angiotensin-i and Lung-Diseases

Topics: Angiotensin I; Angiotensins; Humans; Lung Diseases; Molecular Weight; Peptidyl-Dipeptidase A; Sarcoidosis

The renin-angiotensin system (RAS) has long been appreciated as a major regulator of blood pressure, but has more recently been recognized as a mechanism for modulating inflammation as well. While there has been concern in COVID-19 patients over the use of drugs that target this system, the RAS has not been explored fully as a druggable target. The abbreviated description of the RAS suggests that its dysregulation may be at the center of COVID-19.

Topics: Angiotensin I; Angiotensin-Converting Enzyme 2; Animals; Blood Coagulation Disorders; Coronavirus Infections; COVID-19; Cytokines; Humans; Hypertension; Lung; Lung Diseases; Obesity; Pandemics; Peptide Fragments; Peptidyl-Dipeptidase A; Pneumonia, Viral; Receptor, Angiotensin, Type 1; Severity of Illness Index

Serum ACE (s-ACE) activity were determined in 112 sarcoid patients and 60 healthy volunteers. The mean s-ACE activity in sarcoid patients were 39.5 +/- 14.1 U. and in healthy volunteers 22.1 +/- 3.6, U. Significant increase of s-ACE was seen in active sarcoidosis 51.2 +/- 13.7 U. Serum ACE activity increased twice or more in comparison with control values imply activity of the process. Serum-ACE determination may be of use as a prognostic factor in sarcoidosis.

Topics: Adolescent; Adult; Angiotensin I; Female; Humans; Lung Diseases; Male; Middle Aged; Peptidyl-Dipeptidase A; Prognosis; Reference Values; Sarcoidosis; Severity of Illness Index

Five patients with chronic pulmonary diseases (3 pulmonary emphysema, 1 chronic respiratory failure caused by old tuberculosis, 1 diffuse panbronchiolitis) showed a marked increase of plasma angiotensin-I and PRA level, which was accompanied by an increase of angiotensin-II level, however, whose systemic blood pressure was not elevated. The intravenous infusion of angiotensin-II-analogue (1-Sarcosine, 8-Isoleucine-Angiotensin-II) elicited an antagonistic blood pressure response resembling Bartter's syndrome.

Topics: 1-Sarcosine-8-Isoleucine Angiotensin II; Angiotensin I; Angiotensin II; Blood Pressure; Chronic Disease; Female; Humans; Lung Diseases; Male; Renin

1. To learn how pulmonary vascular injury alters the ability of the lung to metabolize vasoactive autacoids, lung vascular lesions were produced in rats by a single subcutaneous injection of monocrotaline (90 mg kg-1), and the blood pressure responses to angiotensin I (AI), angiotensin II (AII), bradykinin, prostaglandin E2 (PGE2) and substance P were examined. Vasoactive agents were given intravenously or intra-arterially. 2. On histological examination of the lung at 3 weeks after monocrotaline treatment, degeneration or necrotization of endothelial cells was evident. 3. The conversion of AI to AII was only slightly depressed by monocrotaline treatment. On the other hand, the depressor response to intravenously injected bradykinin was enhanced in monocrotaline-treated rats. When the rats were pretreated with indomethacin the depressor response to intravenous bradykinin was the same for both control and monocrotaline-treated groups which suggests that endogenous prostaglandins are involved in the enhancement of the response to bradykinin. 4. In monocrotaline-treated rats the depressor response to intravenous PGE2 was significantly enhanced depending on the period following the treatment, while that to the intra-arterial injection did not differ from control. 5. The data suggest that monocrotaline-induced lung injury impairs the metabolism of PGE2 during pulmonary circulation but has little effect on the conversion of AI to AII and the degradation of bradykinin in rats.

Topics: Angiotensin I; Angiotensin II; Animals; Autacoids; Blood Pressure; Body Weight; Bradykinin; Dinoprostone; Injections, Subcutaneous; Lung; Lung Diseases; Male; Monocrotaline; Pyrrolizidine Alkaloids; Rats; Rats, Inbred Strains; Substance P; Time Factors

1. Based on the findings in the preceding paper we investigated the ability of pulmonary endothelial cells to metabolize prostaglandin F2 alpha (PGF2 alpha) and angiotensin I (AI), and to produce endothelium-derived relaxing factor (EDRF) following lung vascular injury induced by monocrotaline in rats. The isometric tension of pulmonary artery rings isolated from rats 3-5 weeks after an injection of monocrotaline or saline was measured. For comparison the responses to drugs of the artery denuded of endothelium by rubbing were tested. 2. Acetylcholine-induced relaxation of the rings precontracted by noradrenaline was diminished in the artery from monocrotaline-treated rats, depending on the duration after treatment. The diminution was comparable to that in the control artery denuded of endothelium. 3. The contractile response to PGF2 alpha was significantly augmented in the artery injured by monocrotaline. The similar augmentation was observed after the mechanical removal of endothelium in the control artery. Decrease of EDRF was not involved in the enhancement of contractile response to PGF2 alpha in the monocrotaline-injured artery. 4. AI caused a contraction, which was sensitive to captopril, in control rings, and also in monocrotaline-injured rings to a similar degree. Removal of endothelium from the control artery did not modify the response to AI or to AII. 5. These results suggest that the monocrotaline treatment of rats suppresses the ability of pulmonary endothelium to produce EDRF and to degrade prostaglandins. The relative resistance of the AI response to endothelial injury suggests that the existence of converting enzyme is not restricted to the endothelium.

Topics: Acetylcholine; Angiotensin I; Angiotensin II; Animals; Dinoprost; Endothelium, Vascular; In Vitro Techniques; Lung; Lung Diseases; Male; Monocrotaline; Muscle Relaxation; Potassium Chloride; Pulmonary Artery; Pyrrolizidine Alkaloids; Rats; Rats, Inbred Strains

Topics: Aldosterone; Angiotensin I; Angiotensins; Chronic Disease; Humans; Hypertension; Hypertension, Pulmonary; Lung Diseases; Male; Middle Aged

Topics: Angiotensin I; Animals; Bradykinin; Humans; Lung; Lung Diseases; Peptides; Peptidyl-Dipeptidase A; Pulmonary Circulation; Rabbits