Drugs online research references
Blood Press. 1994 Nov;3(6):418-27.
Drug-induced endothelium-dependent and -independent relaxations in isolated resistance vessels taken from simultaneously hypertensive and streptozotocin-diabetic rats.
Kam KL, Pfaffendorf M, van Zwieten PA.
Department of Pharmacotherapy, Academic Medical Centre, University of Amsterdam, The Netherlands.
Hypertension and diabetes mellitus often co-exist and both conditions may be expected to cause synergistic vascular damage. Our group has introduced an animal model for simultaneously occurring hypertension and diabetes mellitus by treating spontaneously hypertensive rats with streptozotocin (STZ). We investigated the drug-induced endothelium-independent and -dependent relaxation in isolated mesenteric small arteries (resistance vessels). Concerning the influence of hypertension, the responses to sodium nitroprusside, methacholine, histamine and nifedipine proved unchanged, the vasodilator response to bradykinin was diminished, whereas that to the K(+)-channel opener cromakalim was enhanced. With respect to the influence of STZ-induced diabetes we found that the responses to sodium nitroprusside, methacholine and nifedipine were unchanged, and that to cromakalim was enhanced, also when the preparations were pretreated with glibenclamide. The responses to histamine (STZ WKY versus control WKY) and bradykinin (STZ SHR versus control SHR) proved enhanced in the isolated vessels taken from diabetic animals. These findings suggest that the influence of the diabetic state is more pronounced than that of hypertension. However, our findings do not indicate that either hypertension or diabetes is associated with generalised endothelial damage in the resistance arteries.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7704291&dopt=Abstract
Korean J Intern Med. 1994 Jul;9(2):99-104.
Impairement of endothelium-dependent relaxation in chronic two-kidney, one clip hypertensive rats.
Choi KC, Woo YJ, Park JW, Lee J, Kim WJ, Yoo KJ, Yoo KS, Kang YJ.
Department of Internal Medicine, Chonnam University Medical School, Kwangju, Korea.
OBJECTIVES: Hypertension is commonly associated with an endothelial dysfunction that may contribute to the rise in blood pressure. Little information has been available so far on the role of endothelium-derived nitric oxide(EDNO) in renin-dependent, 2-kidney, 1 clip(2KIC) hypertension. The present study was aimed to determine a role for EDNO in the development and maintenance of 2KIC hypertension. METHODS: The effects of blocking synthesis or supplementation with precursor of EDNO on the development of hypertension were determined in 2KIC rats. Vascular responses to acetylcholine, nitroprusside, atrial natriuretic peptide and nifedipine were examined in 7- and 12-week hypertensive 2KIC rats. RESULTS: NG-nitro-L-arginine-methyl ester caused a sustained increase of blood pressure in normal rats, while it was only partially associated with a more pronounced increase of blood pressure in the developmental phase of hypertension in 2KIC rats. In 7-week and 12-week hypertensive rats, phenylephrine-induced contraction of the isolated thoracic aortic rings was more sensitive compared with control. Their acetylcholine-induced relaxation was attenuated while the responses to nitroprusside or atrial natriuretic peptide were unaltered. Although their blood pressure did not differ between 7-week and 12-week hypertensive groups, the attenuation in the acetylcholine-induced relaxation was more prominent in the latter with a longer duration of hypertension. Indomethacin did not affect the attenuated relaxation to acetylcholine. The relaxation response to nifedipine was more pronounced in 2KIC rats. CONCLUSION: These results indicate that ENDO has little influence of the 2KIC hypertension, at least during its developmental phase, which is associated with an activated reninangiotensin system. The chronic stage of 2KIC hypertension, however, is associated with an endothelial dysfunction which may contribute to the enhanced vasoconstriction and sustained high blood pressure.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7865495&dopt=Abstract
fhs.McMaster.Ca
The effects of tetrandrine, a Ca2+ antagonist of bis-benzylisoquinoline alkaloid origin, on endothelium-dependent and -independent vascular responsiveness were investigated in perfused rat mesenteric artery. In endothelium-intact preparations pre-contracted with 3 microM phenylephrine and fully relaxed by 0.3 microM acetylcholine tetrandrine caused a rapid transient contraction. In endothelium-denuded preparations, tetrandrine caused only vasorelaxation of phenylephrine-contraction. The biphasic effect of tetrandrine in acetylcholine-relaxed preparations could also be mimicked by sequential applications of atropine/tetrandrine or N(G)-nitro-L-arginine-methylester (L-NAME)/tetrandrine, but atropine or L-NAME alone caused only vasoconstriction. This tetrandrine-induced transient vasoconstriction was also observed in preparations relaxed with ATP, histamine or thapsigargin (TSG), but not those relaxed with A23187, sodium nitroprusside or nifedipine. The present results suggest that tetrandrine, in addition to its known inhibitory effects on vascular smooth muscle by virtue of its Ca2+ antagonistic actions, also inhibits NO production by the endothelial cells possibly by blockade of Ca2+ release-activated Ca2+ channels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10374903&dopt=Abstract
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