Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The state of microcirculatory haemostasis was studied in 145 patients with essential hypertension with reference to the severity of their disease. It was noted that along with the growing duration and severity of the disease the aggregation activity of the platelets is decreasing. Intravenous administration of Heparin, 5, 10, 15, 20 and 25 thousand units, significantly activates the platelets of normal individuals (30 persons) and of hypertonics. The activation develops by the end of Heparin infusion, persists for 2 hours and is clearly perseptible 48 hours following a course of Heparin therapy. The sanogenic role of Heparin-induced activation of the microcirculatory haemostasis in the adaptation-haemostatic reactions is discussed.
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PMID:[State of microcirculatory hemostasis in arterial hypertension and its changes under the effect of heparin]. 88 49

Vascular smooth muscle cell proliferation has been shown to be an important factor in atheromatous plaque formation, hypertrophy associated with essential hypertension, and failure of balloon angioplasty procedures. Investigators have shown that a number of different agents stimulate vascular smooth muscle cell proliferation, including epidermal growth factor, platelet-derived growth factor, angiotensin II, and catecholamines. Previously, we have demonstrated that these agents also cause immediate changes in ion transport and second messenger generation in vascular smooth muscle cells. We have proposed that these immediate changes may be linked to each other and to cell proliferation. In contrast to the many agents that have been shown to stimulate vascular smooth muscle cell proliferation, only a few agents (e.g., heparin sodium or transforming growth factor-beta) have been shown to inhibit vascular smooth muscle cell proliferation. In the present study we have investigated whether heparin inhibits serum- or growth factor-stimulated changes in ion transport and second messenger generation in vascular smooth muscle cells. We found that heparin inhibits serum- or growth factor-stimulated Na(+)-H+ exchange in a concentration-dependent manner that is not dependent on the ability of heparin to function as an anticoagulant agent. In addition, other glycosaminoglycans were not found to be inhibitory, and the inhibitory effects of heparin were discovered to be limited to vascular smooth muscle cells. Heparin does not appear to be acting by binding to growth factors, or by directly inhibiting the Na(+)-H+ exchange protein. However, heparin did inhibit serum- or growth factor-stimulated inositol trisphosphate release and calcium mobilization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin inhibits Na(+)-H+ exchange in vascular smooth muscle cells. 215 14