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)

Hypertension in pregnancy and gestational diabetes have in common a lack of universally accepted classification and nomenclature that hinders comparison of data between research groups and contributes to the lack of consensus in the literature on these conditions. The inter-relationship of hypertension and gestational diabetes can be considered from three viewpoints according to whether hypertension is present before, during, or after the pregnancy. The first question is whether hypertension predating pregnancy predisposes to gestational diabetes. Epidemiological evidence and physiological argument based on the common etiologic factor of insulin resistance would suggest that gestational diabetes should be more common in the presence of preexisting hypertension. The limited clinical data available support this hypothesis. There are three issues concerning the coexistence of hypertension and gestational diabetes: whether gestational diabetes predisposes to pregnancy-induced hypertension, whether pregnancy-induced hypertension predisposes to gestational diabetes and what effect the combination has on morbidity and mortality. A number of studies have investigated whether pregnancy-induced hypertension is more common in women with gestational diabetes, but no consensus has been reached. There is little direct clinical evidence on the reverse issue, but data are presented to suggest that pregnancy-induced hypertension may only predispose to gestational diabetes when its etiology is gestational hypertension and not preeclampsia. The issue of how the coexistence of pregnancy-induced hypertension and gestational diabetes affects maternal or neonatal morbidity and mortality is largely unanswered. The last question is whether gestational diabetes has any prognostic significance with regard to the future development of hypertension in the mother. It is well known that gestational diabetes predisposes to subsequent NIDDM and that NIDDM is associated with a high incidence of essential hypertension. Once again insulin resistance may be a unifying factor. However, there is no direct clinical evidence that gestational diabetes predisposes to future hypertension.
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PMID:Hypertension in women with gestational diabetes. 970 24

Insulin action starts with binding to a membrane receptor (insulin receptor-tyrosine kinase) and with activating an insulin receptor substrate 1 (IRS-1) and substrate 2 (IRS-2). Insulin receptors interact at least with three cascade reactions, phosphorylating G proteins and IRS-1, that activate PLC "ras" and PI-3-K. NIDDM can be defined as a disease caused by defective transduction of insulin signals and IR as a complex phenotype manifesting itself, emphasized by individual and environmental factors, in the cellular systems of signal transduction. IRS is a syndrome characterized by NIDDM, hypertension, visceral obesity, CHD: the X syndrome. Up to day the described mutations of the insulin-receptor gene are rare (e.g. the leprechaunism): genetic IR. Obesity is the principal cause of IR by receptorial and post-receptorial defects: metabolic IR. The obese skeletal muscle shows a reduction of insulin receptor and IRS-1 phosphorylation and of PI-3-K activation; the scarce expression of these proteins would determine the muscular IR. IR is a pattern of essential hypertension. Hypertension, dyslipidemia and abnormality of glucose metabolism are linked by IR. The so called high erythrocyte Na(+)-Li+ counter-transport is a new biochemical marker for IR and hypertension. These drugs can reduce IR: metformin, sulphonilureas, fibrats, dexfenfluramine, troglitazone, doxazosin, ACE-inhibitors.
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PMID:[Insulin resistance. Receptor and post-receptor abnormalities]. 984 54

Proteinuria is the hallmark of renal disease and proteinuria exceeding 1 gm a day in patients with renal disease augers a poorer prognosis. Proteinuria has been shown to be tubulotoxic and directly contributes to renal deterioration. Patients with non-selective proteinuria are more likely to have progressive renal disease. Diabetic patients with persistent microhaematuria have about 20 times the risk of developing diabetic nephropathy. In essential hypertension, the onset of de novo proteinuria after years of adequate BP control is a marker of subsequent decline in renal function. In glomerulonephritis, more severe proteinuria is associated with faster rate of progression. Even though the initial phase of proteinuria in patients with glomerulonephritis is usually of immunological origin, in the vast majority of patients with established disease, the latter progressive phase of proteinuric glomerulopathy is the result of glomerular hyperfiltration which shifts glomerular non-selective pores to larger dimensions resulting in excessive leakage of protein in the urine. Endothelial injury resulting from glomerular hyperfiltration causes increase in local generation of Angiotensin II in the kidney as part of the hemodynamic response. ACE inhibitors and angiotensin II receptor antagonists (ATRA) can improve glomerular pore-selectivity by remodelling the glomerular basement membrane. In addition, these agents also have beneficial effects by decreasing TGF-beta production therapy decreasing mesangial cell proliferation, hence ameliorating disease progression in patients with diabetic nephropathy and IgA nephropathy. A number of recent clinical trials have shown that ACEI and ATRA therapy can retard the progression of renal deterioration in patients with NIDDM and those with IgA nephropathy and even restore normal renal function in those with mild renal impairment. Treatment and control of proteinuria in patients with renal disease should be regarded as important as treatment of hypertension as it can prevent renal failure.
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PMID:Proteinuria: clinical signficance and basis for therapy. 1176 58

Case of diabetes mellitus associated with essential hypertension are mostly type 2 diabetes mellitus(NIDDM) in elderly patients. In the JNC VI and JSH 2004, it is recommended that the therapeutic target blood pressure level should be lower then 130/80 mmHg in hypertension complicated with diabetes mellitus, and this target has recently obtained wide acceptance. On the other hand, the target blood pressure in elderly is recommended below 140/90 mmHg. Accordingly, diabetes mellitus in elderly hypertensives should be treated similarly as in the young and middle-aged. Because ACE inhibitors/ARBs or Ca blockers increase insulin sensitivity, these drugs should be used as the first choice in cases of elderly hypertensive patients complicated with diabetes mellitus.
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PMID:[Blood pressure control in eldery hypertension]. 1640 51


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