Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies using human pituitary extracts have not resolved whether the sodium retaining effects of human growth hormone (hGH) are mediated in part by increased aldosterone secretion. We have studied the effects of an authentic biosynthetic GH (bio-hGH) preparation on sodium metabolism and on the activity of the renin-angiotensin system. Six young men were administered this preparation at 0.2 U/kg/d subcutaneously for five consecutive days. Twenty-four-hour urine collections were obtained for measurement of sodium excretion and osmolality and blood collected for quantitating changes in sodium, osmolality, plasma renin activity (PRA), aldosterone, and arginine vasopressin (AVP) concentrations. Bio-hGH administration resulted in a fall in 24-hour urinary sodium excretion (197 +/- 38 to 42 +/- 20 mmol, mean +/- SD, P less than .005), a reduction in urine volume (1,652 +/- 182 to 848 +/- 348 mL, P less than .05) but not osmolality. PRA increased significantly from 1,118 +/- 73 to 3,608 +/- 1,841 fmol angiotensin 1 L/s (P less than .005), which was associated with a sevenfold increase in plasma aldosterone concentration (52 +/- 12 to 402 +/- 99 pg/mL, P less than .001). Plasma osmolality and AVP concentrations did not change significantly. The results show that Bio-GH-induced retention of sodium involves the activation of the renin-angiotensin system. This mechanism may explain in part the occurrence of plasma volume expansion and hypertension in acromegaly and suggests a risk of fluid retention and possibly hypertension in subjects receiving supraphysiological doses of bio-hGH for treatment of short stature.
 ...
PMID:The antinatriuretic action of biosynthetic human growth hormone in man involves activation of the renin-angiotensin system. 240 33

Acromegaly is associated with an increased cardiac morbidity and mortality, but it is not clear whether this is the result of increased incidence of hypertension and coronary heart disease or of a specific disease of heart muscle. Thirty four acromegalic patients were studied by non-invasive techniques. Seven of these patients had raised plasma concentrations of growth hormone at the time of study; three were newly diagnosed and had not received any treatment. Hypertension was present in nine (26%) but only three (9%) had electrocardiographic left ventricular hypertrophy. Echocardiography showed ventricular hypertrophy in 12 (48%) and increased left ventricular mass in 17 (68%) patients. Holter monitoring detected important ventricular arrhythmias in 14 patients. Thallium-201 scanning showed evidence for coronary heart disease in eight patients. Systolic time intervals were normal except when there was coexistent ischaemic heart disease. A comparison between 19 acromegalic patients with no other detectable cause of heart disease and 22 age matched controls showed appreciably abnormal left ventricular diastolic function in the group with acromegaly. The abnormalities shown did not correlate with left ventricular mass or wall thickness. There was no difference in diastolic function between patients with active acromegaly and those with treated acromegaly. Hypertensive acromegalic patients had worse diastolic function than hypertensive controls, suggesting that hypertension may further impair the left ventricular diastolic abnormality in acromegaly. This is the first study to find evidence of subclinical cardiac diastolic dysfunction in acromegaly and it supports the suggestion that there is a specific disease of heart muscle in acromegaly.
 ...
PMID:Subclinical cardiac dysfunction in acromegaly: evidence for a specific disease of heart muscle. 239 Mar 94

We have studied plasma ANF before and after a 4-h intravenous infusion of normal saline in eight subjects with active acromegaly and in eight age and sex-matched control subjects. Plasma ANF, serum aldosterone and blood pressure were measured basally and after 2 and 4 h and plasma renin activity basally and after 4 h. Basal plasma ANF was similar in each group (4.4 +/- 1.5 pmol/l (mean +/- SEM) in acromegalic subjects and 5.3 +/- 0.7 pmol/l in controls NS). Plasma ANF did not rise significantly after saline in the acromegalic group (2-h value, 5.9 +/- 0.9; 4-h value, 5.1 +/- 0.9 pmol/l) but did rise significantly in the control group (2-h value, 8.9 +/- 1.9; 4-h value 9.5 +/- 1.3 pmol/l, both values P less than 0.05 vs basal level). The 4-h ANF value was significantly higher in the control group than in the acromegalic group (P less than 0.05). Basal and stimulated serum aldosterone values were similar in the two groups. Plasma renin activity suppressed to a lesser extent in the acromegalic group after 4 h. The facts that basal plasma ANF was not raised in acromegalic subjects and did not respond to saline stimulation demonstrate that an abnormality of ANF control may be an important factor in the aetiology of the expanded sodium status of patients with acromegaly and hence may contribute to the hypertension seen in patients with growth hormone excess.
 ...
PMID:Basal and saline-stimulated levels of plasma atrial natriuretic factor in acromegaly. 253 66

