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)

In order to estimate the neuroendocrine function of the central nervous system eventually leading to growth hormone (GH) secretion in essential hypertension, 17 patients with mild arterial hypertension (7 obese and 10 with normal body weight) were examined. The control group consisted of 16 normotensive volunteers (7 obese and 9 with normal body weight). The GH secretion was determined by radioimmunoassay during nocturnal sleep. In all the subjects, the serum GH was also measured after placebo and after the centrally acting alpha 2-adrenergic agonist-clonidine administered i.v. in a dose of 0.15 mg. The fasting serum insulin concentration was also measured in all the subjects. Clonidine decreased the mean arterial pressure in all the subjects investigated. However, in response to clonidine an increase in GH secretion in all hypertensive and normotensive cases with normal body weight was demonstrated, whereas in all obese hypertensive and normotensive patients no significant GH rise was found. It indicates that inhibition of GH secretion in patients with essential hypertension is related to coexistent obesity rather than with that of arterial hypertension. A strong (r = 0.76) and significant (p less than 0.0005) correlation demonstrated between the maximal GH concentration during the nocturnal sleep and after clonidine suggests that the mechanism of GH inhibition in response to both these stimuli is similar and it probably is related to the inhibition of neurohormonal secretion of the growth hormone releasing factor (GRF). However, the negative correlation between the fasting insulin concentration and GH response to clonidine shown in obese subjects only, points to a more complex mechanism of GH inhibition in obesity.
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PMID:Growth hormone (GH) secretion during nocturnal sleep and after clonidine in patients with essential hypertension. 328 64

The relationship between the fractional excretion of filtered sodium (FENa) and the peritubular capillary physical factors (PCPF) in the hypertension (HT) of chronic glomerulonephritis (GN) was examined in hydropenia (C) and during sustained isotonic saline volume expansion (E; 3% net increase of body weight) in 32 GN patients (16 with HT), and compared with our previous findings in 20 normal individuals (NORM) and 19 patients with essential hypertension (EH). Fourteen GN patients (seven with HT) had a 75% reduction of glomerular filtration rate (GFR), the others (nine with HT) had normal or near normal GFR. The PCPF were estimated from the intrarenal venous (wedged) pressure (IRVP) and the calculated efferent arteriolar protein concentration (EAPC). In C, IRVP correlated to GFR (r = 0.682, p less than 0.001) and (FENa) (r = -0.357, p less than 0.05), but IRVP and EAPC were similar in HT and normotension at comparable levels of GFR. The increase of FENa during E (delta FENa) was exaggerated in all HT groups even at reduced levels of GRF, and could not be related to changes in renal hemodynamics or PCPF. delta FENa correlated with mean arterial pressure in C both in GN (r1 = 0.702, p less than 0.01) and in the combined NORM/EH group (r2 = 0.478, p less than 0.01), with r1 greater than r2 (p less than 0.005). The findings indicate that the pathogenesis of hypertension of chronic glomerulonephritis is independent of changes in the PCPF, and are compatible with the idea that humoral factors are the main mediators of the altered sodium excretion during saline volume expansion in the HT of both chronic GN and EH.
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PMID:Intrarenal pressure and sodium excretion in hypertension of chronic glomerulonephritis in humans. 684 Aug 24

In obesity there is a clear reduction of both spontaneous and stimulated GH secretion. Furthermore, in obese patients the somatotrope responsiveness to provocative stimulation is selectively refractory to the inhibitory effect of glucose load. It has been hypothesized that hyperinsulinism of obese patients could play a role in the pathogenesis of these alterations. Aim of the present study was to verify the GH response to GHRH and the ability of glucose load to inhibit it in patients with essential hypertension in whom hyperinsulinism and insulin resistance are frequently present. To this goal, 7 patients with essential hypertension (HP, age, mean +/- SE: 29.6 +/- 2.4 yr, 3 females and 4 males, BMI: 21.7 +/- 1.2 kg/m2), 7 obese (OB, 4 females and 3 males, 31.9 +/- 4.1 yr, 35.6 +/- 2.0 kg/m2) and 7 normal subjects (NS, 4 females and 3 males, 28.3 +/- 3.9 yr, 21.0 +/- 1.6 kg/m2) underwent the following tests: GHRH (1 microgram/kg i.v. at time 0) alone and preceded by oral glucose load (OGTT, 100 g po at -45 min). Basal insulin levels were similar in HP and OB (11.3 +/- 0.5 and 12.7 +/- 2.2 microU/ml, respectively); these, in turn, were higher (p < 0.005) than those in NS (6.8 +/- 0.8 microU/ml). Basal plasma glucose levels in HP were similar to those in OB and NS (80.3 +/- 3.6, 86.9 +/- 6.7 and 84.4 +/- 1.7 mg/dl, respectively). In HP and OB and NS basal GH (1.0 +/- 0.5, 1.0 +/- 0.6 and 0.3 +/- 0.1 micrograms/l, respectively) and IGF-I levels (132.6 +/- 14.8, 137.3 +/- 13.2 and 138.8 +/- 12.2 micrograms/l, respectively) were similar. In HP the GH response to GHRH (AUC: 1058.8 +/- 347.8 micrograms/l/min) was similar to that observed in NS (959.0 +/- 167.8 micrograms/l/min) and higher than that in OB (344.8 +/- 67.2 micrograms/l/min, p < 0.01). OGTT clearly blunted (p < 0.01) the GHRH-induced GH response in HP as well as in NS (401.8 +/- 104.4 and 521.6 +/- 76.6 (g/l/min, respectively) but not in OB (387.4 +/- 78.8 (g/l/min). The OGTT-induced insulin levels in HP did not differ from those of OB, both being higher (p < 0.05) than those recorded in NS. Glucose levels after OGTT were similar in the three groups. In conclusion, this study demonstrates that, like in normal subjects but differently from in obese patients the GH response to GHRH is normal in patients with essential hypertension and it is normally inhibited by oral glucose load even when these patients show high insulin levels. Thus, it is unlikely that the low somatotrope secretion and its refractoriness to inhibition by glucose load in obesity is due to hyperinsulinism.
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PMID:The inhibitory effect of glucose on growth hormone secretion is lost in obesity but not in hypertension. 943 20