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Biomedical subjects

R Lammintausta

Publications and source records attributed to R Lammintausta.

At least 55 records · Page 3Linked to original sources
PubMed1981

Plasma AVP after intravenous chlorpropamide.

The proposed ADH-releasing capacity of chlorpropamide was tested after intravenous administration of the drug to nine healthy fasted volunteers. When compared with the placebo experiment, no evidence for increased ADH release was found. On the contrary, the AVP values measured after chlorpropamide injection were slightly lower during the first 2 h than after the saline injection. Serum chlorpropamide concentration was also measured. After a rapid distribution phase, a slow elimination phase followed. The calculated t 1/2 for distribution phase was 1.00 +/- 0.26 hrs (mean +/- s.e.m.).

Arginine Vasopressin↗
PubMed1981

Pharmacokinetics of dihydroergotamine in healthy volunteers and in neurological patients after a single intravenous injection.

The pharmacokinetics of dihydroergotamine (DHE) was studied in healthy volunteers (n = 6) and in neurological patients (n = 12). After a single 1.0 mg intravenous injection (n = 5) DHE quickly disappeared (T 1/2 beta = 32.9 min, Vdss = 0.33 liter/kg, Cltot = 1055.7 ml/min). In saliva (dose 1.0 mg, n =6) and cerebrospinal fluid (dose 0.5 mg, n =12) there were no measurable amounts of DHE after a single i.v. dose. The 32-h cumulative urinary excretion was 0.02-0.04% of the 1.0 mg intravenous dose. In one subject renal (0.18 ml/min) and extrarenal (692.9 ml/min) clearance of DHE was calculated. According to our results DHe is probably eliminated mainly by hepatic metabolism. The pharmacokinetic properties of DHE indicate a fast clinical response without a cumulative action.

Adult↗
PubMed1981

Chlorpropamide bioavailability and pharmacokinetics.

The pharmacokinetics of chlorproamide was studied in eight healthy volunteers after intravenous and oral dosage. A long elimination half-life with considerable variations between subjects was recorded. The normalized areas under the curve were in close agreement between the subjects, suggesting that they had all absorbed the same magnitude of chlorpropamide. The AUCs after i.v. and p.o. administration did not differ significantly from each other. Thus, the differences in the bioavailability do not seem to be a critical factor in the previously reported large interindividual variations in chlorpropamide steady-state concentrations.

Administration, Oral↗
PubMed1980

Estradiol valerate therapy and the renin--aldosterone system in castrated women.

The effect of estradiol valerate (Progynova, 2 mg daily) on the renin--aldosterone system was studied in nine women after bilateral oophorectomy. Plasma renin activity (PRA) and the daily urinary excretion of aldosterone (dU-Ald) were determined 4 mth after the operation -- during which no estrogen was given -- and after 3 mth on estrogen therapy. Plasma estradiol concentration rose in 7 subjects to the normal postovulatory level. No changes were found in PRA or dU-Ald. The results suggest that an effective estradiol valerate therapy is not accompanied with activation of renin--aldosterone system, while synthetic and non-human natural estrogens (Premarin) were shown earlier to increase PRA.

Aldosterone↗
PubMed1980

Digoxin without effect on renin release in healthy subjects.

In the clinical evaluation of renin status, the effect of chronic digitalization is unknown. A 50 per cent decrease in PRA is presented after intravenous digoxin injection. In this study the acute intake of 0.75 mg digoxin decreased PRA slightly (p less than 0,05), but no difference could be found in ten healthy volunteers in regard to PRA after placebo, randomly examined twice after digoxin and once after placebo tablets. Eight healthy volunteers were digitalized with 2.5 mg digoxin in total during four days. Renin release was stimulated by ergometric exercise (900 kpm for 10 min) before and after digitalization, when the mean serum digoxin concentration was 2.0 +/- 0.2 ng/ml (SEM). No difference in basal or exercise-stimulated PRA could be found after digoxin. We conclude that the steady state digitalis therapy does not interfere with renin release. The peripheral vasoconstriction accompanied with the acute intravenous digitalis administration can lead to a transient decrease of PRA.

Adult↗
PubMed1980

The renin-aldosterone system in low-dose chlorothiazide treatment of hypertensive subjects.

