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Aim: To determine the concentrations of nitric oxide (NO) in plasma of women with essential hypertension in prehypertensive phase, its effect on blood pressure, and correlation with other vasoactive substances that regulate systemic and renal vascular tonus., Methods: The study performed at the Department of Nephrology, Hospital Center in Skopje, Macedonia, included 26 women with essential hypertension in prehypertensive phase and 11 normotensive women as healthy controls. Vasodilating factors NO and 6-keto-prostaglandin F1 alpha (6-keto-PGF1alpha) were determined in plasma. Thromboxane B2 (TXB2) as a vasoconstricting factor and electrolytes Na+, K+, and Ca2+ were determined in urine. Blood pressure was monitored over 24 hours. Systolic, diastolic, mean blood pressure were presented as average 24-hour values., Results: The concentrations of NO and 6-keto-PGF1alpha were significantly lower in women with essential hypertension in prehypertensive phase than in their normotensive controls (NO: median 22, range 11-35 vs median 37.5, range 11-66; 6-keto-PGF1alpha: 64.8+/-14.35 vs 98.21+/-43.45 micromol/L; P<0.001). The index of vascular reactivity (TXB2/6-keto-PGF1alpha ratio) was higher in women in prehypertensive phase than in normotensive women (1.3 vs 0.8, P<0.001). Urinary calcium to creatinine ratio was significantly lower in the prehypertensive group (0.06+/-0.03 vs 0.24+/-0.13, P<0.001). No direct correlations were found between NO, TXB2, and 6-keto-PGF1alpha, or between NO and electrolytes in the urine. Low NO and urinary Ca2+ were significant indicators of increased blood pressure (P=0.013 and P=0.024, respectively; backward stepwise multiple regression analysis)., Conclusions: NO and 6-keto-PGF1alpha were significantly lower in women in prehypertensive phase of essential hypertension. Lower NO correlated with increased systolic blood pressure, but not with on natriuresis and calciuresis. These findings, together with the higher vascular reactivity index, indicate that endothelial dysfunction precedes the establishment of essential hypertension.

A number of laboratory tests are available for evaluation of hypertension in pregnancy. These tests can be used to either predict and/or prognosticate preeclampsia and other hypertensive disorders of pregnancy. The aim of this study was to evaluate alterations in fibronectin homeostasis in normotensive pregnancy and in hypertensive disorders of pregnancy subclassified into chronic hypertension, preeclampsia superimposed on chronic hypertension, and pregnancy induced hypertension. A prospective, longitudinal study was conducted in 115 pregnant women aged 20-39 years, divided into four groups: normotensive (n = 40), chronic hypertension (n = 18), preeclampsia superimposed on chronic hypertension (n = 20), and pregnancy induced hypertension (n = 37). Plasma concentrations of fibronectin were measured by using single radial immunodiffusion assay (RIA) in the 8th, 18th, 23rd, 28th, 32nd and 36th week of gestation. Plasma fibronectin concentration showed no significant changes in normotensive pregnancy, but was significantly elevated in the third trimester in women destined to become preeclamptic or with preeclampsia in whom it reached a mean (+/- SD) of 0.40 +/- 0.09 g/L in the 36th week of gestation. In the groups with preeclampsia superimposed on chronic hypertension and with pregnancy induced hypertension, there was a significant difference between plasma fibronectin concentrations in 32nd (p < 0.01) and 36th (p < 0.001) week of gestation compared with either other levels in the respective group (in the 8th, 18th, 23rd and 28th week of gestation) or those recorded in other groups in the same period of pregnancy. These results suggested that the measurement of plasma fibronectin might be of diagnostic value in preeclampsia but could not be considered a useful predictor for preeclampsia.

