Biomedical subjects

P M Williamson

Publications and source records attributed to P M Williamson.

At least 19 recordsLinked to original sources

PubMed1999

The sydney multicentre study of Parkinson's disease: progression and mortality at 10 years.

OBJECTIVES: To report on a 10 year follow up of patients with idiopathic Parkinson's disease, particularly with respect to mortality and the effect of early treatment with bromocriptine. METHODS: The patients are from the 149 new patients recruited for a double blind, randomised study of low dose levodopa-carbidopa versus low dose bromocriptine. Patients were examined neurologically at least yearly. Neuropsychological examinations were performed at 0, 3, 5, and 10 years. Mortality and cause of death in these patients were compared with the Australian population using standardised mortality ratios (SMRs). Mortality and disease progression were compared by sex and treatment group. Predictors of death within 10 years, nursing home admission, and progression in Columbia score of >/=20 points were examined by logistic regression analysis. RESULTS: Thirteen patients were excluded as having atypical Parkinsonism and six were lost to follow up. All available patients have been followed up for 10 years. Fifty patients (38%) were dead by 10 years and 63 by the last follow up. The SMR was 1.58 for all patients (p<0. 001). There was no significant difference in SMRs between the sexes. The mean duration of disease until death was 9.1 years. Parkinson's disease was thought to have contributed substantially to the death of 30 patients. The most common cause of death was pneumonia. Women progressed at a similar rate to men until 8 years, when the severity of their disease as measured by Hoehn and Yahr stage became greater (p<0.05). Older age of onset correlated with increased risk of death but the SMR was increased even in those aged <70 years (SMR 1.80, p=0.03). Early use of bromocriptine did not reduce mortality or slow progression of disease. One quarter of all patients had been admitted to nursing homes by 10 years. Only four patients were still employed. CONCLUSIONS: Mortality in Parkinson's disease remains increased despite low dose levodopa-carbidopa therapy and no additional benefit was gained from early use of bromocriptine. Duration of disease was similar to that in the era before levodopa.

Age Distribution↗

PubMed1998

Muscle sympathetic vasoconstrictor activity in hydrocortisone-induced hypertension in humans.

AIM: This study was undertaken to test the hypothesis that increased sympathetic vasomotor drive is responsible for cortisol-induced hypertension. METHODS: Ten healthy male subjects on a fixed sodium diet (150 mmol/day) were randomized to five days of treatment with cortisol (200 mg/day) or placebo in a double-blind crossover study. On day 5 of each treatment, multi-unit muscle sympathetic activity was recorded from the common peroneal nerve. Resting muscle sympathetic activity (MSA) was measured in the recumbent position and stimulated MSA was measured in the final 20 sec of end-inspiratory capacity apnoea and end-expiratory apnoea and in the second minute of a cold pressor stimulus. A subgroup of six subjects also underwent identical MSA measurements following 5 days treatment with dexamethasone (3 mg/day). MAJOR FINDINGS: Cortisol, but not placebo, significantly increased systolic (115+/-2 vs 129+/-3 mmHg precortisol vs cortisol day 5, p < 0.001) and diastolic blood pressure (53+/-3 vs 61+/-3, p < 0.05). Resting MSA was significantly reduced by cortisol (23.9+/-2.3 to 5.0+/-2.0 bursts/min, placebo vs cortisol, p < 0.01). Cortisol significantly attenuated the increase in MSA observed at end-inspiratory apnoea (56.3+/-3.9 vs 35.4+/-6.6, p < 0.05) and end-expiratory apnoea (50.5+/-3.5 vs 26.3+/-6.2 bursts/min, n = 8, p < 0.05), and during the cold pressor response (55.0+/-12.7 vs 21.4+/-7.6, n = 5, p < 0.05). Dexamethasone significantly increased systolic blood pressure and suppressed resting and stimulated MSA. No changes in body weight, haematocrit or angiotensin II concentrations occurred during dexamethasone treatment. CONCLUSION: MSA is significantly suppressed by cortisol treatment. As suppression of MSA is also observed during treatment with the pure glucocorticoid dexamethasone, suppressed MSA cannot be attributed to increased plasma volume or to changes in angiotensin II concentration. We conclude that cortisol-induced hypertension is not due to increased muscle sympathetic vasomotor drive.

Adult↗

PubMed1998

Cortisol and hypertension.