Eight patients with essential hypertension were treated with chlorothizide 250 mg daily for 4 weeks with 500 mg daily for further 8 weeks. Both systolic and diastolic blood pressures (BP) decreased significantly during the lower dosage (p < 0.05). Only the diastolic BP continued decrease during the higher dosage regimen of chlorothiazide (p < 0.05). Plasma renin activity (PRA) and plasma aldosterone (PA) did not increase during the lower dosage of chlorothiazide. During 4 weeks on the dosage of 500 mg of chlorothiazide daily, PRA increased by 79 per cent (p < 0.001) and PA by 66 per cent (p < 0.001) from the level of the lower dosage. During the next 4 weeks, no changes in PRA or PA were seen. The result shows the strong compensatory activation renin-aldosterone system on the usual chlorothiazide therapy. In spite of a decrease in BP, the lower dosage was not accompanied with any significant compensation. Renin-aldosterone system during diuretic therapy not only causes the so-called false tolerance to antihypertensive effect, but also potentiates the loss of potassium. This can best be avoided by using the minimal effective dosage of the diuretic drug.

Adolescent↗
PubMed1980

Endogenous oestrogens and the renin-aldosterone axis--castration of women with high or normal oestradiol level.

Oestrogens increase plasma renin activity (PRA) by inducing synthesis of renin substrate in the liver. This is proved clinically by the synthetic oestrogens of oral contraceptives and by the equine conjugated oestrogens in postmenopausal therapy. The effect of endogenous oestrogen production on the activity of the renin-aldosterone system is not clear, but progesterone is an important stimulus of renin release in the luteal phase of menstrual cycle. We studied 15 premenopausal women undergoing bilateral oophorectomy. Eight women had high mean serum oestradiol level 1.2 +/- 0.6 (SD) nmol/l for follicular cysts or for a prolonged climacteric proliferation phase. Seven women had normal follicular oestradiol level (0.2 +/- 0.1 nmol/l). In PRA or daily urinary aldosterone excretion (dU-Ald) no differences could be found between the groups. In one month after oophorectomy no changes in PRA or dU-Ald were found in either group, while the serum oestradiol fell to unmeasurable levels. The results suggest that endogenous oestrogens are not to cause activation of the renin-aldosterone axis as measured by the clinically useful PRA and dU-Ald. The result is in agreement with previous reports of postmenopausal therapy with oestriol succinate or oestradiol valerate.

Adult↗
PubMed1980

Response of renin, aldosterone and antidiuretic hormone to furosemide and furosemide-triamterene combination.

Plasma renin activity (PRA), antidiuretic hormone (ADH), urinary aldosterone excretion (U-Aldo) and electrolyte excretions were studied in a randomized study after furosemide (80 mg) (F), furosemide + triamterence (80 + 100 mg) (F + T), and after placebo were administered to seven healthy volunteers. F + T preparation showed a slower absorption of furosemide, a slower natriuresis and a slower excretion of potassium as compared to F-präparation. After application of the diuretics, PRA reached the maximal level in four hours, three times higher than the control level after F and four times higher after F + T. At 24 hrs after drug intake PRA did not differe from the control level. No significant difference could be found between F and F + T. U-Aldo of 24 hrs increased 1.9-fold after F and 2.2-fold after F + T, as compared with placebo. Between the individual natriuretic and hormonal responses no correlation could be found. After F + T, U-Aldo and U-K showed a positive correlation (P < 0.05). ADH did not change after diuretics from the pretreatment fasting level. The results show a fast but transient response of the renin-aldosterone system after furosemide and the furosemide-triamterene combination which could not be correlated with the natriuretic effects. The result differs from that found earlier with hydrochlorothiazide.

Adult↗
PubMed1979

Pharmacokinetics of nitrazepam in saliva and serum after a single oral dose.

The pharmacokinetics of nitrazepam in saliva and serum was studied in 12 healthy volunteers after a single administration of a 5 mg nitrazepam tablet. The binding of nitrazepam to plasma proteins was determined 4 hours after the administration by ultracentrifugation. The analysis of nitrazepam concentrations was performed by 63Ni-EC-GLC. The pharmacokinetic parameters were evaluated manually or by AUTOAN-program in serum, and manually in saliva. The concentrations of nitrazepam in serum and saliva correlated significantly (r = 0.472, P less than 0.001, n = 97). The ratio saliva: serum was, however, time dependent. The protein free fraction in serum was significantly higher (P less than 0.01) than the salivary concentration at the same time (4 hours after administration). The peak concentrations in serum and saliva were 40.7 and 1.9 ng/ml (P less than 0.001) and the times to reach the peak maximum 2.4 and 2.5 hours, respectively (difference not significant). The mean half-life of nitrazepam in serum was 30.5 hrs and in saliva 39.9 hrs, the difference being significant at P less than 0.05. The distribution phase parameters, poorly described before, were calculated. The clinical value of nitrazepam analysis in saliva seems to be negligible.

