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Biomed Pharmacother. 2000 Jun;54 Suppl 1:83s-85s.
Clinical characteristics of primary aldosteronism: its prevalence and comparative studies on various causes of primary aldosteronism in Yokohama Rosai Hospital.

Nishikawa T, Omura M.

Department of Medicine, Yokohama Rosai Hospital, Yokohama City, Kanagawa, Japan.

We studied 1,020 patients with hypertension visiting our outpatient clinic during a five-year period, from 1995 until 1999.Those subjects were screened by determining plasma renin activity (PRA) and plasma aldosterone concentration (PAC) after testing routine laboratory examinations in order to differentiate secondary hypertension from essential hypertension. All patients with low-reninemic hypertension were examined by furosemide plus the upright test. This led to an increase in diagnoses of primary aldosteronism (PA) (confirmed by captopril-loading test). Our studies demonstrated that the incidence of PA is 5.4%, and also that the plasma potassium level is not always beneficial for suspecting the presence of PA, because 28% of the patients with PA show only hypokalemia. We would like to emphasize that adrenal venous sampling plays a critical role in establishing the optimal management for patients with PA, because CT imaging is limited to detection of adrenal masses.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10914999&dopt=Abstract




Brain Res. 2000 Aug 4;873(1):75-82.
Angiotensin-(1-7) causes endothelium-dependent relaxation in canine middle cerebral artery.

Feterik K, Smith L, Katusic ZS.

Departments of Anesthesiology, Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905, USA.

The heptapeptide, angiotensin-(1-7), is an active member of the renin-angiotensin system. The present study was designed to characterize the role of endothelium in relaxations of large cerebral arteries to angiotensin-(1-7). Rings of canine middle cerebral arteries were suspended in organ chambers for isometric force recording. The levels of cyclic guanosine 3',5'-monophosphate (cGMP) were assessed by radioimmunoassay. During contraction to uridine 5'-triphosphate (UTP, 3x10(-6) to 10(-5) mol/l), angiotensin-(1-7) (10(-9) to 3x10(-5) mol/l) caused concentration-dependent relaxations in arteries with endothelium, but not in endothelium-denuded vessels. Angiotensin-(1-7) significantly increased formation of cGMP. Nitric oxide synthase inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME, 3x10(-4) mol/l), and selective soluble guanylate cyclase inhibitor, 1 H-[1,2, 4]oxadiazolo[4,3-a]quinozalin-1-one (ODQ, 3x10(-6) mol/l), abolished angiotensin-(1-7)-induced relaxations. Angiotensin receptor antagonists, losartan (10(-5) mol/l), PD 123319 (10(-5) mol/l), [Sar(1),Thr(8)]-angiotensin II (10(-5) mol/l) [Sar(1),Val(5), Ala(8)]-angiotensin II (10(-5) mol/l) or [7-D-Ala]-angiotensin 1-7 (10(-6) mol/l) did not affect these relaxations. However, angiotensin-converting enzyme inhibitor, captopril (10(-5) mol/l) augmented relaxations to angiotensin-(1-7). Finally, bradykinin B(2) receptor antagonist, [D-Arg(0),Hyp(3),Thi(5),D-Tic(7), Oic(8)]-bradykinin (HOE 140, 5x10(-8) mol/l) significantly reduced the effect of angiotensin-(1-7), while bradykinin B(1) receptor antagonist, des-Arg(9), [Leu(8)]-bradykinin (6x10(-9) mol/l) did not influence the vascular response to the heptapeptide. These findings indicate that (1) angiotensin-(1-7) produces relaxation of canine middle cerebral arteries by the release of nitric oxide from endothelial cells, (2) angiotensin receptors do not mediate endothelium-dependent relaxations to the heptapeptide, and (3) this effect appears to be dependent on activation of local production of kinins. Our studies support the concept that angiotensin-(1-7), as a natural vasodilator hormone, may counterbalance the hemodynamic actions of angiotensin II.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10915812&dopt=Abstract




Hepatogastroenterology. 2000 May-Jun;47(33):767-70.
Effects of single dose of 50mg captopril in patients with liver cirrhosis and ascites.

Lee JK, Hsieh JF, Tsai SC, Ho YJ, Kao CH.

Department of Nuclear Medicine, China Medical College Hospital, Taichung, Taiwan.

BACKGROUND/AIMS: In patients with liver cirrhosis and ascites, the renin angiotensin system is usually activated. Such a correlation supports the hypothesis that activation of the renin-angiotensin system plays an influential role in the pathogenesis of ascites in liver cirrhosis. METHODOLOGY: In this study, 25 patients with liver cirrhosis and ascites (10 females, 15 males; age: 45-67 years) were enrolled. We evaluated the acute effects of converting enzyme inhibitor (a single dose of 50 mg captopril taken orally) on glomerular filtration rate, effective renal plasma flow, filtration fraction, plasma renin activity, and plasma aldosterone. RESULTS: Oral intake of a single 50 mg dose of captopril significantly decreased glomerular filtration rate (65 +/- 6 mL/min/1.73 m2 vs. 53 +/- 9 mL/min/1.73 m2), filtration fraction (21.2 +/- 2.7% vs. 15.5 +/- 4.1%), and plasma aldosterone (340 +/- 80 pg/mL vs. 247 +/- 42 pg/mL), but increased plasma renin activity (2.65 +/- 2.19 ng/mL/hr vs. 11.58 +/- 2.70 ng/mL/hr) and effective renal plasma flow (312 +/- 41 mL/min/1.73 vs. 356 +/- 60 mL/min/1.73 m2). CONCLUSIONS: We suggest that oral intake of a single dose of 50 mg captopril can block the renin-angiotension system, and result in changes in renal hemodynamics and function in cirrhotic patients with ascites.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10919029&dopt=Abstract












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