1. In humans, the hypertensive effects of adrenocorticotropic hormone (ACTH) infusion are reproduced by intravenous or oral cortisol. Oral cortisol increases blood pressure in a dose-dependent fashion. At a dose of 80-200 mg/day, the peak increases in systolic pressure are of the order of 15 mmHg. Increases in blood pressure are apparent within 24 h. 2. Cortisol-induced hypertension is accompanied by a significant sodium retention and volume expansion. Co-administration of the type I (mineralocorticoid) receptor antagonist spironolactone does not prevent the onset of cortisol-induced hypertension. Thus, sodium retention is not the primary mechanism of cortisol-induced hypertension. 3. Direct and indirect measures of sympathetic activity are unchanged or suppressed during cortisol administration, suggesting that cortisol-induced hypertension is not mediated by increased sympathetic tone. 4. Preliminary evidence in humans suggests that suppression of the nitric oxide system may play a role in cortisol-induced hypertension. 5. These potential mechanisms of cortisol action may be relevant in a number of clinical contexts, including Cushing's syndrome, apparent mineralocorticoid excess, the hypertension of liquorice abuse and chronic renal failure. There is also preliminary evidence suggesting a role for cortisol in essential hypertension.

Adrenocorticotropic Hormone↗

PubMed1998

The nitric oxide system and cortisol-induced hypertension in humans.

1. The aim of the present study was to assess the role of the nitric oxide (NO) system in cortisol-induced hypertension in humans. 2. Plasma and urinary nitrate/nitrite concentrations and plasma concentrations of arginine and symmetric (SDMA) and asymmetric (ADMA) dimethyl arginine were measured in six subjects on a restricted nitrate diet who were treated with 80 mg/day cortisol and in subjects on an unrestricted nitrate diet who were treated with cortisol (80 mg/day, n = 6, or 200 mg/day, n = 10) for 5 days. 3. Cortisol significantly increased systolic and mean arterial pressure. Significant reductions in plasma nitrate/nitrite concentrations were observed in subjects on a restricted nitrate diet on days 3, 4 and 5 of cortisol treatment (to 11 +/- 1, 10 +/- 1, 11 +/- 1 pmol/L, respectively) compared with pretreatment (16 +/- 1 pmol/L; P < 0.01). There were no significant changes in plasma arginine, ADMA or SDMA concentrations. 4. Cortisol treatment significantly increased blood pressure and reduced plasma nitrate/nitrite concentrations. Reductions in plasma nitrate concentrations are not explained by changes in substrate availability or in endogenous nitric oxide synthase inhibitors. These data support a role for the NO system in cortisol-induced hypertension in humans.

Arginine↗

PubMed1997

Autonomic blockade amplifies cortisol-induced hypertension in man.

1. We investigated the role of the autonomic nervous system (ANS) in cortisol induced hypertension using the technique of total autonomic blockade (AB). 2. Four healthy young males were given 50 mg cortisol 6 hourly for 6 days. On the day prior to, and the last day of, cortisol treatment, AB was produced using oral prazosin 1 mg, intravenous clonidine 300 micrograms, propranolol 0.2 mg/kg and atropine 2 mg. The adequacy of blockade was assessed using the haemodynamic response to Valsalva manoeuvre. 3. Cortisol produced a significant rise in systolic blood pressure (130 +/- 2 vs 110 +/- 1 mmHg, pre vs post cortisol; P < 0.01). On the final treatment day, AB augmented the increase in diastolic blood pressure (delta DBP), mean arterial pressure (delta MAP) and heart rate (delta HR) compared to the pretreatment day, delta DBP: 43 +/- 6 vs 17 +/- 4 mmHg, post vs pre cortisol, P < 0.005, delta MAP: 39 +/- 4 vs 14 +/- 4 mmHg, P < 0.001, delta HR: 45 +/- 5 vs 26 +/- 4 b.p.m., P < 0.05. The change in systolic blood pressure (delta SBP) was not statistically significant (32 +/- 4 vs 7 +/- 3 mmHg, P = 0.065). 4. These results suggest that the ANS exerts a modulating influence on the hypertensive effect of cortisol.

Adrenergic alpha-Antagonists↗

PubMed1997

Reflex sympathetic function in cortisol-induced hypertension in humans.

