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Biomedical subjects

H Vapaatalo

Publications and source records attributed to H Vapaatalo.

At least 19 recordsLinked to original sources
PubMed1992

L-cysteine augments the vasorelaxation induced by sodium nitrite and SIN-1 but not that due to acetylcholine.

The effects of 1 mM L-cysteine on sodium nitrite-, 3-morpholinosydnonimine (SIN-1)- and acetylcholine-induced relaxation and cyclic GMP accumulation were studied in isolated noradrenaline-precontracted rat mesenteric arterial rings. L-Cysteine augmented the relaxation and cyclic GMP increase induced by sodium nitrate and SIN-1 but not those induced by acetylcholine. The effects of L-cysteine on relaxation were independent of the presence of intact endothelium. The results suggest that L-cysteine protects exogenously released nitric oxide.

Acetylcholine↗
PubMed1992

Inhaled budesonide fails to inhibit the PAF-induced increase in plasma leukotriene B4 in man.

1. We studied the ability of inhaled budesonide to modulate PAF-induced acute effects in nine healthy nonsmoking volunteers. Responses in inflammatory cells and mediators in peripheral blood as well as in pulmonary function and circulation were monitored. 2. Inhalation of increasing doses of PAF (total cumulative dose of 500 micrograms) caused a rapid and profound decrease in circulating white blood cells, especially in granulocytes (P less than 0.01), which was turned to an increased number of these cells (P less than 0.05, P less than 0.025, respectively) in the blood samples taken 8 min after completion of the PAF challenge. No changes in the circulating platelets or their thromboxane production were found. Plasma concentrations of histamine or methylhistamine remained unchanged during PAF-inhalation, while plasma LTB4 tripled from the baseline level at 10 min (P less than 0.0005) and was returned to the pre-PAF value at 60 min. 3. PAF inhalation induced a bronchial obstruction (P less than 0.025), but no bronchial hyperresponsiveness to methacholine was found in any of our subjects when measured 24 h after the PAF challenge. Furthermore, PAF caused a decrease in systolic blood pressure (P less than 0.05). 4. Budesonide pretreatment of 400 micrograms twice daily during the preceding 5 days had no effect on any PAF-induced events measured in our study. That fact may also contradict the role of bronchial resident or alveolar cells as a source of the PAF-induced LTB4 burst in plasma. 5. We conclude that in healthy volunteers inhaled PAF induces a marked increase in plasma LTB4, which is not inhibited by inhaled budesonide.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1992

Endothelium-dependent and -independent effects of exogenous ATP, adenosine, GTP and guanosine on vascular tone and cyclic nucleotide accumulation of rat mesenteric artery.

1. The effects of exogenous guanosine 5'-triphosphate (GTP) and guanosine on vascular tone and cyclic nucleotide accumulation of noradrenaline-precontracted endothelium-intact and endothelium-denuded rat mesenteric artery rings were compared with the effects of the known purinoceptor agonists adenosine 5'-triphosphate (ATP) and adenosine. 2. GTP (10 microM-1 mM) dose-dependently relaxed endothelium-intact mesenteric artery rings by producing a rapid initial response followed by sustained relaxation resembling the relaxant response to acetylcholine. GTP also slightly relaxed endothelium-denuded artery rings. The acetylcholine- and GTP-induced relaxations of endothelium-intact rings were attenuated by NG-nitro L-arginine methyl ester (L-NAME, 330 microM) which attenuation was reversed with L-arginine (1 mM). 3. Guanosine (10 microM-1 mM) relaxed both endothelium-intact and -denuded artery rings in a dose-dependent manner. The relaxations were more pronounced in endothelium-intact preparations and were only slightly attenuated by L-NAME (330 microM). 4. ATP (1 microM-1 mM) and adenosine (10 microM-1 mM) dose-dependently relaxed endothelium-intact and -denuded artery rings. The responses were more pronounced in endothelium-intact vascular preparations. 5. GTP (100 microM) and guanosine (100 microM) increased guanosine 3':5'-cyclic monophosphate (cyclic GMP) accumulation in both endothelium-intact and -denuded artery rings corresponding to the relaxations observed. The concentrations of adenosine 3':5'-cyclic monophosphate (cyclic AMP) were not affected. 6. ATP (100 microM) increased cyclic GMP concentration of endothelium-intact artery rings. The concentrations of cyclic AMP were not affected by ATP (100 microM) and adenosine (100 microM) in endothelium-intact and -denuded vascular preparations.7. These results provide evidence that exogenous GTP and guanosine relax precontracted endothelium-intact and -denuded rat mesenteric artery rings by increasing cyclic GMP accumulation. The response to GTP of endothelium-intact rings can mainly be explained by the release of endothelium-derived relaxing factor (EDRF), but that of guanosine is only partly due to EDRF, and is a combination of endothelium-dependent and -independent effects. The endothelium-independent response of GTP and guanosine is a direct, unknown effect on smooth muscle and guanylate cyclase.

