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It has been demonstrated that pepstatins isolated from streptmyces inhibit the renin activity and among pepstatins and other renin inhibitory substances, pepstatin A, isovaleryl pentapeptide is known as a most potent renin inhibitor (1, 2, 3). The solubility of this compound limits application in many studies. In the present work, the renin inhibitory activity of a soluble acid protease inhibitor, N-acetyl-pepstatin, was demonstrated both in vitro and in vivo. N-acetyl-pepstatin was found in a culture filtrate of streptmyces naniwa ensis by Murao and Satoi (4). The chemical structure is N-acetyl-valyl-valyl-4-amino 3-amino-hydroxy-6-methylheptanyl-alanyl-4-amino-3-amino-hydroxy-6-methylheptanic acid;M.W. 644 (5). The same acetyl pentapeptide was also found from strain MD494-Al of streptmyces parvisporogenes by Aoyagi et al (6). N-acetyl-pepstatin is soluble in phosphate buffer at pH 7.4 in concentrations higher than 20 mg/ml.In vitro experiments were carried out using partially purified dog renin and dog renin substrate as described in previous papers (7, 8). One tenth ml of 50 ng angiotensin I equiva lent per hour (Ang-I Eq•hr) of renin and 0.2 ml of 200 ng Ang-I Eq of renin substrate were incubated for 1 hr at 37'C with N-acetyl-pepstatin dissolved in 1/3M phosphate buffer (0.2 mnl, pH 7.4) containing 8 mM EDTA and 0.02% Neomycin. The angiotensin I formed in this mixture was determined by radioimmunoassay. Inhibitory activity of N-acetyl pepstatin was expressed as percentage reduction in the production rate of angiotensin I. Average inhibitions of the renin activity by N-acetyl-pepstatin in a concentration of 10-6 and 10-5 M were 30.9±7.2% and 64.8 -+ 3.2%, respectively (n=8), while those with the same concentration of pepstatin A were 49.7+7.8 % and 89.2+3.7 %, respectively (n=6).Renin inhibitory effect of N-acetyl-pepstatin in vivo was determined by inhibition of

from so called GOPD (bronchial asthma, chronic bronchitis and chronic pulmonary emphysema), brochiectasis or alveolitis, has been noted since 1966 in Japan '. Through clinical, radiologic, physiologic and pathologic analysis based on accumulated data by Homma and Yamanaka1^, a nationwide survey with the cooperation of 30 universities, national and municipal institutions throughout the country was organized in 1980 to investigate the incidence and the morbidity of the disease under the aid of the Ministry of Health and Welfare of Japan6*. The results obtained by this project team during 1980 to 1982 disclosed the features of clinical and pathological findings, the gist of which was already reported7'19. As stated later, DPB is associated with HLA-Bw54 antigen which is found specifically in Japanese and Chinese and not in Caucasians, suggesting that DPBmay be an ethnically specific disease.

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