Nine healthy male subjects underwent measurement of reflex sympathetic function, pressor responsiveness and baroreflex sensitivity to phenylephrine (PE) and glyceryltrinitrate (GTN) before (C1) and following six days of treatment (E6) with cortisol (F), 200 mg/day. Seven subjects had washout studies (W) performed at least two weeks following the end of treatment. The BP responses to head tilt, isometric exercise and mental arithmetic were unaltered by F, however, there was a significant diminution of the diastolic BP response to cold pressor stimulus (delta DBP: 19 +/- 3 vs 25 +/- 5 vs 27 +/- 5 mmHg; E6 vs C1 vs W, p < 0.05 C1 vs E6 and W). Baroreflex sensitivity to PE was increased (28 +/- 3 vs 19 +/- 2 ms/mmHg, E6 vs C1, p = 0.03). These data demonstrate that increased BP during F treatment is not attributable to increased SNS activity, and suggest that SNS activity may be decreased by F.

Adult↗

PubMed1996

Ambulatory blood pressure monitoring (ABPM) in the normal menstrual cycle and in women using oral contraceptives. Comparison with conventional blood pressure measurement.

This study was undertaken to determine if blood pressures (BP) assessed by routine sphygmomanometry and 24 h ambulatory monitoring (ABPM) alter throughout the normal menstrual cycle or in the cycle of women using oral contraceptive pills (OCP), and the interrelationships between urinary sodium (Na) and potassium (K) excretion and ABPM throughout the menstrual cycle. Eleven women with a normal ovulatory cycle (ovulatory) and ten age-matched women taking an oral contraceptive pill (OCP) were studied three times in random order during their menstrual cycle, within days 1 to 5, 13 to 16, and 25 to 28. Twenty-four hour urine Na, K, and creatinine (Cr) excretion and serum Na, K, Cr, cortisol, estradiol, progesterone and plasma renin, angiotensinogen, and aldosterone concentrations were measured. BP was measured by a mercury sphygmomanometer and by 24 h BP (Accutracker II). On days 1 to 5, daytime systolic BP was higher in OCP [mean: 123 mm Hg, 95% confidence interval: 117, 128] than ovulatory women [114 mm Hg (109, 118); P = .011] though daytime diastolic BPs were similar [OCP: 71 (68, 75), ovulatory: 69 (66, 72)]. This difference in daytime systolic BP between groups was also apparent at both of the other stages of the menstrual cycle. Nighttime systolic BPs were significantly higher in OCP users on days 13 to 16 (P < .05) and days 25 to 28 (P < .01). In women taking OCPs, daytime ABPM for days 1 to 5 were higher than their office readings by 15 (7,23)/11 (7,15) mm Hg (P = .001), whereas office and ABPM readings were similar in ovulatory women. This pattern was evident at all three stages. There was no significant change in BP throughout the menstrual cycle within either group, and no correlation between urine Na or K and BP. Systolic BPs are higher throughout the menstrual cycle in women who take OCPs than in ovulatory women but this difference is only detected when ambulatory blood pressure is assessed. Blood pressure does not change subsequently in either ovulatory or OCP-taking women throughout the menstrual cycle.

Adult↗

PubMed1996

Dose-response relationships and mineralocorticoid activity in cortisol-induced hypertension in humans.

OBJECTIVE: This study was designed to define the dose-response relationships for cortisol-induced hypertension in humans and to test the hypothesis that cortisol-induced hypertension is a consequence of classical mineralocorticoid actions using the mineralocorticoid antagonist spironolactone. METHODS: In study 1, six normal men were given cortisol orally every 6 h for 5 days at doses of 40, 80 and 200 mg per day. In study 2, six normal men were given spironolactone at 400 mg/day for 6 days and cortisol at 80 mg/day for 5 days, commencing on the second day of spironolactone treatment. RESULTS: Systolic blood pressure increased significantly with cortisol at 80 and 200 but not 40 mg/day. There was no difference between 80 and 200 mg/day. Weight increases were seen at the two higher doses and serum potassium concentration fell with each dose. Spironolactone prevented the increase in body weight and the decrease in serum potassium but did not affect the increase in blood pressure produced by cortisol. CONCLUSIONS: Cortisol at 80 and 200 mg per day produces similar blood pressure and metabolic effects. Spironolactone blocked the mineralocorticoid effects of cortisol but not the blood pressure rise, suggesting that these mineralocorticoid effects are not responsible for cortisol-induced hypertension.

Adult↗

PubMed1995

Mechanisms of cortisol-induced hypertension in humans.

