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)

To investigate the role of Angiotensin II in the release of ACTH, the response of adrenocorticotrophic hormone to hypoglycaemia was studied before and during treatment with an angiotensin converting enzyme inhibitor, enalapril, in 15 male patients with essential hypertension. Plasma levels of ACTH were measured before and 60, 90 and 120 min after an i.v. bolus of normal saline, as placebo, and, 3 days later, after an i.v. bolus of regular insulin (0.15 U/Kg b.w.). Enalapril treatment was then started and both placebo and hypoglycaemic tests were repeated 15 days thereafter. No changes in ACTH plasma levels were observed after acute normal saline either before or during enalapril treatment. On the contrary, hypoglycaemia induced a sharp increase of ACTH before enalapril (from 19.5 +/- 4.1 to 74.4 +/- 13.0 pg/ml, p less than 0.01 60 min after insulin) but not during ACE inhibition (from 26.1 +/- 6.2 to 34.6 +/- 5.9 pg/ml, NS, at min 60 of the study). The present data confirm our previous observation on the reduction of the hypoglycaemic-induced ACTH release during ACE inhibition with captopril and support the hypothesis that circulating Ang II may exert a facilitating role on adrenocorticotrophic hormone release.
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PMID:Angiotensin converting enzyme inhibition reduces ACTH release due to hypoglycaemia. 303 30

1. Repeated observations indicate that ACTH administration causes hypertension. 2. Development of hypertension requires 17 alpha-hydroxyprogesterone and 17 alpha,20 alpha-dihydroxy-4-pregnene-3-one to be present in association with other steroids. 3. The hypertensinogenic activity of corticosteroids is distinct from their glucocorticoid and mineralocorticoid effects. 4. The location of central and peripheral receptors for this hypertensinogenic activity is not clear. 5. The physiological mechanisms that mediate the response are unknown, though a number of potential mediating effects has been demonstrated. 6. The overall importance of unusual steroids and steroid actions in human essential hypertension still requires elucidation.
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PMID:Receptors and steroid-dependent hypertension. 307 74

In order to determine arterial pressure and vasoactive hormone relationships in normotensive man, we measured intra-arterial pressure continuously along with hourly venous hormone levels (renin, angiotensin II, aldosterone and catecholamines) for 24 hours in 5 healthy volunteers under standardized conditions. Mean 24-hour levels of intra-arterial pressure 106/63 +/- 5.4/4.9 mmHg were much lower than in patients with mild essential hypertension studied earlier. A common diurnal pattern was seen for plasma renin, angiotensin II, and catecholamines, with higher levels in the day time and lower levels at night. Aldosterone levels however, paralleled those of cortisol at night. Plasma norepinephrine levels showed close, positive correlations with arterial pressure in all volunteers. We conclude that the level of blood pressure as measured continuously over 24 hours is lower than might be expected from regular clinic recordings; that aldosterone regulation is contributed to by ACTH in the nocturnal hours; and that fluctuations in arterial pressure and sympathetic activity over 24 hours are closely coupled.
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PMID:Diurnal patterns of blood pressure, heart rate and vasoactive hormones in normal man. 352 53

A non-ACTH aldosterone-stimulating factor(s) has been implicated in the pathogenesis of idiopathic hyperaldosteronism (IHA). Although this factor has not been fully characterized, some evidence suggests that it may be related to a pro-gamma-melanotropin (pro-gamma-MSH), derived from the NH2-terminal region of pro-opiomelanocortin. In the present study, plasma immunoreactive (IR-) gamma-MSH levels at 0800 h in patients with IHA were evaluated (90 +/- 17 fmol/ml; range: 13-173 fmol/ml) and found to be significantly higher (P less than 0.05) than those in subjects with aldosterone-producing adenomas (33 +/- 8 fmol/ml), essential hypertension (33 +/- 6 fmol/ml), and normotensive controls (19 +/- 2 fmol/ml). Seven of nine IHA subjects had circulating IR-gamma-MSH levels above the normal range (greater than 35 fmol/ml). In plasmas sampled at 1200 h, IR-gamma-MSH was significantly higher in patients with IHA (95 +/- 26 fmol/ml) and adenomas (63 +/- 23 fmol/ml), as compared with essential hypertensives (31 +/- 6 fmol/ml) and normotensives (19 +/- 3 fmol/ml). Mean plasma IR-ACTH, plasma cortisol, and urinary cortisol levels did not differ significantly between any of these groups. In order to evaluate the effect of a pro-gamma-MSH in vitro, adrenal adenoma tissue was obtained from two patients, one with elevated IR-gamma-MSH (61 fmol/ml) and a second with low IR-gamma-MSH (12 fmol/ml). Aldosterone secretion by dispersed adenoma cells from the former, but not the latter, underwent a fourfold dose-dependent (10(-14)-10(-9) M) increase in response to human Lys-gamma 3-MSH. These data suggest that a pro-gamma-MSH may be implicated as a pathogenic factor in a subset of patients with primary aldosteronism, particularly among those differentially diagnosed as having IHA.
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PMID:Plasma immunoreactive gamma melanotropin in patients with idiopathic hyperaldosteronism, aldosterone-producing adenomas, and essential hypertension. 401 76

