Drugs online research references
Clin Hemorheol Microcirc. 1998 Jul;18(2-3):185-90.
Effects of Ramipril and Isradipin on hemorheological profiles in patients with arterial hypertension.
Muravyov AV, Zaitsev LG, Muravyov AA, Yakusevich VV, Sirotkina AM.
Department of Biol. and Med. Problems, Yaroslavl University, Russia.
In this study, the effect of the angiotensin-converting-enzyme inhibitor (ACE inhibitor) Ramipril (5 mg/day) and calcium antagonist Isradipin (5 mg/day) treatment of two groups of hypertensive patients (n = 22 in each of group) was evaluated. The parameters of the hemorheological profile (blood and plasma viscosity, red blood cell aggregation and deformation, plasma protein concentration and its osmolality, hematocrit and ratio of Hct/blood viscosity) were measured in basal conditions (before treatment) and after 3 weeks of treatment. The patients showed some increased blood, plasma viscosity, RBC aggregability and fibrinogen concentration in basal conditions. In both groups of patients, three main parameters of the hemorheological profile (plasma viscosity, Hct and RBC aggregation) decreased after treatment. No significant changes in red cell deformability was found. In conclusion, ACE inhibition with Ramipril and calcium channel blocking with Isradipin lead to a moderate improvement of blood rheology in patients with hypertension. This may be explained by the pronounced vasodilatatory effect of ACE inhibitor and calcium antagonist, though their acting mechanism is different.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9699040&dopt=Abstract
Adv Exp Med Biol. 1989;247A:39-48.
Significance of kallikrein-kinin and renin-angiotensin systems in the hypotensive mechanism of angiotensin-I converting enzyme inhibitors in essential hypertensives.
Iimura O, Shimamoto K.
Second Department of Internal Medicine, Sapporo Medical College, Japan.
This study was undertaken to further clarify the role of kallikrein-kinin and renin-angiotensin systems in the hypotensive mechanisms of the angiotensin-I converting enzyme inhibitor by using highly sensitive and specific radioimmunoassays in patients with essential hypertension. Captopril was administered for 14 days (chronic effect), and the acute effects of captopril, alacepril and ramipril were also studied in the in-patients with essential hypertension. All of these converting enzyme inhibitors rapidly decreased the blood pressure and plasma angiotensin II levels, and increased plasma and urinary kinin and plasma renin activity in the acute effect. Following the administration of captopril for 14 days, these decreases and increases were maintained. The change of blood pressure was significantly correlated negatively with that of plasma kinin levels and positively with that of plasma angiotensin II levels in both the acute and chronic effect of converting enzyme inhibitors. Urine volume and urinary sodium excretion were markedly augmented, while both the change of urine volume and that of urinary sodium excretion were negatively correlated with the change of blood pressure in the chronic effect. These findings suggest that the hypotensive effect of converting enzyme inhibitors might be caused by an increase of plasma kinin and a decrease of plasma angiotensin II, and in part by an augmentation of urine volume and urinary sodium excretion. In this drug treatment, the renal kallikrein-kinin system may also play some role in the increase of urine volume and urinary sodium excretion through the increased kinin in the kidney.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2532450&dopt=Abstract
Diabetes. 1997 Jan;46(1):107-12.
Interactions of the kallikrein-kinin and renin-angiotensin systems in experimental diabetes.
Vora JP, Oyama TT, Thompson MM, Anderson S.
Division of Nephrology and Hypertension, Oregon Health Sciences University, Portland 97201-2940, USA.
The kallikrein-kinin system (KKS) has been postulated to play a role in modulation of hemodynamic function in diabetes and to contribute to the hemodynamic effects of angiotensin-converting enzyme inhibition (CEI). To further explore the KKS and its interactions with the renin-angiotensin system (RAS), studies were conducted in nondiabetic control rats and in moderately hyperglycemic diabetic rats. In protocol 1, control and diabetic rats were studied before and after administration of one of two dissimilar B2 kinin receptor antagonists (BK2As), or vehicle. At a low dose (0.5 microg x kg-1 x min-1), the first generation antagonist D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin significantly reduced the glomerular filtration rate (GFR) and renal plasma flow rate in diabetic rats, despite variable effectiveness in blocking the hypotensive response to injected bradykinin. However, a similar hemodynamic effect occurred in nondiabetic rats, suggesting that the observed effect was not specific to diabetes. Higher doses (20 microg bolus, then 1 microg x kg-1 x min-1 infusion) did not affect hemodynamics in either group, perhaps because of partial agonist effect. The second BK2A tested was the newer compound, icatibant (Hoe 140; D-Arg,[Hyp3,Thi5,D-Tic7,Oic8]-bradykinin). Hoe 140 consistently blocked the vasodepressor action of injected bradykinin, but had no effect on systemic or renal hemodynamics in either control or diabetic rats. In protocol 2, control and diabetic rats were pretreated with the CEI ramipril for 1-2 weeks, after which renal function was studied before and after Hoe 140 (0.1 mg s.c. and i.v.) or vehicle. CEI lowered blood pressure in both groups. Hoe 140 did not affect renal function in control rats, but in diabetic rats pretreated with ramipril, it induced a modest but significant decline in GFR. Ramipril induced the predicted changes in the systemic and intrarenal RAS, while acute BK2A had no consistent effect on RAS parameters. These studies suggest that the endogenous KKS has only a minor role in modulation of renal hemodynamics in the euvolemic diabetic rat, in the absence of KKS stimulation by CEI. However, angiotensin-converting enzyme is also kininase II, which serves to increase endogenous kinin activity. The increased kinin activity resulting from CEI treatment may participate, to a modest degree, in hemodynamic regulation of the diabetic kidney.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8971089&dopt=Abstract
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