There is emerging evidence that cortisol plays a significantly greater role in human hypertension than previously thought. Apart from the well recognized role of cortisol in the hypertension of Cushing's syndrome, local cortisol excess has been recognized as responsible for rare forms of hypertension such as apparent mineralocorticoid excess and licorice abuse and more recently implicated in the hypertension of chronic renal failure, hypertension related to low birth weight and essential hypertension. Although cortisol-induced hypertension is characterized by sodium retention and volume expansion, studies with synthetic glucocorticoids or sodium restriction suggest that the hypertension is, to a substantial degree, independent of sodium and volume. Increase in cardiac output is not essential for cortisol-induced blood pressure rise but the precise role of increases in total or regional peripheral resistance as a primary mechanism has nto been determined. Increased pressor responsiveness, particularly to catechols, is a prominent feature but whether these changes are sufficient to account for the hypertension remains unclear. There is no evidence for increased sympathetic nervous activity as judged by measurements of plasma catcholamines, neuropeptide-Y, or resting noradrenaline spillover rate. Responses to mental stress or maximal hand-grip are unchanged and baroreflex sensitivity is increased. Octreotide profoundly reduced the elevated plasma insulin concentrations seen with cortisol administration but had no effect on the rise in blood pressure.

Hemodynamics↗

PubMed1995

Age at onset: the major determinant of outcome in Parkinson's disease.

Factors at presentation which influenced the course of the disease and response to treatment were assessed in 125 de novo patients with Parkinson's disease. Ninety-eight patients were available for re-assessment at 5 years. Older patients presented earlier after the onset of symptoms, deteriorated more rapidly, and were significantly more likely to develop dementia and impairment of balance. Increasing age and symmetrical disease predicted the new appearance of imbalance. Age of onset did not predict dyskinesia or end of dose failure. A low tremor score at baseline and female gender were predictive of the early appearance of dyskinesia. Patients who experienced end of dose failure were taking a significantly higher dose of levodopa. Once dose and duration of treatment were corrected for, no baseline features were predictive of end of dose failure. The dose of levodopa at 5 years was positively correlated to baseline disease severity as measured by the Columbia score. We conclude that the age of onset of symptoms of Parkinson's disease is a major determinant of the course of the disease and response to treatment.

Adult↗

PubMed1995

11 beta-Hydroxysteroid dehydrogenase and its inhibitors in hypertensive pregnancy.

Preeclampsia is accompanied by amplification of the sodium retention that is a feature of normal pregnancy. Recent evidence suggests that mineralocorticoid receptor activation is increased in preeclampsia, but classic mineralocorticoids (aldosterone, 11-deoxycorticosterone) are not present in excess. Cortisol can act as a mineralocorticoid receptor agonist only when its renal inactivation to cortisone by 11 beta-hydroxy-steroid dehydrogenase is impaired, for example, in congenital enzyme deficiency and after administration of exogenous inhibitors (eg, licorice). Endogenous inhibitors of this enzyme have been detected in human urine and are increased in pregnancy. To establish whether cortisol causes mineralocorticoid excess in hypertensive pregnancy and whether endogenous inhibitors of 11 beta-hydroxysteroid dehydrogenase are responsible, we studied 25 hypertensive pregnant patients (13 with preeclampsia and 12 with gestational hypertension), 16 normotensive pregnant subjects, and 13 nonpregnant control subjects. Concentrations of plasma renin and aldosterone were increased in pregnancy, but less so in hypertensive pregnancy. Plasma potassium and urinary electrolytes were not different between the groups. Plasma cortisol was increased in pregnancy but not different in hypertensive pregnancy, and urinary cortisol, plasma and urinary cortisone, and urinary tetrahydrocortisol and tetrahydrocortisone were not different between the groups. Endogenous inhibitors of 11 beta-hydroxysteroid dehydrogenase were more active in urine from pregnant women but were not increased further in hypertensive pregnancy. There were no differences in these parameters between patients with preeclampsia and gestational hypertension. We conclude that deficient inactivation of cortisol to cortisone does not contribute to the sodium retention of normotensive or hypertensive pregnancy and that endogenous inhibitors of 11 beta-hydroxysteroid dehydrogenase have no evident pathophysiological significance in pregnancy.

11-beta-Hydroxysteroid Dehydrogenases↗

PubMed1995

Experimental studies on cortisol-induced hypertension in humans.

