No abstract available.
Angiotensin I ; Angiotensin II* ; Angiotensins* ; Autoradiography ; Receptors, Angiotensin* ; Renin* ; Renin-Angiotensin System*

No abstract available.
Angiotensin I ; Angiotensin II* ; Angiotensins* ; Autoradiography ; Receptors, Angiotensin* ; Renin* ; Renin-Angiotensin System*

PURPOSE: Angiotensin(ANG) II regulates tone of penile smooth muscle for erection. ANG III is a product converted from ANG II by aminopeptidase A. The effects of ANG III have not been clarified in the penile corpus cavernosum. The purpose of the present experiment was to determine whether the ANG III has regulatory function in the control of rabbit corpus cavernosum smooth muscle tone. MATERIALS AND METHODS: A strip of rabbit corpus cavernosum was mounted in an organ chamber to measure the isometric tension. We compared the effects of ANG III(10-7M to 10-5M), ANG II(10-8M to 10-6M) and ANG I(10-7M to 10-5M) on the contractility of the corpus cavernosum smooth muscle. RESULTS: ANG III, ANG II, and ANG I contracted corpus cavernosum smooth muscle strips dose-dependently. The contraction of smooth muscle induced by ANG III was 10 fold less by ANG II. Contractile response to ANG III was not attenuated by captopril(angiotensin converting enzyme inhibitor). Contractile response to ANG III was significantly inhibited by Dup 753 of 10-7M(type 1 specific ANG II receptor inhibitor) but not inhibited by PD 123,319 of 10-6M(type 2 specific ANG II inhibitor). CONCLUSIONS: The present results suggest that ANG III is involved in the regulation of corpus cavernosum smooth muscle tone, and contractile effect to ANG III produced via activation of type 1 ANG II (AT1) receptor. The rank order of potency of contraction was as follows, ANG II>ANG IIIANG I.
Angiotensin I* ; Angiotensin II* ; Angiotensin III* ; Angiotensins* ; Glutamyl Aminopeptidase ; Losartan ; Muscle, Smooth*

BACKGROUND: Angiotensin-converting enzyme inhibitors(ACEi) do not decrease plasma angiotensin II levels in chronic use to the same extent as in acute use. this reincrease in angiotensin II level is explained either by a renin-mediated reactive rise in plasma angiotensin I or by non-ACE dependent angiotensin II generation. The aim of this study was to compare the additive effects of an ACEi and angiotensin II receptor antagonist(AT1a) in antiproteinuric effect, hyperkalemia, and hypotension. METHODS: 58 outpatients with chronic renal insufficiency were included and they were randomly classified into two groups : Group I(prescribed AT1a only), Group II(AT1a and ACEi combination therapy), and the changes of serum creatinine, the amount of proteinuria, the developement of hyperkalemia, and hypotension were evaluated. RESULTS: In group I, the amount of proteinuria decreased to 92.8% of initial amount at 1 month after the start of drugs. 2 of 28 patients(7.1%) developed hyperkalemia, and serum creatinine did not change (1.686+/-1.415mg/dL 1.821+/-1.301mg/dL, p=0.289). But in combination therapy group, serum creatinine level increased from baseline value of 1.466+/-0.619mg/dL to 1.800+/-0.881mg/dL(p=0.05), proteinuria did not change (101% of initial amount), and 7 of 30 patients(23.3%) developed hyperkalemia. CONCLUSION: Combination therapy seems to have no additive antiproteinuric effect, but serum creatinine and potassium levels should be closely monitered during the combination therapy.
Angiotensin I ; Angiotensin II* ; Angiotensins* ; Creatinine ; Humans ; Hyperkalemia ; Hypotension ; Outpatients ; Peptidyl-Dipeptidase A* ; Plasma ; Potassium ; Proteinuria ; Receptors, Angiotensin* ; Renal Insufficiency, Chronic

