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A simple, rapid and sensitive HPLC method has been developed for the simultaneous determination of ramipril and hydrochlorothiazide in their dosage forms. Acetonitrile: sodium perchlorate solution (0.1 M) adjusted to pH 2.5+/-0.2 with phosphoric acid (46:54 v/v), was used as the mobile phase, at a flow rate of 1.5 ml/min. A supelcosil LC-8 column (5 microm), 15 cm x 4.6 mm i.d. was utilized as stationary phase. Detection was affected spectrophotometrically at 210 nm. Clobazam was used as an internal standard. The method was also applied for the determination of ramipril in the presence of its degradation products. Linearity ranges for ramipril and hydrochlorothiazide were 4.5-45 and 0.6-14 microg/ml, respectively. Minimum detection limits (S/N = 2) obtained were 180 and 23 ng/ml for ramipril and hydrochlorothiazide, respectively. The proposed method was further applied to the analysis of tablets containing the two drugs, the percentage recoveries +/- S.D. (n = 5) were 100.45%+/-0.63 and 99.55%+/-0.78 for ramipril and hydrochlorothiazide, respectively.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11199212&dopt=Abstract
Hypertension. 2001 Jan;37(1):121-128.
Effect of Chronic Blockade of the Kallikrein-Kinin System on the Development of Hypertension in Rats.
Rhaleb NE, Yang XP, Nanba M, Shesely EG, Carretero OA.
Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Mich.
-The kallikrein-kininogen-kinin system is an important vasodilator and vasodepressor component of the cardiovascular system. Acting mainly through B(2) receptors, kinins may counterbalance the pressor effect of angiotensin II, salt, and mineralocorticoids plus salt. Using rats lacking the bradykinin precursors low- and high-molecular-weight kininogen or a B(2) kinin receptor antagonist (icatibant), we investigated whether absence or blockade of the kallikrein-kinin system alters blood pressure (BP) in rats given (1) chronic infusion of Ang II, (2) a normal or high salt diet, or (3) chronic administration of deoxycorticosterone acetate (DOCA) plus salt. We confirmed the genotype and phenotype of Brown Norway Katholiek rats (BNK) and found that they had a G-to-A point mutation on the kininogen gene compared with Brown Norway (BN) and Sprague-Dawley (SD) rats, very low levels of high-molecular-weight kininogen (17+/-3 ng/mL) compared with BN and SD (1814+/-253 and 2397+/-302 ng/mL, respectively; P:<0.01), and plasma low-molecular-weight kininogen concentrations below detectable limits compared with 1773+/-74 and 1781+/-140 ng/mL for BN and SD, respectively. Basal BP was the same in BNK and BN. Chronic infusion of icatibant did not alter BP in BN or Wistar rats. At doses that blocked the acute effect of bradykinin, icatibant did not potentiate the pressor effect of a chronic subpressor or pressor dose of angiotensin II in male and female Wistar rats nor that of a high salt diet (2%) plus unilateral nephrectomy in male Wistar rats. Moreover, blockade of the kallikrein-kininogen-kinin system in either BN rats given a very high dose of icatibant or kinin-deficient rats (BNK) did not potentiate the pressor effect of angiotensin II (nonpressor dose) or a high salt (3% NaCl) diet given for 2 weeks. Established DOCA-salt hypertension was not exaggerated in rats treated with icatibant but was partially attenuated by ramipril (1.5 mg. kg(-)(1). d(-)(1) for 7 days; P:<0.002). This antihypertensive effect was abolished by icatibant (P:<0.002, ramipril versus ramipril plus icatibant). These results suggest that endogenous kinins do not participate in the maintenance of normal blood pressure or antagonize the development of hypertension induced by chronic infusion of angiotensin II, a high salt diet, or DOCA-salt. However, kinins appear to play an important role in the antihypertensive effect of angiotensin-converting enzyme inhibitors in DOCA-salt hypertension.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11208766&dopt=Abstract [PubMed - as supplied by publisher]
Pflugers Arch. 2000 Dec;441(2-3):235-40.
Cyclooxygenase 2 and neuronal nitric oxide synthase expression in the renal cortex are not interdependent in states of salt deficiency.
Castrop H, Kammerl M, Mann B, Jensen BL, Kramer BK, Kurtz A.
Institut fur Physiologie I, Universitat Regensburg, Germany.
Neuronal nitric oxide synthase (nNOS) and cyclooxygenase-2 (COX-2) expression in the kidney are localized to the cortical thick ascending limb of the loop of Henle (cTALH), including the macula region, and increase after salt restriction. Because of the similar localization and regulation of nNOS and COX-2 expression, we have examined whether there is a functional interrelationship between the expression of the two enzymes. Male Sprague Dawley rats were fed for 1 week either a low-salt diet (0.02% w/w) which produced moderate increases of nNOS and COX-2 expression, or low salt combined with the angiotensin I converting enzyme inhibitor ramipril (10 mg/kg per day), which produced strong increases of renocortical nNOS and COX-2 expressions. To inhibit nNOS or COX-2 activities, animals received in addition N(G)-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg per day) or rofecoxib (10 mg/kg per day) for 1 week, respectively. L-NAME treatment did not change COX-2 expression and conversely rofecoxib treatment did not change nNOS expression in the kidney cortex under any experimental conditions. L-NAME but not rofecoxib attenuated renin mRNA levels. Rofecoxib markedly reduced renal prostanoid excretion. These findings suggest that under these conditions the control of nNOS and COX-2 gene expression in the macula densa regions of the kidney cortex are not dependent on each other.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11211108&dopt=Abstract
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