Administration, Oral↗
PubMed1979

Maternal and fetal plasma renin activity during ritodrine infusion to the mother.

The effect of ritodrine to the mother on plasma renin activity (PRA) in the mother and fetus was examined in 10 mothers coming to elective cesarean section. 10 comparable mothers without ritodrine infusion served as controls. At the end of 2 h infusion of ritodrine, the mean maternal PRA was significantly (p less than 0.001) higher than in the control group. Also the mean PRA levels in the umbilical vein (p less than 0.001) and umbilical artery (p less than 0.01) were significantly higher after ridodrine infusion to the mother than the respective levels in the control group.

Adult↗
PubMed1979

The effect of methysergide, pimozide, and sodium valproate on the diazepam-stimulated growth hormone secretion in man.

Diazepam-induced GH secretion was tested on 28 male volunteers before and after a 3-day treatment with methysergide, pimozide, or sodium valproate. Serum GH, diazepam, and blood glucose levels were determined. Without prior medication, the mean serum GH level increased 336% 1 h after diazepam administration. Treatment with the serotonin antagonist, methysergide, had no effect on the diazepam-stimulated GH secretion, whereas pimozide, the selective dopamine receptor-blocking agent, reduced the GH response to diazepam by 50% (P less than 0.05). Sodium valproate, a gamma-aminobutyric acid transaminase inhibitor, also inhibited diazepam-induced GH secretion; stimulated GH levels were 51% at 30 min (P less than 0.025), 39% at 60 min (P less than 0.025), and 46% at 90 min (P less than 0.025) relative to the stimulated levels without medication. No difference was found in blood glucose or serum diazepam levels after the drug treatments relative to the values obtained under basal conditions. It is suggested that diazepam-induced GH secretion is at least partly mediated via dopaminergic mechanisms. Serotonin does not seem to be involved. It is further proposed that gamma-aminobutyric acid plays an inhibitory role in GH secretion.

Adult↗
PubMed1979

Stimulatory effect of acute baclofen administration on human growth hormone secretion.

The effect of acute administration of the gamma-amino-butyric acid (GABA) derivative, baclofen, on human GH secretion was tested. In eight of the nine volunteers, both 5 and 10 mg baclofen (Lioresal) significantly basal GH secretion. Previoulsy, it has been reported that subacute baclofen treatment inhibits the GH response to insulin hypoglycemia and arginine. Thus, the present study shows that baclofen is able to modify GH secretion via different mechanisms, depending on the test situation and duration of treatment. As a putative GABA agonist, the effect of baclofen may be mediated via GABA-ergic pathways. Because of variable results, the evaluation of a possible physiological role of GABA in GH secretion requires further study.

Aminobutyrates↗
PubMed1979

Effect of melatonin on L-tryptophan- and apomorphine-stimulated growth hormone secretion in man.

The effect of subacute melatonin (250 mg every 8 h over a period of 40 h) and placebo treatment on L-tryptophan- and apomorphine-stimulated GH secretion was tested in 13 volunteers. Melatonin premedication significantly reduced the GH response to peroral L-tryptophan loading, suggesting that melatonin affects GH secretion in man by interfering with serotonergic transmission. In the apomorphine test, no significant difference in GH response was observed after melatonin when compared to placebo treatment. This suggests that dopaminergic mechanisms do not have a central role in mediating actions of melatonin on the hypothalamic-pituitary axis. It is further proposed that melatonin influences GH secretion at a suprahypophyseal level.

Adult↗
PubMed1979

Effect of oral contraceptive containing a new progestin (ORG 2969) on plasma renin activity, growth hormone and immunoreactive insulin.

Plasma renin activity (PRA), Growth hormone (GH) and immunoreactive insulin (IRI) were studied in seven healthy subjects during the ovulatory menstrual cycle and during the first and third cycles of oral contraception with 0.05 mg of ethinylestradiol and 0.100 mg or 0.125 mg of a new progestogen, 17 alpha-ethinyl-18-methylene-4-estren-17 beta-ol. The PRA level in the second half of the control cycle was significantly higher than in the beginning of the cycle. At the end of the treated cycles it was significantly higher than at the end of the control cycle. Neither GH nor IRI showed significant changes during the control cycle. GH was significantly higher at the end of the first and third treated cycles than at the end of the control cycle. IRI was significantly higher both in the beginning and at the end of the first treated cycle than the corresponding IRI levels in the control cycle. IRI at the end of the third treatment cycle was not significantly different from corresponding means at the end of the control cycle or the first treated cycle.

Adult↗