Angioedema is a non-pitting edema that occurs in the skin and mucus membranes. It is known that major etiologies include hereditary deficiency of C1 esterase inhibitor, temperature extreme, trauma, food sensitivity, and medications such as penicillin, aspirin, NSAIDS and ACE inhibitors. ACE inhibitors are blocking the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, and increasing local levels of bradykinin, a potent vasodilator. This increased bradykinin has been theorized to cause angioedema and cough in patients on ACE inhibitors. However, there has been very few causes of angioedema induced by angiotensin II receptor blocker. This is the first report of a patient presenting angioedema induced by losartan -angiotensin II receptor blocker- in this century.
Angioedema* ; Angiotensin I ; Angiotensin II ; Angiotensin-Converting Enzyme Inhibitors ; Anti-Inflammatory Agents, Non-Steroidal ; Aspirin ; Bradykinin ; Cough ; Edema ; Hereditary Angioedema Types I and II ; Humans ; Losartan* ; Membranes ; Mucus ; Penicillins ; Receptors, Angiotensin ; Skin

The renin-angiotensin system (RAS) plays an important role in the pathogenesis of diabetic nephropathy. Recently, the activation of local RAS in mesangial cells by high glucose has been reported. However, little is known about the changes of RAS in podocytes under diabetic conditions. In this study, we examined whether RAS activation was induced in high glucose- stimulated podocytes. Immortalized mouse podocytes were exposed to medium containing 5.6 mM glucose (NG), NG+24.4 mM mannitol, or 30 mM glucose(HG). mRNA and protein expression of RAS components were determined by real time-PCR and Western blot, respectively. Angiotensin I (AI) and angiotensin II (AII) concentrations, angiotensin-converting enzyme (ACE) levels, and renin activity were also determined. Angiotensinogen (AGT) mRNA expression was significantly increased in HG-stimulated podocytes. In addition, AI and AII concentrations were significantly higher in HG-treated cell lysates and in their conditioned media. However, there were no differences in renin activity and ACE levels among the groups. AII type 1 receptor (AT1R) mRNA and protein expression were also increased by 288% (p<0.01) and 170% (p< 0.05) in HG-stimulated podocytes compared to NG- treated cells. In conclusion, HG induced AGT mRNA expression, resulting in increases in AI and AII levels. These findings suggest that increased AII production along with increased AT1R expression in podocytes under diabetic conditions may well be considered as factors actively involved in the pathogenesis of diabetic nephropathy.
Angiotensin I ; Angiotensin II ; Angiotensinogen ; Animals ; Blotting, Western ; Culture Media, Conditioned ; Diabetic Nephropathies ; Glucose* ; Mannitol ; Mesangial Cells ; Mice ; Podocytes* ; Renin ; Renin-Angiotensin System* ; RNA, Messenger

To investigate the mechanisms underlying the cholinergic agonist carbachol-induced cardiovascular responses, changes of renin-angiotensin system were examined in fetal hormonal systems. In the ovine fetal model under stressless condition, the cardiovascular function was recorded. Blood samples were collected before (during baseline period) and after the intravenous administration of carbachol. Simultaneously, the levels of angiotensin I (Ang I), angiotensin II (Ang II) and vasopressin in the fetal plasma were detected by immunoradiological method. Also, blood gas, plasma osmolality and electrolyte concentrations were analyzed in blood samples. Results showed that in chronically prepared ovine fetus, intravenous infusion of carbachol led to a significant decrease of heart rate (P < 0.05), and a transient decrease followed by an increase of blood pressure (P < 0.05) within 30 min. After the intravenous infusion of carbachol, blood concentrations of Ang I and Ang II in near-term ovine fetus were both significantly increased (P < 0.05); however, blood concentration of vasopressin, values of blood gas, electrolytes and plasma osmolality in near-term ovine fetus were not significantly changed (P > 0.05). Blood levels of Ang I and Ang II in the atropine (M receptor antagonist) + carbachol intravenous administration group was lower than those in the carbachol group without atropine administration (P < 0.05). In conclusion, this study indicates that the near-term changes of cardiovascular system induced by intravenous administration of carbachol in ovine fetus, such as blood pressure and heart rate, are associated with the changes of hormones of circulatory renin-angiotensin system.
Angiotensin I ; blood ; Angiotensin II ; blood ; Animals ; Blood Pressure ; Carbachol ; pharmacology ; Cholinergic Agonists ; pharmacology ; Fetus ; Heart Rate ; Renin-Angiotensin System ; Sheep ; Vasopressins ; blood

