We measured the internal diameters of small muscular pulmonary arteries in the right and left lower lobes of lungs rapidly frozen in the anesthetized, open-thorax cat. In every cat the right lower lobe was ventilated with the test gas and all other lobes were ventilated with O 2 . In 4 cats, the test gas supplied to the right lower lobe was also O 2 (control experiments); in 6, it was 100% N 2 and in 6 it was 90% N 2 -10% CO 2 . In the 4 controls, there was no difference between the internal diameters of corresponding arteries in the right and left lower lobes. In the other 12 cats, there was a highly significant decrease in the diameter of arteries in the right lower lobe that correlated well with a large decrease in blood flow to that lobe, calculated using a shunt equation. Ventilation of the right lower lobe with 10% CO 2 in air (4 cats) did not affect the diameter of arteries and ligation of the pulmonary artery to the right lower lobe resulted in only a slight decrease in arterial dimensions in 3 of 4 cats.These data show that in regional alveolar hypoxia without systemic hypoxia the muscular pulmonary arteries of the terminal respiratory units in the hypoxic region actively constrict. The constriction occurs with or without alveolar hypercapnia. ADDITIONAL KEY WORDS altitudecarbon dioxide lung oxygen pulmonary artery pulmonary circulation respiration local regulation of pulmonary circulation pulmonary vasoconstriction hypoxia hypercapnia pulmonary artery occlusion anesthetized cats• Most investigators now agree that reduced partial pressure of oxygen in alveolar air leads to an acute increase in pulmonary vascular resistance in several species of mammal, including man.1 -2 The vasoconstriction occurs both when decreased oxygen is not associated with increased carbon dioxide concentration, as at high altitude, 8 and when the two occur together, as during hypoventilation at sea level. 4 The most recent evidence indicates a positive correlation between the vasoconstrictor response and the presence of This work was supported in part by U. S. Public Health Service Grants HE-06285 and HE-5251, the California Tuberculosis and Health Association and Nonr Contract 222(55).Dr. Kato was a Trainee of the National Heart Institute.Accepted for publication April 11, 1966. both alveolar hypoxia and mixed venous blood (tissue) acidosis. 5A constrictor response can be mediated entirely within the lung, for it can be induced in isolated perfused lungs.6 ' 7i 8 In intact animals, when one lung breathes air low in oxygen but systemic hypoxia is prevented by having the other lung breathe a mixture rich in oxygen, the constriction is confined to the hypoxic lung. 9 ' 10 As to the location of the change in resistance, the major pulmonary vascular resistance normally 11 ' 12 and during alveolar hypoxia is in vessels beyond the tip of any catheter.8 ' 18 The control site must be somewhere in the small muscular pulmonary arteries, 14 "18 the capillaries 17 or small veins. ' 18~21All of these vessels are exposed to t...

Alcohol dehydrogenase (Adh) is the key enzyme in alcohol fermentation. We analyzed Adh expression in order to clarify the role of Adh of soybeans (Glycine max) to flooding stress. Proteome analysis confirmed that expression of Adh is significantly upregulated in 4-day-old soybean seedlings subjected to 2 days of flooding. Southern hybridization analysis and soybean genome database search revealed that soybean has at least 6 Adh genes. The GmAdh2 gene that responded to flooding was isolated from soybean cultivar Enrei. Adh2 expression was markedly increased 6 h after flooding and decreased 24 h after floodwater drainage. In situ hybridization and Western blot indicated that flooding strongly induces Adh2 expression in RNA and protein levels in the root apical meristem. Osmotic, cold, or drought stress did not induce expression of Adh2. These results indicate that Adh2 is a flooding-response specific soybean gene expressed in root tissue.

Background: Regulation of vascular smooth muscle tone by cGMP-dependent protein kinase I␣ (PKGI␣) through RhoA inhibition is not understood. Results: PKGI␣ binds RhoA, through cGMP-induced binding, and inhibition of RhoA requires PKGI␣ activity. Conclusion: RhoA-PKGI␣ co-interaction regulates RhoA function. Significance: Understanding RhoA regulation by PKGI␣ is important for understanding the regulation of vascular tone in vivo and in human diseases such as hypertension.

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Assessment of tumor microvasculature is therefore probably one of the most important prognostic predictors in renal cell carcinoma.

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The effect of olmesartan medoxomil (OLM), an angiotensin II receptor blocker (ARB), on advanced nephropathy and mortality was evaluated in Zucker Diabetic Fatty (ZDF) rats, a type 2 diabetes model. OLM was administered from 36 weeks of age, when the animals developed advanced proteinuria. OLM effectively suppressed the progression of proteinuria. The ZDF rats started to die at 50 weeks of age, which was accompanied by abrupt increase in blood urea nitrogen, suggesting that the cause of death was renal insufficiency. OLM suppressed increases in blood urea nitrogen and increased the survival rate of the ZDF rats. The histological examination revealed that the renal damage was ameliorated by OLM. The macrophage infiltration and monocyte chemoattractant protein-1 (MCP-1) expression was increased in the glomeruli and tubulointerstitium of the ZDF rat kidneys, and the increase was lessened by OLM. In a separate study, albumin increased MCP-1 release from cultured tubular epithelial cells. These results suggest that protein leakage from the glomeruli stimulates MCP-1 production in tubular cells and that MCP-1 released into the interstitial space induces macrophage infiltration and inflammation. It is conceivable that the beneficial actions of ARB on diabetic nephropathy are, at least in part, due to decrease of proteinuria and the subsequent reduction of inflammatory changes in tubular cells.

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