Acetylcholine↗
PubMed1992

Adrenaline stimulates thromboxane and inhibits leukotriene synthesis in man.

Catecholamines and other catecholic compounds have opposite effects on the cyclooxygenase and 5-lipoxygenase pathways of arachidonic acid metabolism in human polymorphonuclear leukocytes and whole blood in vitro. The hypothesis that high levels of adrenaline, found e.g. in myocardial infarction, are involved in the regulation of arachidonic acid metabolism was tested. Adrenaline (0.1 micrograms/kg per min for 45 min and thereafter 0.2 micrograms/kg per min for 15 min) was infused to healthy male volunteers to mimic relationships between high levels of adrenaline and arachidonic acid metabolism in myocardial infarction. Adrenaline infusion increased Ca ionophore A23187-induced TXB2 formation in whole blood. The effect was smaller when spontaneous clotting was used as a stimulus. Urinary 11-dehydro-TXB2 excretion, an indicator of total in vivo thromboxane synthesis, increased twofold. Adrenaline infusion decreased both LTB4 and LTE4 synthesis in A23187-stimulated whole blood. These results demonstrate that high levels of adrenaline influence the cyclooxygenase and 5-lipoxygenase pathways of arachidonic acid metabolism differentially in man.

Adult↗
PubMed1979

Tolfenamic acid is as effective as ergotamine during migraine attacks.

Tolfenamic acid (a potent inhibitor of prostaglandin biosynthesis), ergotamine tartrate, acetylsalicylic acid, or placebo was administered during 160 migraine attacks in twenty women in a double-blind, cross-over study. Tolfenamic acid and ergotamine were equally effective in reducing the duration and intensity of attacks, but side-effects, especially nausea, were less common with tolfenamic acid. This probably accounted for the patients' preference for tolfenamic acid. The effectiveness of tolfenamic acid in acute migraine attacks accords with the postulated role of prostaglandins in migraine.

Adolescent↗
PubMed1979

The effects of a beta 1-blocking agent, atenolol, on blood pressure, plasma renin activity and prostaglandin F2 alpha excretion in patients with essential hypertension.

The antihypertensive action of beta-blocking agents has been suggested to be associated with the decrease in plasma renin activity (PRA) and can be antagonized by indomethacin, a prostaglandin (PG) synthesis inhibitor. We studied the acute and long-term effects of a beta 1-blocking agent, atenolol (50 mg b.i.d.), on blood pressure (BP), PRA and urinary PGF2 alpha excretion in 12 male patients (40 years old) with essential hypertension. BP was measured by means of a brachial cuff. PRA and PGF2 alpha were estimated radioimmunologically. One day after the initiation of atenolol treatment, BP fell significantly, the supine values from 159/114 to 143/104 mmHg and the erect from 158/118 to 140/106 mmHg. In six weeks BP decreased further to 135/94 and 134/96 mmHg, respectively. After the cessation of atenolol for three weeks BP rose to the pre-atenolol level. When the dose was readjusted (25-150 mg daily for 26 weeks), diastolic BP remained at 100 mmHg or higher in only two patients. During the atenolol treatment PRA declined to one-third of the pre-atenolol level in one day and to one-half in six weeks. The urinary excretion of PGF2 alpha was not affected by atenolol. Our results suggest that 1) the antihypertensive action of atenolol and the reduction of PRA are substantial already in one day, and 2) the decrease in BP or PRA is not associated with PGF2 alpha production.

Adult↗
PubMed1979

A comparative, double-blind study on tolfenamic acid in the treatment of rheumatoid arthritis.

Sixty patients with diagnosed rheumatoid arthritis were treated at random with tolfenamic acid, a new nonsteroid anti-inflammatory analgesic, in a daily dose of 600 mg, or with phenylbutazone 300 mg or acetylsalicylic acid 1,500 mg daily. Both the patients and the physician found that tolfenamic acid had a clearly better effect than phenylbutazone or the low-dose acetylsalicylic acid used as a control. Tolfenamic acid and acetylsalicylic acid were well tolerated. Serious side-effects (leukopenia and thrombocytopenia in one case, hematemesis and melena in another) only occurred in those patients who received phenylbutazone.

Administration, Oral↗
PubMed1979

Tolfenamic acid in the treatment of rheumatoid arthritis.

In an open trial of three months' duration the clinical effect of tolfenamic acid, a new nonsteroid anti-inflammatory analgesic, was found to be good in 85 patients suffering from rheumatoid arthritis. Both subjective and objective parameters clearly improved, and corticoid therapy could be abandoned by 21% of the patients. Tolfenamic acid was for the most part better than or as good as, the previous medication by which the disease had been brought to a stabile state. Side-effects were mild, no severe adverse reactions were observed which could be definitely attributed to tolfenamic acid.