The aim of our echocardiographic study was to characterize cardiac function and anatomy of 14 acromegalics (A: 9 women, 5 men; mean age: 42.4 yrs) more closely. The duration of acromegaly in 4 of these patients was between 3 and 12 years; the disease was diagnosed for the first time in the other patients. Double M-mode echocardiography was performed in all patients and the results compared with data obtained from a control group of 24 healthy volunteers (N: 22 men, 2 women; mean age: 23 yrs). The mean left ventricular diameter at end-diastole was greater in the acromegalics than in the controls (A: 55 +/- 6 mm, N: 50 +/- 4 mm; p less than 0.005, means +/- SD). After correction for age and body surface area, it, however, was outside the 95% confidence interval in 5 patients. Left ventricular hypertrophy was present in 3 patients, one of whom had coexistent arterial hypertension. A total of 3 patients were hypertensive. Significantly higher values for the maximal velocity of systolic wall thickening (A: 6.1 +/- 0.6 cm/s, N: 4.2 +/- 0.6 cm/s, p less than 0.001) and diameter change (A: 12.4 +/- 2.0 cm/s, N: 10.6 +/- 1.0 cm/s, p less than 0.005) indicate increased contractility with concurrently increased relaxation; fractional shortening did not differ significantly (A: 38 +/- 5%, N: 37 +/- 5%, ns). The isovolumetric relaxation period at diastole was slightly longer in the acromegalics (A: 70 +/- 17 ms, N: 61 +/- 13 ms, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Cardiac function in endocrine diseases: I. Acromegaly. 258 16

As previously shown, in essential hypertension postprandial plasma insulin concentrations are elevated. In order to determine a relationship of high blood pressure and plasma insulin levels in acromegaly and in obesity 59 subjects with normal glucose tolerance were studied. They were divided into three groups: (I) patients with acromegaly: 7 normotensives and 8 hypertensives, (II) 12 obese normotensives and 12 obese hypertensives and (III) 10 non-obese hypertensives, and 10 healthy subjects. Blood glucose and plasma insulin concentrations were measured in a fasting state and after an oral glucose load of 75 g. The fasting insulin concentrations in all the acromegalics and in all the obese patients were higher than those in healthy subjects. The insulin response to the glucose load was significantly enhanced in all the three groups of hypertensive patients compared with those of matched normotensive controls. The results indicate that insulin may play a role in the regulation of blood pressure in essential hypertension, and in such hyperinsulinaemic disorders as acromegaly and obesity.
 ...
PMID:High blood pressure and hyperinsulinaemia in acromegaly and in obesity. 266 41

Fifty to sixty percent of clinical hypertension is sensitive to sodium (Na) intake: known causes, primary aldosteronism, bilateral renal artery stenosis, mild azotemia, acromegaly, and low-renin hypertension account for only a fraction. We have identified a group of normal-renin hypertensives characterized by inability to modulate normally their renal vascular and adrenal responsiveness to angiotensin II. These patients handle shifts in Na intake abnormally, show more positive balance on a high-salt diet, and raise their blood pressure when shifted to a high-salt diet. Renal blood flow does not shift with Na intake, but does respond strikingly to converting enzyme inhibition, which also corrects altered renal and adrenal responsiveness, ability to handle a sodium load, and hypertension. These patients have a striking family history of hypertension; 50% of the offspring of hypertensives show similar features, including a renal vasodilator response to converting enzyme inhibitors or calcium channel blocking agents. Accumulating evidence suggests that the abnormality is inherited and may be the most common form of hypertension.
 ...
PMID:Sodium-sensitive hypertension. Implications of pathogenesis for therapy. 267 76

