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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In previous studies short-term cortisol increased cold pressor responses and the rise in forearm vascular resistance accompanying intra-arterial norepinephrine without an increase in overall resting sympathetic nervous activity. The present study examined whether these alterations in pressor response are glucocorticoid or mineralocorticoid effects, or both. Normal male subjects (n = 12) received either fludrocortisone, 0.3 mg daily (n = 6), or dexamethasone, 3 mg daily (n = 6), for 7 days. Hemodynamic studies were performed before and on day 7 of treatment. Fludrocortisone increased body weight from 69.3 +/- 1.8 to 71.1 +/- 2 kg (p less than 0.001), cardiac output from 5.0 to 6.0 l/min (+/- 0.1, p less than 0.01), mean arterial pressure from 82 +/- 1 to 91 +/- 1 mm Hg (p less than 0.001), cold pressor responsiveness from 13.0 to 39.0 mm Hg/ml per 100 ml per minute (R units) (+/- 4.3, p less than 0.01), and forearm vascular response to intra-arterial norepinephrine (F = 59.4, p less than 0.01) and angiotensin II (F = 30.8, p less than 0.01) infusions. Total peripheral resistance fell from 22.0 to 20.1 mm Hg/l per minute (+/- 0.3, p less than 0.05). Dexamethasone did not increase cardiac output, 5.1 to 5.2 l/min (+/- 0.1), or body weight but did increase mean arterial pressure from 82 +/- 3 to 91 +/- 3 mm Hg (p less than 0.001), cold pressor responsiveness from 8.6 to 17.1 R units (+/- 2.8, p less than 0.05), and forearm vascular response to intra-arterial norepinephrine (F = 33.0, p less than 0.01) and angiotensin II (F = 54.9, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Jun
PMID:Pressor responsiveness in corticosteroid-induced hypertension in humans. 159 52

To gain insight into the role of the sympathetic nervous system in the development of mineralocorticoid hypertension, we determined noradrenaline and adrenaline in plasma and urine before, during and after administration of the synthetic steroid, fludrocortisone, for a period of 6 weeks in normotensive volunteer subjects. In addition, pressor reactivity to exogenous noradrenaline, platelet alpha 2- and lymphocyte beta 2-receptors, and platelet intracellular free calcium were determined. Fludrocortisone induced a fall in free and sulpho-conjugated plasma noradrenaline and after 6 weeks, a rise in free and sulpho-conjugated noradrenaline excretion. The number of alpha 2- and beta 2-adrenergic binding sites decreased. A marked increase in platelet free intracellular calcium was found after the first week of fludrocortisone administration followed by a decrease in the following weeks. Reactivity to exogenous noradrenaline was found to be enhanced and this could be a factor contributing to the development of hypertension. Whereas the decrease in plasma noradrenaline observed would suggest a diminution in sympathetic tone, the finding of a rise in urinary noradrenaline excretion after 6 weeks of steroid administration in the presence of suppressed plasma levels points to an increased renal sympathetic drive. The decreased number of platelet alpha 2- and lymphocyte beta 2-receptors observed would also be consistent with the assumption of an increased sympathetic tone.
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PMID:Sympathetic tone and pressor response to noradrenaline during mineralocorticoid-induced blood pressure rise in man. 300 4

The effect of treatment with 9 alpha-fluorocortisol (9 alpha FF), a steroid which causes hypertension in sheep, was examined in sheep with ACTH-induced hypertension. ACTH treatment alone increased mean arterial pressure (MAP), plasma Na concentration, water intake and urine volume and decreased plasma K concentration. 9 alpha FF treatment, for 3 days during continuing ACTH administration, did not change blood pressure but increased heart rate, water intake and urine volume and decreased urinary K excretion. As 9 alpha FF did not cause a further increment in blood pressure in sheep with ACTH-induced hypertension it is possible that both ACTH and 9 alpha FF may produce hypertension by similar mechanisms.
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PMID:The effect of the 'hypertensinogenic' steroid, 9 alpha-fluorocortisol on blood pressure in sheep with ACTH-induced hypertension. 301 28

Normal subjects, normal-renin hypertensive patients, and low-renin hypertensive patients were evaluated by intravenous saline infusion and with a fludrocortisone acetate (Florinef) protocol to clarify diagnostic criteria for primary aldosteronism that are recommended for the saline infusion protocol. The patients consumed a 200 mEq sodium, 70 mEq potassium diet for 6 days, and on the last 3 days received Florinef 0.5 mg orally twice daily. On Days 3 and 6, urinary aldosterone and tetrahydroaldosterone excretions were determined, and on Days 4 and 7 plasma aldosterone (PA) was determined at 0600 after overnight recumbency and at 0800 after 2 hours of walking. Although the level of normal PA suppression by saline infusion has been commonly defined as 10 ng/dl, a value of 5 ng/dl was originally recommended. In 20 normal subjects and 45 normal-renin hypertensive patients, we found that the PA was almost always suppressed below 5 ng/dl. In 18 of 75 low-renin patients including five with aldosterone-producing adenoma (APA), the PA was never suppressed below 10 ng/dl; thus, these 18 patients had classical primary aldosteronism by generally accepted criteria. The Florinef protocol was performed in eight of these 18 patients and was abnormal in all. An abnormal Florinef protocol was also found in seven of 15 patients studied with PA suppression after saline infusion to between 5 and 10 ng/dl, but in only one of 24 patients studied with PA suppression below 5 ng/dl. Additional studies in the subgroup with abnormal results from the Florinef protocol indicated that none of these patients had evidence of APA, so they had nontumorous primary aldosteronism (NTPA).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Further evaluation of saline infusion for the diagnosis of primary aldosteronism. 638 37

