Normotensive subjects with family history of hypertension (FHT) have been reported to have increased left ventricular mass index and reduced ventricular compliance. Of interest is whether blood pressure variability (BPV), which has been associated with target organ damage, is then part of this complex inherited syndrome? The objectives of this study are to determine whether there are any significant differences in BPV, arterial compliance and humoral factors in subjects with FHT as compared to controls. Thirty-five subjects with self reported FHT and 35 matched controls underwent 24 hour BP monitoring (BR-102, Schiller Inc. Germany). Arterial compliance was measured using systolic pulse wave tonometry (HDI/Pulsewave Cardiovascular Profiling Instrument, Hypertension Diagnostic Inc. USA). None of the subjects were hypertensive or diabetic. Out of these numbers, 25 subjects with FHT and 26 controls had measurements of plasma catecholamines, plasma renin and serum aldosterone. Catecholamines were assayed with high performance liquid chromatography, while both renin and aldosterone measurements were by radioimmunoassay. Subjects with FHT have higher night time BPV. There was no significant difference in arterial compliances between both groups. There were increased level of norepinephrine (NE) in subjects with FHT but epinephrine (E), renin and aldosterone levels were similar in both groups. There were no correlations between NE and BPV but E was negatively associated with daytime and mean arterial systolic BPV. In conclusion subjects with FHT demonstrated a higher night time BPV and NE level as compared to controls.
We report a case of a young hypertensive male who was first seen in 1998 with a right thalamic haemorrhage and uncontrolled hypertension. CT abdomen showed a right adrenal tumour and a hyperplastic left adrenal gland. Laparoscopic adrenalectomy performed followed by histopathological examination confirmed the diagnosis of adrenal adenoma. He subsequently presented to us again a year later with persistent hyperkalaemia and asymptomatic hyponatraemia. Further investigations strongly suggested the presence of isolated mineralocorticoid deficiency with normal cortisol levels. This was confirmed to be due to partial or late-onset congenital adrenal hyperplasia (CAH). We discuss the association of partial CAH and adrenal tumours and the unmasking of the mineralocorticoid deficiency following adrenalectomy.
Serum concentrations and urinary output of calcium, magnesium, sodium and potassium were analysed in normotensive pregnant women and in women with pregnancy-induced hypertension during the third trimester. In addition, plasma renin activity (PRA) was also determined. Significantly lower serum total calcium, urinary calcium and magnesium excretions and plasma renin activity were evident in women with PIH. Urine output and creatinine clearance were not significantly different between the two groups. No significant correlation was evident between serum calcium, magnesium and PRA. The relationship between these parameters and high blood pressure is not immediately apparent. They nevertheless suggest of a disturbance in electrolyte metabolism in women with PIH, that may underly the pathogenesis of this disorder.
Blood samples were collected from clinically healthy female cynomolgus monkeys imported from Indonesia, the Philippines and Malaysia. These animals were maintained under uniform environmental conditions for four to five years. The blood samples were examined for their hematological, serum biochemical and hormonal values. The ranges of the values as well as their arithmetic means and standard deviations have been tabulated with respect to each examination item.
Essential hypertension is a major public health concern worldwide where its prevalence accounts for various cerebrovascular diseases. A common molecular variant of angiotensinogen (AGT), the precursor of potent vasoactive hormone angiotensin II, has been incriminated as a marker for genetic predisposition to essential hypertension in some ethnics. This case-control study was designed not only to determine the association of the AGT M235T gene variants with essential hypertension, but also its relationship to Plasma Renin Activity (PRA) in subjects attending the Health Clinic, Kuala Lumpur, Malaysia.
The effect of thyroid hormones on the renin-angiotensin-aldosterone system has not been fully resolved. Highly specific immunoassays for measurement of renin, aldosterone, free T4 (fT4), free T3 (fT3) and ultrasensitive TSH enables a direct and more accurate measurement of these hormones. We investigated the relationship between plasma renin, aldosterone and thyroid hormones in the basal state and after intravenous frusemide. This is a cross-sectional study involving 37 patients with thyrotoxicosis, 42 rendered euthyroid with normal fT4, fT3 and TSH levels, 17 with euthyroid levels of fT4 and fT3 but suppressed TSH, and 11 with hypothyroidism. Basal plasma renin was significantly higher in thyrotoxicosis (63.4 +/- 9.8 microU/ml, mean +/- SEM) compared to euthyroid (32.7 +/- 4.4 microU/ml) and hypothyroid (26.7 +/- 9.8 microU/ml). Basal plasma renin for euthyroid with suppressed TSH (41.0 +/- 7.4 microU/ml) was significantly higher than hypothyroid (p = 0.02). Basal plasma aldosterones were not significantly different except for suppressed TSH (157.7 +/- 13 pg/ml), which was higher than normal (109.9 +/- 10.4 pg/ml; p = 0.04). Following frusemide, plasma renin and aldosterone were significantly increased in all groups. Plasma renin was highly correlated to fT3 (r = 0.405, p < 0.001), total T3 (r = 0.359, p < 0.001), fT4 (r = 0.331, p < 0.001) and TSH (r = 0.300, p < 0.001) in the basal state, but less to total T4 (r = 0.248, p < 0.01). Plasma renin correlated poorly to serum aldosterone (r = 0.212, p < 0.03). This study clearly showed that regulation of renin was mainly influenced by fT3, and that aldosterone response to frusemide was blunted in thyrotoxicosis despite normal electrolytes.