Studies in humans have shown that cortisol administration (200 mg/day) increases cardiac output, renal vascular resistance, glomerular filtration rate, plasma volume, extracellular fluid volume, exchangeable sodium, plasma glucose, insulin, renin substrate and atrial natriuretic peptide concentrations as well as urinary kallikrein excretion. Cortisol treatment decreases renin and angiotensin II concentrations while catecholamines and vasopressin are decreased or unchanged. We have clear evidence from a number of studies that cortisol-induced hypertension is modulated by, but not dependent on, exogenous sodium. The increase in cardiac output normally seen with cortisol administration is not essential for the blood pressure rise. The role of the increase in renal vascular resistance in the genesis of the hypertension is unclear. Studies using measurements of noradrenaline spillover and assessment of reflex function have not shown any increase in sympathetic nervous system activity but changes in vascular responsiveness, particularly to phenylnephrine and noradrenaline are marked. Cortisol is known to have a variety of effects on brain, heart, kidneys, blood vessels and body fluid volumes. To what extent the observed changes are epiphenomena, amplifiers or modulators, or are causal is unclear. Cortisol hypertension may reflect a complex interplay of these factors varying with the steroid concentrations achieved, underlying genetic factors and the particular experimental circumstances.

Extracellular Space↗

PubMed1994

Hyperinsulinemia is not a cause of cortisol-induced hypertension.

There is much interest in the relationship of hypertension to hyperinsulinemia. Six male volunteers received cortisol, 50 mg orally four times daily, for 5 days. Plasma insulin concentration increased from 11.8 +/- 3.0 mU/L to 16.1 +/- 4.0 mU/L (P = .034). Fasting glucose increased from 4.7 +/- 0.3 to 5.8 +/- 0.1 mmol/L (P = .001). The insulin-to-glucose ratio was unchanged. Octreotide has been reported to lower blood pressure in obese, hyperinsulinemic, hypertensive patients. The hypothesis that cortisol-induced hypertension might be secondary to steroid-induced hyperinsulinemia was examined by determining whether reversal of hyperinsulinemia by octreotide would reverse cortisol-induced hypertension. Five healthy men were given two subcutaneous injections of 0.05 mg of octreotide before and on the fifth day of cortisol administration. Cortisol increased blood pressure, weight, plasma glucose concentration, and white cell count, with decreases in plasma potassium concentration and packed cell volume. Plasma cortisol concentrations were unchanged following octreotide in the control period but decreased after cortisol treatment. Insulin concentrations were reduced profoundly after octreotide, both in the control period (12.5 +/- 3.7 mU/L, falling to 1.1 +/- 0.3 mU/L at 30 min) and on cortisol (22.3 +/- 4.5 to 2.3 +/- 0.5 mU/L at 30 min). Octreotide did not lower pressure before or after cortisol treatment. Thus, octreotide was effective in lowering plasma insulin concentrations but di not lower blood pressure in normal subjects with cortisol-induced hypertension. These data do not support the notion that steroid-induced hyperinsulinemia is responsible for steroid-induced hypertension.

Adult↗

PubMed1994

Neuropeptide Y in cortisol-induced hypertension in male volunteers.

1. Cortisol-induced blood pressure rises in men are not accompanied by increases in plasma catecholamines. The present study examines the effects of cortisol on the sympathetic co-transmitter, neuropeptide Y (NPY). 2. Eight normal men were given cortisol 200 mg/day over 5 days and haemodynamic, metabolic and hormonal measures were taken. Plasma NPY-like immunoreactivity (NPY-LI) concentrations were measured by direct radio-immunoassay. 3. Cortisol significantly increased systolic, diastolic and mean arterial pressure, bodyweight, plasma glucose and total white cell concentration and decreased plasma potassium and total eosinophil count, as in previous studies. Plasma NPY concentrations were not altered significantly during cortisol treatment, but increased following cessation of cortisol treatment (P = 0.006). 4. The essentially unchanged pattern for NPY concentration with cortisol treatment resembles that previously reported for adrenaline and noradrenaline, but the increase in NPY on cortisol withdrawal was not seen for adrenaline or noradrenaline. These data do not support a role for sympathetic activation in the genesis of cortisol-induced hypertension.

Adult↗

PubMed1994

The Sydney Multicentre Study of Parkinson's disease: a randomised, prospective five year study comparing low dose bromocriptine with low dose levodopa-carbidopa.

