidneys were taken to weigh and to measure renin content. The ANP-infused group showed an attenuation of increases in blood pressure compared to the non-infused control group. PRA was lower in the ANP-infused group than in the non-infused group. Cortical renal renin content (RRC) of the clipped kidneys was not different between ANP-infused and non-infused groups. The clipped kidneys showed a higher RRC and weighed less than the non-clipped contralateral kidneys within each group. In contrast, sham-clipped rats did not show significant changes in any of the parameters examined regardless of whether ANP was infused or not. These results demonstrate that chronic ANP infusion does not prevent but does attenuate the development of hypertension in 2-K, 1-C rats. It is suggested that ANP plays a role in the long-term regulation of blood pressure, at least in part, by antagonizing the renin-angiotensin-system.