Essential hypertension has long been assumed to be a multifactorial disease. However, recent evidence suggests that it is a syndrome rather than a disease with a common symptom--an elevated blood pressure. One large segment of the hypertensive population--approximately 60%--has in common an increased blood pressure sensitivity to salt intake. Further analysis of this subgroup suggests that it is also heterogeneous, consisting of at least six major entities: renal parenchymal disease, bilateral renal artery stenosis, primary aldosteronism, acromegaly, low renin essential hypertension, and the most recently described entity--nonmodulating essential hypertension. This subset's name is derived from the fact that sodium intake does not modify (modulate) renovascular and adrenal responses to angiotensin II, as occurs in normotensives and modulating hypertensive patients. The following abnormalities have been reported in these patients: (1) a failure of renal blood flow to increase with salt loading; (2) a reduced ability to excrete a salt load; (3) reduced renin suppression both by salt and angiotensin II; and (4) a hypertensive response to salt load. These patients also have a strong family history for hypertension and an increase in erythrocyte sodium countertransport. With a better understanding of the mechanisms underlying the elevated blood pressure in a specific patient, a more rational approach to therapy is possible. For example, in the salt-sensitive hypertensive patient a diuretic would be the presumed treatment of choice. While this is correct for some salt-sensitive hypertensives, in nonmodulators diuretics may be relative ineffective while converting enzyme inhibitors may be more effective because they specifically correct the underlying pathophysiologic derangement.
 ...
PMID:Sodium-sensitive essential hypertension: emerging insights into an old entity. 269 48

Clinical examination and blood pressure measurement over the ankle in 31 patients with acromegaly, showing signs of active disease, did not reveal manifestations of obliterative arterial disease in the lower limbs. Sixteen of the patients had a normal blood pressure; in none of them did the authors find a deviation of blood flow in the foot and in the calf at rest and during reactive hyperaemia following 5-minute ischaemia. Fifteen patients with hypertension were found to have increased resting blood flow in the foot and calf and increased blood flow in the foot during reactive hyperaemia.
 ...
PMID:Peripheral circulation in hypertensive and normotensive acromegalics. 276 53

Using mice transgenic for the growth hormone gene (TGHM), we have studied the effects of a systemic elevation of growth hormone on vascular growth with the aim of investigating the role of vascular mass changes in producing hypertension. In contrast to human acromegaly or gigantism, there was no elevation of blood pressure in TGHM, but there were significant increases in vascular wall mass. In accordance with a presumably increased perfusion of larger organs, the medial cross-sectional areas of thoracic aorta and mesenteric resistance vessels were greater in the TGHM. These differences could be normalized in the aorta by body weight and in the mesenteric vessel by small intestine weight. Furthermore, the brain was not significantly heavier in the TGHM, and their carotid and cerebral vessels also were not larger. Wall-to-lumen ratios were similar in the aorta, carotid, and middle cerebral arteries suggesting that wall stress was the controlling factor in wall thickness. Surprisingly, the mesenteric vessels had increased wall-to-lumen ratio, which was similar to that seen in hypertensive vascular remodeling but in a normotensive animal. In an attempt to explain this finding it was noted that the pattern of mesenteric vascular networks and even organized structure within the vessel wall itself appeared to be fixed, perhaps by genetic mechanisms. Thus, vascular network structure may be a potentially limiting factor in the ability of the vessel wall to remodel and may have been responsible for the greater wall-to-lumen ratio in TGHM mesenteric vessels. A similar situation in human acromegaly or gigantism could result in a circulation marginally able to correct for other demands on blood flow resulting in about one third of cases being hypertensive.
 ...
PMID:Vascular remodeling in the growth hormone transgenic mouse. 280 41

In order to elucidate the role of the dopaminergic system in the control of aldosterone secretion in acromegaly with arterial hypertension 10 patients and 10 healthy volunteers were studied. Plasma aldosterone and prolactin were determined by radioimmunological methods after dopaminergic receptor blockade with metoclopramide and sulpiride. Plasma aldosterone was also determined after adrenal stimulation with synthetic corticotrophin (Synacthen). In patients with acromegaly and hypertension, the aldosterone secretion in response to metoclopramide was completely inhibited whereas induced with corticotrophin was lower than in controls. Also prolactin secretion in response to metoclopramide or sulpiride was markedly lower as compared with that in controls. Sulpiride did not stimulate aldosterone secretion either in patients or in healthy controls. The results indicate that the dopaminergic control of aldosterone secretion in acromegaly with arterial hypertension is altered.
 ...
PMID:Arterial hypertension in acromegaly: altered dopaminergic control of aldosterone secretion. 283 67


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>