149 previously untreated patients with Parkinson's disease were recruited over a three year period and randomly allocated to either low dose levodopa-carbidopa (< or = 600/150 mg/day) or low dose bromocriptine (< or = 30 mg/day). A five year follow up is reported on the 126 patients who completed the dose titration and who have not developed features of atypical Parkinsonism. Levodopa-carbidopa in low dosage adequately controlled symptoms in most patients and delayed the appearance of dyskinesia and end of dose failure for about two years longer than conventional doses. Only a few patients could be managed for more than one year on low dose bromocriptine alone; these patients had mild disease and asymmetric signs. Patients randomised to bromocriptine did not develop dyskinesia or troublesome end of dose failure until levodopa-carbidopa was added. The prevalence of dyskinesia in this group was lower than in patients given levodopa-carbidopa alone. The prevalence of end of dose failure was similar in the two randomisation groups once levodopa was introduced.

Adult↗

PubMed1994

Haemodynamic and metabolic effects of carbenoxolone in normal subjects and patients with renal impairment.

Carbenoxolone inhibits the enzyme complex 11 beta-hydroxysteroid dehydrogenase. Functional deficiency of this complex might contribute to the hypertension of renal parenchymal disease. We have compared the effects of carbenoxolone (300 mg/day for 5 days) in six normal subjects and seven patients with renal disease. Patients with renal disease had higher blood pressure, plasma creatinine concentration (0.15 +/- 0.01 mmol/L cf. 0.09 +/- 0.01 mmol/L) and urine protein excretion than normals. In normal subjects carbenoxolone increased body weight and plasma chloride and decreased initial urine sodium excretion, packed cell volume, plasma albumin, renin and aldosterone concentrations. In patients with renal disease, carbenoxolone also produced these effects, but in addition significantly increased systolic, (129 +/- 3 to 135 +/- 5 mm Hg) mean (97 +/- 3 to 101 +/- 3 mm Hg) and diastolic blood pressure (81 +/- 3 to 85 +/- 2 mm Hg) and lowered plasma potassium (4.1 +/- 0.1 to 3.8 +/- 0.1 mmol/L) and urine sodium:potassium ratio (1.57 +/- 0.22 to 2.60 +/- 0.54). These results are consistent with the notion that partial deficiency of 11 beta-hydroxysteroid dehydrogenase contributes to the hypertension of renal parenchymal disease.

11-beta-Hydroxysteroid Dehydrogenases↗

PubMed1993

Reliability of the Columbia scale for assessing signs of Parkinson's disease.

Inter- and intrarater reliability in scoring the signs of Parkinson's disease using the original Columbia scale and a modified version of this, the Sydney scale, were assessed in five neurologists participating in a long-term study of Parkinson's disease. Scoring was done on video recordings of 41 patients whose disability ranged from mild to severe. Although all the neurologists were familiar with the scales and had received training designed to produce uniformity of scoring, interrater reliability was poor. The mean score for the Columbia scale varied from 18.6 to 30 and for the Sydney scale from 15.2 to 23.2. By contrast, intrarater reliability was good. This study highlights the limitations of clinical rating scales in Parkinson's disease when more than one rater is used. In designing clinical trials, every effort should be made to ensure that the same patient is always assessed by the same rater.

Analysis of Variance↗

PubMed1993

Effects of cortisol on blood pressure and salt preference in normal humans.

1. Adrenocorticotrophic hormone (ACTH) and corticosteroids stimulate salt appetite in laboratory animals. The hypothesis tested was that cortisol administration increases salt preference in humans. 2. Sodium taste studies (detection and recognition thresholds, taste intensity and preference tests) were conducted before, during and after cortisol administration (200 mg/day for 5 days) in normal men on a free diet. 3. Cortisol significantly increased systolic blood pressure (SBP), 113 +/- 3 - 130 +/- 4 mmHg, P < 0.05; diastolic blood pressure (DBP), 65 +/- 3 - 81 +/- 2 mmHg, P < 0.05; mean arterial pressure (MAP), 81 +/- 2 - 97 +/- 3 mmHg, P < 0.05; and bodyweight, 72.9 +/- 3.0 - 75.4 +/- 3.3 kg, P < 0.05. 4. Salt detection and recognition thresholds, taste intensity and preference for sodium chloride were unchanged following cortisol.

Adult↗