Objective: To determine the relationship between endothelin-1 (ET-1), human atrial natriuretic peptide (hANP), plasma-renin activity (PRA) and 24-h urinary excretion of aldosterone (U-Ald) in pregnancy-induced hypertension (PIH)., Design and Methods: Plasma hANP (pg/ml), ET-1 (pg/ml), PRA (ng/ml per h) and U-Ald (microg/24 h) were measured and 24 h ambulatory mean arterial pressure (MAP) was monitored in 178 normotensive subjects (NT) and 79 gravidas with PIH at the 8th, 18th, 23rd, 28th, 32nd and 36th weeks., Results: The PIH group had higher MAP than the NT group from the 23rd week (91.64 +/- 8.76 versus 83.48 +/- 4.36 mmHg, P< 0.01) until the end of the pregnancy. ET-1 levels (pg/ml) in both groups were identical at the beginning of pregnancy and different in the 23rd week [(NT versus PIH) (35.11 +/- 17.42 and 40.2 +/- 19.51, respectively, P < 0.05)] and the 36th week (37.36 +/- 18.07 and 42.7 +/- 16.43, P< 0.05). hANP levels (pg/ml) in the NT group decreased insignificantly from the 8th till the 32nd week, then increased to 101.94 +/- 17.4 in the 36th (P< 0.001 versus any other week). In the PIH group, hANP increased from 104.8 +/- 26.8 pg/ml at the 8th week to 161.3 +/- 28.6 pg/ml at the 36th week (P< 0.0001). hANP correlated with MAP in the NT group (r = 0.252, P< 0.0005) but not the PIH group. U-Ald in the NT group increased from 23.52 +/- 6.83 microg/24 h at the 8th week to 54.07 +/- 19.62 microg/24 h at the 36th week (P < 0.0001) and in the PIH group it increased from 27.90 +/- 11.6 to 53.66 +/- 20.4 microg/24 h (P< 0.0001). In the PIH group, PRA was lower compared with the NT group from the 8th (2.99 +/- 1.26 versus 4.10 +/- 1.82 ng/ml per h, P< 0.05) until the 36th week (3.34 +/- 2.16 versus 4.46 +/- 2.13 ng/ml per h). In the forced multiple regression analysis model with hANP as a dependent variable, a value of P< 0.003 was found with PRA, U-Ald and MAP, which indicates an interaction between the two vasoactive and homeostatic systems: the renin-angiotensin-aldosterone system and hANP., Conclusions: In PIH, elevated hANP might be important as a counterbalance to the presence of the active vasopressors and sodium retention. By inhibiting renin release, enhancing the transcapillary fluid migration and with its action as vasodilator, it acts as a corrective factor of the imbalance between the contracted circulating fluid volume and the vasoconstricted vascular bed.

In 24 young normotensive subjects (mean age 22.25 +/- 5.65 years) with one hypertensive parent (FH(+)-), 22 subjects (mean age 23.55 +/- 5.17 years) with two hypertensive parents (FH+ +/-), and a control group of 16 age and gender matched subjects (mean age 22.50 +/- 6.00 years) with two normotensive parents (FH--), creatinine clearances and microalbuminuria (MA) were measured. Blood pressure was monitored for 24 hours and mean arterial pressure (MAP) was calculated and compared between groups. No significant differences were recorded. FH(+)- and FH++ subjects had significantly higher MAP over the sleeping period than FH-- subjects (78.63 +/- 1.71, 78.95 +/- 1.27; and 72.91 +/- 1.35 mmHg respectively; p < 0.02). Creatinine clearance was higher in FH(+)- and FH++ group compared to FH-- subjects (2.39 +/- 0.17; 2.29 +/- 0.17; and 1.66 +/- 0.11 ml/sec respectively; p < 0.01). Hyperfiltration correlated with MAP in FH++ subjects (2.29 +/- 0.17 ml/sec; 92.45 +/- 7.39 mmHg; r = 0.52 i p < 0.03). MA correlated neither with creatinine clearance nor with MAP. Our results suggest that hypertension may develop as a consequence of the long-lasting, higher GFR, which may accelerate the age-related process of sclerosis both in the small arterioles and the glomeruli.

In 48 men, 42, 1 +/- 8.8 yrs old, with untreated mild essential hypertension, serum uric acid, total cholesterol triglycerides and glucose were examined at 8 a.m after 16 hour overnight fasting. All patients were overweight, with body mass index: 26.9 +/- 2.4 kg/m2, (normal value: 19-24.9); serum uric acid 293.1 +/- 89.3 mmol/l; cholesterol 6.3 +/- 1.4; triglycerides 2.0 +/- 1.3 and glucose 5.4 +/- 0.9 mmol/l. File out of 48 (10.4%) patients had hyperuricemia, nine (18.7%) had hypercholesterolemia, twenty (41.7%) had hypertriglyceridemia and 19 (39.6%) had hyperglycemia. Significant correlation between serum uric acid and triglycerides only (r = 0.35; p < 0.01), was found. A correlation exists between the diastolic blood pressure and cholesterol (r = 0.35; p < 0.01); as well as, between mean arterial blood pressure and cholesterol (r = 0.34; p < 0.02). Only three out of 48 (6.2%) patients with hypertension had all four biochemical parameters above normal levels. Our results suggest that interrelation of all these metabolic disorders are important in essential hypertension, and especially the association of high serum uric acid and triglyceride level.