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)

An increase in glomerular filtration rate and in tubular Na+ reabsorption from the parenteral administration of insulin-like growth factor I (IGF-I) have been reported in human subjects. To evaluate whether glomerular hyperfiltration and Na+ hyper-reabsorption present in some essential hypertensives are associated to an excess of IGF-I, the plasma levels of this factor and several parameters of renal function were studied in 30 non-treated essential hypertensives and in 30 normotensive controls. IGF-I levels were higher in hypertensive as compared to controls. With the 95% (upper) limit of the normotensive population as a cut-off point, a subgroup of six hypertensives had an abnormally high IGF-I level. Mean blood pressure was slightly lower in these six patients (112 +/- 7 mmHg) than in the remaining patients (120 +/- 2 mmHg). As compared to normotensives and hypertensives with normal IGF-I levels, patients with increased IGF-I levels were characterized by lower (P < 0.01) fractional Na+ excretion and higher (P < 0.05) creatinine clearance. The analysis of the relation of plasma renin activity and the concurrent daily rate of Na+ excretion showed that patients with increased IGF-I were low-renin hypertensives and patients with normal IGF-I were normal-renin hypertensives. These results indicate that an association exists between exaggerated circulating levels of IGF-I and abnormalities of renal function present in some patients with essential hypertension. It is suggested that IGF-I can play a role in low-renin essential hypertension.
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PMID:Abnormalities of renal function in essential hypertension with increased circulating levels of insulin-like growth factor I. 148 57

An excess of circulating insulin-like growth factor I (IGF-I) has been found in patients with essential hypertension and left ventricular hypertrophy (LVH). In addition, an increase in collagen type III synthesis has also been reported in hypertensive patients. Since IGF-I is a positive effector of collagen type III expression, we have investigated whether a relationship exists between circulating IGF-I and collagen type III synthesis in patients with essential hypertension. The relationship between plasma concentrations of IGF-I and an index of tissue synthesis of collagen type III (serum concentrations of procollagen type III aminoterminal peptide [PIIIP]) was investigated in 37 patients with essential hypertension before and after six months of treatment with lisinopril. The control group consisted of 30 age- and sex-matched normotensive subjects without LVH. Baseline concentrations of IGF-I were higher in hypertensive patients than in normotensive controls (285 +/- 25 vs. 240 +/- 15 ng/ml; P < 0.01). Mean IGF-I levels were higher in hypertensive patients with LVH (n = 10, 330 +/- 49 ng/ml) than in those without LVH (n = 27, 252 +/- 25 ng/ml; P < 0.05). Baseline concentrations of PIIIP were higher in hypertensive patients than in normotensive controls (10.07 +/- 0.54 vs. 8.47 +/- 0.77 ng/ml; P < 0.01). Mean PIIIP levels were higher in hypertensives with LVH than in those without LVH (12.20 +/- 0.78 vs. 7.97 +/- 0.55 ng/ml; P < 0.05). There was no correlation between IGF-I and PIIIP at baseline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin-like growth factor I and collagen type III synthesis in patients with essential hypertension and left ventricular hypertrophy. 780 9

In a previous work we have found than an association exists between the presence of left ventricular hypertrophy (LVH) and increased circulating levels of insulin-like growth factor I (IGF-I) in essential hypertension. To address whether this association is of pathophysiological relevance the relationship between echocardiographically determined LVH and IGF-I levels was investigated in 49 patients with essential hypertension before and after one year of antihypertensive treatment with different regimens (nonpharmacological measures, bisoprolol, captopril). The control group consisted of 30 normotensive subjects without LVH. Before treatment IGF-I levels were higher (p < 0.05) in hypertensives with LVH, n = 17, (81.3 +/- 14.3 ng/ml) compared with hypertensives without LVH, n = 32, (57.4 +/- 3.9 ng/ml) and controls (61.3 +/- 3.9 ng/ml). A positive correlation was found between IGF-I levels and LVMI in the whole group of hypertensives (r = 0.32, p < 0.05). After one year of treatment hypertensives with initial LVH separated in two subgroups: those in which LVH regressed (n = 10) and those in which LVH persisted (n = 7). A similar diminution of BP was observed in the two subgroups of hypertensives. The IGF-I levels decreased significantly in patients in which LVH regressed (101.6 +/- 21.7 vs. 61.2 +/- 8.5 ng/ml; p < 0.05) and increased slightly in patients in which LVH persisted (51.2 +/- 8.9 vs. 68.5 +/- 7.9 ng/ml). Six patients in which LVH regressed showed a diminution of IGF-I after treatment. These six patients had received captopril as treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of antihypertensive therapy on left ventricular hypertrophy of essential hypertension: a role for insulin-like growth factor I? 826 89

Depletion of intracellular free magnesium (Mg(i)) is a characteristic feature of insulin resistance in essential hypertension, but it is not clear to what extent low Mg(i) levels contribute to insulin resistance, result from it, or both. As insulin-like growth factor I (IGF-I) may improve insulin resistance, we investigated whether this peptide could similarly improve Mg(i) responsiveness to insulin in hypertension, and whether this effect was related to any direct IGF-I effect on Mg(i). 31P-Nuclear magnetic resonance spectroscopy was used to measure Mg(i) in erythrocytes from 13 fasting normotensive and 10 essential hypertensive subjects before and 30, 60, and 120 min after incubation with a physiologically maximal dose of insulin (200 microU/mL) and with different doses of recombinant human IGF-I (0.1-100 nmol/L). In normotensive subjects, IGF-I elevated Mg(i) (P < 0.05) in a dose- and time-dependent fashion, as did insulin (P < 0.05). However, in hypertensive subjects, maximal Mg(i) responses to insulin, but not to IGF-I, were blunted [insulin, 163+/-11 to 177+/-10 micromol/L (P=NS); IGF-I, 164+/-6 to 190+/-11.7 micromol/L (P < 0.05)]. Furthermore, for insulin, but not for IGF-I, cellular Mg(i) responsiveness was closely and directly related to basal Mg(i) levels (insulin: r=0.72; P < 0.01; IGF-I: r=0.18; P=NS). Lastly, blunted Mg(i) responses to insulin could be reversed by preincubation of hypertensive cells with IGF-I. We conclude that 1) both IGF-I and insulin stimulate erythrocyte Mg(i) levels; 2) cellular Mg(i) responses to insulin, but not to IGF-I, depend on basal Mg(i) levels, i.e. the higher the Mg(i) the greater the sensitivity to insulin; and 3) IGF-I potentiates insulin-induced stimulation of Mg(i) at doses that themselves do not raise Mg(i). These effects of IGF-I may underlie at least in part its ability to improve insulin sensitivity clinically. Together, these data support a role for IGF-I in cellular magnesium metabolism and emphasize the importance of magnesium as a determinant of insulin action.
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PMID:Magnesium responsiveness to insulin and insulin-like growth factor I in erythrocytes from normotensive and hypertensive subjects. 985 85