In this study, the effects of angiotensin II (A II, Asn-Arg-Val-Tyr-Val-His-Pro-Phe) and angiotensin III (A III, Arg-Val-Tyr-Ile-His-Pro-Phe) on blood pressure (B.P.), pulse rate, several hormones [plasma renin activity (PRA), plasma aldosterone (PA), ACTH, plasma cortisol (PC), urinary catecholamines and urinary aldosterone] and urinary electrolytes were investigated in 9 male patients with essential hypertension [mean age 36.2 +/- 4.1 (S.E.) years]. A II and A III infusions (8 ng/kg/min, 60 min) were started from 0900 h and blood samples were drawn before, at 15, 30, 45, 60 min after the beginning of the infusions, and at 15 min after their cessation. Urinary samples were collected within 2 hrs before and after the infusions, respectively. A II significantly increased B.P.(p less than 0.01) during the infusions, whereas A III did not increase B.P.. PRA significantly decreased after the infusions of A II and A III (p less than 0.05), but the potency of A II was significantly greater than that of A III (p less than 0.01). PA was increased after both infusions, but in response to A III, a peak was observed at 30 min after the infusion and subsequently, the levels decreased gradually. Significant differences between both responses were found at 45 and 60 min (p less than 0.05) after the infusions. ACTH was unchanged during the infusions, but PC was equipotentially suppressed during the infusions, with the suppression of A II being similar to that of A III. In the responses of urinary catecholamines, noradrenaline and dopamine were equipotentially decreased after the infusions (p less than 0.05). The results of the present study clearly indicate that several differences exist between the biological activities of A II and those of A III. Further systematic experimental studies are needed to resolve the details.
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PMID:[Changes in responses of blood pressure and several hormones to infusions of angiotensin II and angiotensin III in patients with essential hypertension]. 609 61

A total of 192 subjects with borderline hypertension, essential hypertension (labile and stable patterns) and practically normal persons (controls) were examined. The basal plasma concentration of aldosterone, progesterone and cortisol as well as blood renin activity was measured in all the subjects in the orthostatic position. After intravenous injection of ACTH in a dose of 12.5 Units the blood was collected for analysis after 60 and 120 minutes. The basal level of corticosteroids underwent the most distinct alterations in patients with the labile and stable patterns of essential hypertension. The ACTH test pointed to definite changes in corticosteroid secretion in some subjects with borderline arterial hypertension. The test enabled one to identify a clear-cut dissociation in the aldosterone and progesterone reactions in subjects with stable essential hypertension. The ACTH test also made it possible to reveal a distinct functional relationship between the renin-angiotensin system and adrenal cortex, which was considerably impaired in stable essential hypertension.
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PMID:[Effect of ACTH on serum corticosteroid level in patients with hypertension]. 609 45

