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*

No abstract available.
Angiotensin II* ; Angiotensins*

The present study was aimed at investigating the molecular regulation of the renin- angiotensin system (RAS) in two-kidney, one clip (2K1C) hypertension. The expression of renin, angiotensinogen and angiotensin II receptor genes was determined by Northern blot analysis in rats made 2K1C hypertensive for 2 or 4 weeks. The expression of renin gene was increased in the clipped kidney and decreased in the contralateral non-clipped kidney at weeks 2 and 4. The expression of angiotensinogen gene was not significantly altered at week 2, but increased at week 4 in the clipped kidney. However, it was not significantly altered in the contralateral kidney either at week 2 or 4. Nor was the expression of angiotensinogen gene significantly altered in the liver either at week 2 or 4. On the other hand, the expression of angiotensin II receptor gene was decreased at week 2, and increased at week 4 in the clipped kidney, whereas it was not significantly changed in the contralateral kidney either at week 2 or 4. In the liver, the expression of angiotensin II receptor gene was not significantly altered at week 2, but decreased at week 4. These results suggest that the components of RAS are transcriptionally regulated in 2K1C hypertension in a manner dependent on tissues and duration of hypertension.
Angiotensin II* ; Angiotensinogen* ; Angiotensins* ; Animals ; Blotting, Northern ; Hand ; Hypertension ; Kidney ; Liver ; Rats* ; Receptors, Angiotensin* ; Renin

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*

No abstract available.
Angiotensin II* ; Angiotensins* ; Hydrocortisone* ; Insulin*

No abstract available.
Angiotensin II ; Angiotensins ; Lithium ; Receptors, Angiotensin

Mesangial cells are found to have renin and angiotensin II-AT1 receptors, but the presence of other components of the renin-angiotensin system and production of angiotensin II within the cell have not been demonstrated. The presence of the renin-angiotensin system components in the glomerular epithelial cell has not been previously reported. We studied expression of each component of the renin-angiotensin system in primary cultured rat glomerular epithelial cells and mesangial cells. We assessed mRNA expression by RT-PCR and the presence of angiotensin II by immunocytochemistry. Both cultured glomerular epithelial cells and mesangian cells expressed mRNA for components of the renin-angiotensin system such as renin, angiotensinogen and angiotensin II type 1A and 1B receptor subtypes. Immunocytochemical studies with specific antibody for angiotensin II demonstrated significant immunoreactivity in both glomerular epithelial cells and mesangian cells. These results, for the first time, provide direct evidence that both the glomerular epithelial cells and mesangian cells contain a complete renin-angiotensin system and generate angiotensin II with intracellular mechanisms. Further studies are required to define the subcellular localization of angiotensin II with electron microscopy and to elucidate the physiological importance of the intracellular reninangiotensin system.
Angiotensin II ; Angiotensinogen ; Angiotensins ; Animals ; Epithelial Cells ; Immunohistochemistry ; Mesangial Cells* ; Microscopy, Electron ; Rats* ; Renin ; Renin-Angiotensin System* ; RNA, Messenger*

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

No abstract available.
Angiotensin II* ; Angiotensins* ; Animals ; Hemorrhage* ; Rats*