Administration, Oral↗
PubMed1979

Prostaglandins in the regulation of circulation and blood pressure.

Endogenous prostaglandins (PGs) participate in the regulation of local circulation, and presumably also in the control of systemic blood pressure. Vasodilatory PGs synthesized in resistance vessels seem to maintain the basal blood flow in some tissues. Vasoconstriction stimulates the PG synthesis in vessel walls, and the vasodilatory PGs antagonize this constriction in several vascular beds. Circulating vasodilatory PGs or their metabolites may function as antihypertensive hormones. Reports on the effect of intrarenal PG production on renal function are contradictory. The renin-angiotensin-aldosterone and kallikrein-kinin systems have complex interrelations with PGs. PGs may also participate in the mechanism of action of some cardiovascular drugs.

Aldosterone↗
PubMed1978

Effects of prostaglandins on rat cardiac adenylate cyclase.

A significant stimulatory action of PGE1 on adenylate cyclase of the particulate membrane preparation of rat heart was observed at 1 X 10(-4) M. PGE1 caused a positive inotropic effect on isolated spontaneously beating rat atria 1 X (10(-5) M, and an increase in atrial cyclic AMP level at 1 X 10(-6) M. PGE2 stimulated the atrial but not the whole heart particulate adenylate cyclase. PGF 2alpha had no effect on these enzyme preparations. Our results suggest that: (i) The inotropic response of isolated spontaneously beating rat atria to PGE1 may be connected with an increase in cyclic AMP level; (ii) the effect of prostaglandins on heart in vivo must be indirect, because the concentrations needed to stimulate isolated atria and particulate adenylate cyclase were high, compared with the doses effective in vivo.

Adenylyl Cyclases↗
PubMed1978

Effects of reserpine and propranolol on urinary excretion of histamine and 5-hydroxytryptamine in severe cold exposure in normal and cold-acclimated Guinea-pigs.

The effects of cold-acclimation, reserpine and propranolol were investigated on the survival time, rectal temperature and urinary excretion of histamine and 5-HT in guinea-pigs at -20 degrees C. Both reserpine and propranolol shortened survival time by 3 hours and 1.5 hours respectively, the shortest time being in the cold-acclimated reserpine-treated animals. There was a trend in severe cold exposure to increased excretion of histamine both in the non-acclimated and in cold-acclimated animals. Reserpine did not change the excretion but increased the concentration of histamine from 0.08 to 0.25 microgram/ml. Propranolol proved to be a histamine liberator by increasing the excretion in non-acclimated from 0.10 to 1.40 microgram/h and concentration from 0.10 to 4.52 microgram/ml and in cold-acclimated animals the excretion from 0.20 to 2.85 microgram/h and the concentration from 0.08 to 3.23 microgram/ml. Severe cold increased the excretion of 5-HT in the non-acclimated animals from 0.08 to 0.21 microgram/h and cold acclimation increased this to 0.17 microgram/h. Reserpine diminished the excretion from 0.08 to 0.03 microgram/h in the non-acclimated animals, but propranolol had no effect. The results showed that the excretion of histamine and 5-HT into urine are changed in cold and can be modified with drugs. The application of the findings in proving a cold stress deserves further study.

Acclimatization↗
PubMed1978

The effect of inhibition of prostaglandin synthesis on plasma renin activity and blood pressure in essential hypertension.

The influence of oral indomethacin treatment (75 mg daily for a week) on urinary excretion of prostaglandin (PG) F2alpha, plasma renin activity (PRA), blood pressure (BP) and electrolyte excretion (Na+ and K+) was studied in 21 patients with untreated essential hypertension (9 women and 12 men, aged from 40 to 45 years). PGF2alpha excretion and PRA were markedly suppressed by indomethacin in both sexes. A close correlation was found between the decreases in PGF2alpha excretion and PRA. 13,14dihydro-15keto-PGF2alpha (a metabolite of PGF2alpha) excretion also tended to be lowered during the indomethacin treatment. BP tended to increase but urine volume and electrolyte excretion were unchanged during the indomethacin period. The results suggest that in essential hypertension inhibition of the PG synthesis causes a concomitant suppression in PRA and may slightly increase BP.

Adult↗
PubMed1978

Effect of lowering of the temperature on the tissue levels of cAMP, cGMP, PGE and PGF2 alpha in spontaneously beating rat atria preparation.

Tissue levels of cAMP, cGMP, PGE, and PGF2 alpha were measured in spontaneously beating rat atria preparation at 20C and 37C. At 20C the formation of cAMP increased in correlation with the markedly increased amplitude and reduced frequency. The other biochemical parameters were not significantly affected by the low temperature.

Adaptation, Physiological↗