9 alpha-Fluorocortisol (9 alpha FF) is an analogue of cortisol with 'mineralocorticoid', 'glucocorticoid' and 'hypertensinogenic' activity. 9 alpha FF was infused at 2 mg/day for 5 days to sheep receiving a normal Na intake (100 mmol/d) and a high K intake (congruent to 800 mmol/d). K loading modified the Na retaining effects of 9 alpha FF but had no effect on the development of the hypertension. These experiments suggest that the effects of K loading on the development of 9 alpha-FF hypertension are not related simply to the effects that K has on modifying the Na retaining effects of the steroid.
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PMID:The influence of potassium loading on the pressor and metabolic effects of 9-alpha-fluoro-cortisol in sheep. 650 88

Hypertension and hypokalemia were found in a 60-yr-old woman suffering from primary hyperparathyroidism. Laboratory investigations in this patient disclosed 1) elevated levels of plasma aldosterone (PA) which could not be suppressed by a high sodium diet alone or in combination with fludrocortisone (Florinef); 2) a decline of the elevated PA levels after 4 h of ambulation; and 3) low PRA which was unresponsive to stimulation by a low sodium diet coupled with diuretic-induced volume depletion and 4 h of ambulation. These findings were consistent with the diagnosis of primary hyperaldosteronism. Extirpation of a parathyroid adenoma reduced the patient's serum calcium level to normal, and subsequently, a normalization of her blood pressure, serum electrolytes, PA, and PRA were observed. On the basis of these data is is suggested that in this case hyperaldosteronism may have been caused directly or indirectly by primary hyperparathyroidism.
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PMID:Primary hyperparathyroidism: possible cause of primary hyperaldosteronism in a 60-year-old woman. 699 17

Urinary kallikrein excretion has been reported to be decreased in patients with essential hypertension and elevated in patients with primary aldosteronism as a reflection of mineralocorticoid activity. Low renin essential hypertension (LREH) has been postulated to result from excess production of an unknown mineralocorticoid(s). Urinary kallikrein excretion was compared in outpatients with essential hypertension, mineralocorticoid hypertension (primary aldosteronism and 17alpha-hydroxylase deficiency), and in normal subjects of the same race. No significant difference in urinary kallikrein excretion of patients with LREH vs. normal renin essential hypertension (NREH) was found for either black (4.1+/-0.4 vs. 4.8+/-0.5 esterase units (EU)/24 h, mean+/-SE, for 27 LREH and 38 NREH, respectively) or white patients (12.2+/-2.3 vs. 11.7+/-1.4 EU/24 h for 13 LREH and 25 NREH, respectively). Urinary kallikrein was decreased in black vs. white hypertensive patients and normal subjects. However, in patients with normal renal function (creatinine clearance >/=80 ml/min) urinary kallikrein was not significantly decreased in either black hypertensive vs. black normal subjects (4.3+/-0.3 vs. 5.4+/-0.6 EU/24 h) or in white hypertensive vs. white normal subjects (11.9+/-1.2 vs. 8.4+/-0.9 EU/24 h). In contrast, hypertensive patients with mild renal insufficiency (creatinine clearance of 41.8+/-78.5 ml/min) had reduced (P < 0.05) urinary kallikrein (3.3 EU/24 h with creatinine clearance of 63.6+/-2.0 for 24 black patients and 4.2+/-0.7 EU/24 h with creatinine clearance of 67.0+/-3.5 for 6 white patients). These results suggest that a reduction in urinary kallikrein excretion rate is an early accompaniment of hypertensive renal injury. Urinary kallikrein excretion in response to a 6-d 10-meq sodium diet and a 3-d Florinef (0.5 mg b.i.d.) administration was compared in hypertensive patients with normal renal function vs. race and age-matched normal subjects. Stimulation of urinary kallikrein excretion by Florinef was equal in black and white normal subjects vs. hypertensive patients (black normals = 12.3+/-2.7 [n = 9], NREH = 11.7+/-1.8 [n = 10], LREH = 10.9+/-1.5 [n = 12]; white normals = 21.2+/-2.9 [n = 11], essential hypertension = 20.9+/-3.2 [10 NREH, 5 LREH]). Stimulation of urinary kallikrein excretion with low sodium diet was decreased (P < 0.05) only in black LREH (black normals = 11.2+/-2.4 [n = 10], NREH = 10.1+/-2.7 [n = 10], LREH = 7.4+/-1.1 [n = 13]; white normals = 19.1+/-2.7 [n = 13], essential hypertension = 17.5+/-2.3 [nine NREH, four LREH]). However, during low sodium diet, black patients with LREH had evidence for less sodium depletion as manifested by a decreased rise in urinary aldosterone excretion (16.3+/-2.7 vs. 33.3+/-6.4 mug/24 h for black normals) and a failure to achieve metabolic balance in 11/13 patients. Thus, the lesser kallikrein stimulation appeared to result from these two factors. Black and white hypertensives with creatinine clearance <80 ml/min had little increase in urinary kallikrein excretion with Florinef or low sodium diet.5 of 12 patients with primary aldosteronism or 17alpha-hydroxylase deficiency did not have an elevated urinary kallikrein excretion rate. Mild renal insufficiency may have contributed to this finding in two of these five patients. Nevertheless, this finding illustrates a limitation to the use of urinary kallikrein excretion rate as an index of mineralocorticoid activity. However, it appears that the majority of patients with LREH have no evidence for excess production of an unknown mineralocorticoid. The failure to find a decrease in urinary kallikrein excretion in racially matched patients with essentil hypertension and normal renal function questions the postulate of a role of the kallikrein-kinin system in the initiation of essential hypertension.
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PMID:Urinary kallikrein excretion in essential and mineralocorticoid hypertension. 735 84

