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Biomedical subjects

H Bultasová

Publications and source records attributed to H Bultasová.

At least 19 recordsLinked to original sources

[Changes in plasma renin and aldosterone after parathyroidectomy in patients with hyperparathyroidism].

The plasma renin activity and its changes after parathyroidectomy indicate a preserved internal secretory renal function in dialyzed patients. The PRA values before parathyroidectomy are not unequivocally related to the blood pressure reading. After parathyroidectomy during the initial months the renin and aldosterone plasma levels decline in patients with secondary and primary HPT (p < 0.001), the urinary Na/K quotient rises in primary HPT (p < 0.05) and the systemic blood pressure declines in dialyzed patients with secondary HPT (p < 0.001). The findings suggest relations between the two hormonal systems during hyperparathyroidism and in the early stage after parathyroidectomy. Parathormone probably stimulates renin secretion. After a prolonged time interval following operation the parathormone levels in the blood steam reach normal levels and the same probably applies to intracellular calcium in cells of the iuxtaglomerular apparatus along with PRA.

Adult↗

Vasoactive humoral systems and sodium transport in erythrocytes of normotensive offsprings of essential hypertensive subjects.

Urinary excretion of sodium, potassium and some hormones influencing their transport was investigated before and after i.v. furosemide administration in 10 offsprings of normotensive subjects who had a normal Na(+)-K+ cotransport activity and in 26 normotensive men with a positive family history of essential hypertension. The latter group was divided into two subgroups with regard to the activity of red cell Na(+)-K+ cotransport. The Co[-] subjects with a decreased Na(+)-K+ cotransport activity had lower urinary excretion of sodium and vasodilators (kallikrein, dopamine, PGE2 and prostacyclin) after furosemide administration. The urinary excretion of vasopressor factors (PGF2 alpha, thromboxane) was unchanged as compared with that in the control group. There was a significant correlation between Na(+)-K+ cotransport activity and kallikrein excretion. These results suggest a deficit in the secretion of renal substances with vasodilating or natriuretic effects in Co[-] subjects. This could negatively affect their sodium excretion.

Adult↗

Circadian rhythms of urinary sodium, potassium and some agents influencing their excretion in young borderline hypertensives.

The circadian rhythms of sodium (Na+), potassium (K+), aldosterone (ALDO), 11-deoxycorticosterone (DOC), 18-hydroxy-DOC (18-OH-DOC), cortisol (F), corticosterone (B), adrenaline (A), noradrenaline (NA), dopamine (DA), metanephrine (MN), normetanephrine (NMN), homovanillic acid (HVA), kallikrein (KE) and prostaglandins E (PGE) and F2 alpha (PGF2 alpha) excretion were studied in eight young borderline hypertensive men (BHT) and in six healthy age-matched normotensive subjects (NT) during hospitalization, after adaptation to the hospital regimen and a diet containing 135 mmol Na+ and 90 nmol K+. Urine samples were collected in 4 h periods for 24 h: 1. at normal daily activity, 2. during a 24 h bed rest. The results were evaluated by means of cosinor analysis. The circadian rhythms of ALDO, F, B, 18-OH-DOC and PGF2 alpha excretion were similar in both groups, with the exception of higher mesors of urinary ACTH-dependent corticosteroids in BHT at normal daily activity. Differences were observed in the rhythms of Na+, A, NA, DA, HVA and PGE excretion, this, however, above all during the normal daily regimen. The curve of urinary Na+ was flat in BHT due to a higher portion of Na+ excreted during the night. In the rhythms of A, NA and PGE excretion, the acrophases were shifted to the later hours in BHT, and the mesors of A and NA were also significantly higher. In contrast, DA and HVA excretion curves were flat with a lower mesor. These changes normalized, or at least mitigated, during a 24 h bed rest. The results of the study show that the circadian rhythm of Na+ excretion are disturbed already in the initial stage of hypertension. The likely cause is the exaggerated rise in adrenergic activity in the kidney during the day, induced by orthostasis and the concomitant physical (and mental?) activity, which is inadequately compensated for by the activation of natriuretic mechanisms.

Adolescent↗