Angiotensin-converting enzyme (ACE), a dipeptidyl carboxypeptidase, hydrolyzes angiotensin I to the active angiotensin g and also inactivates bradykinin. Activity of ACE was first identified in plasrna by Skeggs et al in 1956. In 1975 Lieberman first reported elevation of serum ACE level in patients with active sarcoidosis and suggested clinical application of the assay to confirm a diagnosis of sarcoidosis and to serve as a guide for therapy. The author studied the serurn ACE levels in 21 syphilitic patients (11 men, 10 women) who showed positive responses in both VDRL and TPHA tests and 20 normal healthy controls (7 men, 13 women) by the spectrophotometric method described by Lieberrnan who modified Cushman and Cheungs method. Comparative studies of ACE levels in syphilitic group with normal control group and relationship among the age, sex and treatment were also conducted. The results were summarized as follows : Ages of the syphilitic patients and normal healthy control group ranged from 18 to 51 years (27 1+-8 98 years) and from 14 to 49 years (28 4+9 08 years) respectively. The mean serum ACE level in syphilitic patients was ll 33+-3 25 p/ml, which was significantly higher than that of normal healthy control group, 6 39+-2 RR p/ml, (p<0001) Of the 21 syphilitic patients, 15(71 4%) had ACE activity higher than the upper limit of normal (mean+1SD). There was no significant correlation between age and serum ACE level. -countinue-
Angiotensin I ; Angiotensins* ; Bradykinin ; Diagnosis ; Humans ; Male ; Peptidyl-Dipeptidase A* ; Sarcoidosis ; Syphilis*

Angiotensin I ; Hepatic Stellate Cells ; Insulin-Like Growth Factor Binding Protein 2 ; Peptide Fragments ; Peptidyl-Dipeptidase A

The recently discovered angiotensin-converting enzyme-related carboxypeptidase 2 (ACE2)-[Angiotensin-(1-7)(Ang-(1-7)]-Mas receptor axis has an opposing function to that of the ACE-Angiotensin II (Ang II)-Angiotensin type 1 (AT1) receptor axis. Ang-(1-7) is present in the kidneys at concentrations comparable to those of Ang II and is associated with vasodilation, modulation of sodium and water transport, and stimulation of nitric oxide (NO) synthase. Ang-(1-7) also acts as a physiological antagonist of Ang II by counterbalancing the Ang II-mediated intracellular signaling pathway. In a hypertensive model, increased ACE and decreased ACE2 along with a higher ACE/ACE2 ratio in hypertensive kidneys appeared to favor Ang II generation, leading to hypertensive renal damage. In addition, the administration of a selective Ang-(1-7) receptor blocker or an ACE2 inhibitor was associated with worsening of hypertension and renal function. Ang-(1-7)-mediated increases in renal blood flow were abolished by blockade of the Mas receptor and by inhibition of prostaglandin release and NO in spontaneously hypertensive rats and in Wistar-Kyoto controls. Further research on the function of the ACE2-Ang-(1-7)-Mas receptor axis could lead to a novel target for inhibiting kidney disease progression.
Angiotensin I ; Angiotensin II ; Hypertension ; Kidney ; Kidney Diseases ; Nitric Oxide ; Peptide Fragments ; Peptidyl-Dipeptidase A ; Rats, Inbred SHR ; Renal Circulation ; Sodium ; Vasodilation ; Water ; Axis, Cervical Vertebra