A 56-year-old white female presented with longstanding hyperkalemia, hyperchloremia, and hypertension. Renal function was normal. Plasma renin levels were low as were serum and urinary aldosterone. Plasma cortisol levels were normal. Fludrocortisone was ineffective in lowering serum potassium. Plasma renin and aldosterone levels responded appropriately to salt restriction and to postural changes. Plasma atrial natriuretic hormone (ANH) and urinary prostaglandins (PG) were normal. Salt loading resulted in suppression of renin and aldosterone levels and stimulation of plasma ANH and urinary PG but failed to increase potassium or chloride excretion. The persistent hyperkalemia, hyperchloremia, and suppressed renin-aldosterone axis were consistent with type II pseudohypoaldosteronism. Hydrochlorothiazide was effective in normalizing serum potassium levels and blood pressure. These studies exclude abnormalities in ANH and PG secretion in this disorder and are compatible with an abnormality in chloride reabsorption.
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PMID:Type II pseudohypoaldosteronism. Report of a case and review of the literature. 793 Mar 91

This study examined haemodynamics and noradrenaline spillover in five normal men before and on day 7 of oral fludrocortisone treatment, 0.3 mg/day. Resting systolic (105 to 115 mm Hg, standard error of the difference +/- 2.0, p < 0.01) and diastolic (65 to 73 mm Hg, +/- 3.0, p < 0.05) blood pressure increased, as did cardiac output, from 5.0 to 5.7 L/min (+/- 0.1, p < 0.01). Calculated total peripheral resistance fell from 21.2 to 20.0 mm Hg/L/min (+/- 0.4, p < 0.05). Fludrocortisone produced a fall in plasma potassium, renin and aldosterone concentrations and haematocrit and a rise in body weight. Cold pressor responses were increased by fludrocortisone, from 7.5 to 20 mm Hg (+/- 3.0, p < 0.01), and forearm vascular resistance rose 12 arbitrary resistance units (R) before and 36 R units after treatment (+/- 5.0, p < 0.01). Total body spillover of noradrenaline was decreased from 9.48 to 7.36 ng/kg/min (+/- 0.86, p < 0.05). There were no changes in forearm noradrenaline spillover at rest or during cold pressor stimulation. It appears unlikely that the sympathetic nervous system plays a major role in the pathogenesis of mineralocorticoid hypertension in man.
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PMID:Mineralocorticoid induced hypertension and noradrenaline spillover in man. 819 7

Fludrocortisone reduces plasma norepinephrine in healthy humans, but forearm vascular and pressor responses to norepinephrine are potentiated. The effects of fludrocortisone on sympathetic nerve activity in healthy humans are not known. To investigate these effects we evaluated muscle sympathetic nerve activity, heart rate, and arterial pressure in 11 healthy volunteers during three protocols: (1) before and on day 7 of fludrocortisone (0.4 mg/d) treatment with ad libitum diet (n = 6); (2) before and on day 7 of fludrocortisone (0.4 mg/d) or placebo with a 150 mmol/24 h (mEq/24 h) sodium diet (n = 7); and (3) before and on day 2 of fludrocortisone (0.4 mg/d) or placebo with a 150 mmol/24 h (mEq/24 h) sodium diet (n = 4). Placebo did not alter any parameter.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1994 Jan
PMID:Effects of fludrocortisone on sympathetic nerve activity in humans. 828 23


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