Recent studies using the ratio of plasma aldosterone concentration (PAC) to PRA as the screening test for primary aldosteronism in hypertensive populations suggested that the prevalence may be as high as 5-15%, with well over half of the subjects having normal serum potassium concentrations. Despite an increasing clinical awareness of this entity, many clinicians are reluctant to consider routine screening for primary aldosteronism in essential hypertensive patients because there are few community-based prevalence studies of primary aldosteronism in different populations. Furthermore, genetic and environmental differences may affect the prevalence and presentation of primary aldosteronism in distinct populations. This study was designed to determine the prevalence of primary aldosteronism in the predominantly Chinese population in Singapore. Three hundred and fifty unselected adult hypertensive patients attending two primary care clinics had random ambulatory measurements for PAC (nanograms per dL) and PRA (nanograms per mL/h). Serum urea, creatinine, and electrolyte measurements were obtained simultaneously. Subjects with renal insufficiency (serum creatinine, >140 micromol/L) and those treated with glucocorticoids or spironolactone were excluded. Screening was considered positive if the PAC: PRA ratio was more than 20 and the PAC was more than 15 ng/dL (>416 pmol/L). Primary aldosteronism was confirmed with the determination of PAC after 2 L saline administered iv over 4 h. Adrenal computed tomographic (CT) scans were performed in biochemically confirmed cases of primary aldosteronism. Further localization with adrenal vein sampling was carried out in selected patients with equivocal findings on adrenal CT scan. Sixty-three (18%) of the 350 hypertensive patients (215 women and 135 men; age range, 23-75 yr) were screened positive for primary aldosteronism. Only 13 of these 63 subjects (21%) were hypokalemic (serum potassium, <3.5 mmol/L). Confirmatory studies were carried out in 56 (89%) of the subjects with a positive PAC:PRA ratio. Using a PAC above 10 ng/dL (>277 pmol/L) after saline infusion as the diagnostic cut-off, 16 of the 56 patients had biochemically confirmed primary aldosteronism. Hypokalemia was found in 6 of the 16 patients (37.5%) with primary aldosteronism. Subtype evaluation with adrenal CT scan and adrenal vein sampling indicated that half of the patients with primary aldosteronism may have had potentially curable unilateral adrenal adenoma. Our data suggest that primary aldosteronism occurs in at least 5% of the adult Asian hypertensive population, and approximately half of these individuals may have potentially curable, unilateral, aldosterone-producing adrenal adenoma. Our findings also confirm the poor predictive value of hypokalemia in both the diagnosis and the exclusion of primary aldosteronism.
Compared with persons of European descent (ED), persons of African descent (AD) have lower aldosterone (ALDO) levels, with the assumption being that the increased cardiovascular disease (CVD) risk associated with AD is not related to ALDO. However, the appropriateness of the ALDO levels for the volume status in AD is unclear. We hypothesized that, even though ALDO levels are lower in AD, they are inappropriately increased, and therefore, ALDO could mediate the increased CVD in AD. To test this hypothesis, we analyzed data from HyperPATH - 1,788 individuals from the total cohort and 765 restricted to ED-to-AD in a 2:1 match and genotyped for the endothelin-1 gene (EDN1). Linear regression analyses with adjustments were performed. In the total and restricted cohorts, PRA, ALDO, and urinary potassium levels were significantly lower in AD. However, in the AD group, greater ALDO dysregulation was present as evidenced by higher ALDO/plasma renin activity (PRA) ratios (ARR) and sodium-modulated ALDO suppression-to-stimulation indices. Furthermore, EDN1 minor allele carriers had significantly greater ARRs than noncarriers but only in the AD group. ARR levels were modulated by a significant interaction between EDN1 and AD. Thus, EDN1 variants may identify particularly susceptible ADs who will be responsive to treatment targeting ALDO-dependent pathways (e.g., mineralocorticoid-receptor antagonists).