The response of plasma aldosterone (PA) and plasma renin activity (PRA) to ACTH stimulation (0.25 mg Tetracosactide infusion/10 h) and to insulin-induced hypoglycemia (0.1 U/kg b.w.) has been studied in 34 essential hypertensive (EH) patients. Corticotrophin stimulation increases significantly PA, the percent increase being higher in normal PRA EH patients than in controls but comparable to controls in low PRA EH patients. PRA shows a slight and transient elevation. A significant increase in PA is observed also during the insulin test, but the percent increase is lower than that under ACTH stimulation. The possibility that aldosterone is involved, under severe and frequent stress, in the genesis of essential hypertension is discussed.
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PMID:[Behavior of aldosterone and plasma renin activity after ACTH administration and insulin-induced hypoglycemia in patients with essential arterial hypertension]. 626 56

Plasma concentration of progesterone (P), 17 alpha-hydroxyprogesterone (17 alpha-P), 11-desoxy-cortisol (S), cortisol (F), 11-desoxycorticosterone (DOC), corticosterone (B), aldosterone (ALD), dehydroepiandrosterone-free (DHA-f), dehydroepiandrosterone-sulfate (DHA-s) and testosterone (TEST) were measured in 26 essential hypertension (E.H.) and 6 primary aldosteronism (P.A.) before, 30 min. and 60 min. after the intravenous infusion of ACTH 250 micrograms. Seven E.H. patients were similarly studied in the condition of low and high sodium intake and plasma renin activity (PRA) was also measured at the same time. P.A. showed significantly higher ALD than that of E.H., whereas DHA-f and DHA-s levels of these patients were lower than that of E.H. In men with E.H., TEST level showed step down response to ACTH. Low sodium intake induced a marked increase of ALD and PRA in E.H. In low sodium intake other mineralocorticoids such as DOC and B showed high value at 60 min (20% t value) after ACTh infusion. From these observations, it was suggested that the mineralocorticoids have a good response to ACTh in low sodium intake rather than high sodium intake, especially ALD has a clearly augmented response to ACTh. On the other hand, PRA showed only a reserve response to ACTH infusion.
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PMID:[Response of several adrenal steroids to rapid ACTH stimulation test in essential hypertension and primary aldosteronism (author's transl)]. 627 61

To study effects on pituitary-adrenocortical activity of a sustained block of angiotensin II formation, six 'drug-resistant' patients with essential hypertension were studied before and during treatment with an inhibitor of the angiotensin-converting enzyme (Captopril, SQ 14,225). The drug was given in increasing doses (100-400 mg/day) for 2 weeks whilst patients received a moderately restricted sodium intake (60-80 mmol/day). Immunoreactive ACTH, cortisol, aldosterone, plasma renin activity (PRA) and the activity of the angiotensin-converting enzyme (ACE) were measured in blood samples drawn at 0800-0900 h. Urinary excretion of cortisol and aldosterone were measured in 24-h urine collections. Further information on pituitary-adreno-cortical function was obtained by measuring serial plasma corticosteroid levels after submaximal stimulation with a synthetic ACTH preparation. ACTH and cortisol did not change an observation which does not support the hypothesis that glucocorticoid activity is influenced by a decrease in plasma angiotensin II concentrations.
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PMID:Pituitary - adrenocortical function in patients during treatment with the angiotensin-converting enzyme inhibitor captopril. 627 52

1. The haemodynamic and volume response to ACTH administration was investigated in six patients with mild, untreated essential hypertension and two patients with Addison's disease on maintenance steroids. Blood pressure, heart rate and weight were recorded daily. Plasma volume (125I-HSA) and cardiac output (thermo-dilution) were measured during the control period and on the 5th day of ACTH treatment. 2. In the hypertensive subjects, mean arterial pressure rose from 94.3 +/- 2.2 to 105.7 +/- 2.8 mmHg on the 5th day of ACTH administration (P less than 0.02). Plasma volume rose from 29.8 +/- 2.2 to 34 +/- 2.2 ml/kg. Cardiac index increased from 2.85 +/- 0.21 to 3.32 +/- 0.14 l/min per m2 (P less than 0.05). Cardiac output rose from 5.81 +/- 0.69 to 6.72 +/- 0.59 l/min. Calculated total peripheral resistance, heart rate and body weight were unchanged. No such changes were seen in patients with Addison's disease. 3. The haemodynamic characteristics of ACTH in patients with mild untreated essential hypertension are similar to those in the experimental model of ACTH induced hypertension in sheep.
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PMID:Haemodynamic response to ACTH administration in essential hypertension. 627 65


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