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Biomedical subjects

F Fyhrquist

Publications and source records attributed to F Fyhrquist.

At least 271 records · Page 15Linked to original sources
PubMed1975

Plasma renin activity, blood pressure and sodium excretion during treatment with clonidine.

Clonidine, 225 mug a day, has been given orally for 3 months to 15 patients with essential hypertension. Mean BP was reduced from 159/107 to 143/87 mmHg. The antihypertensive effect of the drug was dissociated from changes in plasma renin activity (PRA) during clonidine treatment. PRA levels decreased initially in 6 patients with the highest PRA values before treatment, but then increased again. In 6 patients with lower pretreatment PRA levels, PRA rose continuously. Opposite patterns of 24-hour urinary sodium excretion were observed in these arbitrary subgroups. The antihypertensive effect of clonidine in essential hypertension appears to be independent of changes in PRA.

Administration, Oral↗
PubMedDate not supplied

Is renin substrate an erythropoietin precursor?

The biogenesis of erythropoietin is incompletely understood. One hypothesis maintains that erythropoietin is synthesized primarily in the kidney while according to another theory an erythropoietin precursor present in plasma is activated by a renal factor, erythrogenin. An attractive candidate for the erythropoietin precursor is renin substrate (angiotensinogen) which has chemical similarities with erythropoietin. We show here that purified renin substrate from human plasma is immunologically related to human erythropoietin. Moreover, purified renin substrate, like erythropoietin, causes the dose-dependent increase of haemoglobin F in cultured human erythroid leukaemia K562 cells. We conclude that renin substrate is a likely precursor of erythropoietin.

Angiotensinogen↗
PubMedDate not supplied

Endothelin in migraine patients.

Endothelins (ETs) are the most potent vasoconstrictors known, and may be the mediators of the vasoconstrictive phase in migraine attacks. We studied 31 previously selected migraine patients with (9) and without (22) aura ictally and interictally to determine their plasma ET-1 values. The mean interictal and ictal values were 5.3 pg/ml (SD 1.8) and 6.4 pg/ml (SD 3.9), respectively. The ictal values were markedly elevated at the beginning of the migraine attack (<2 h) and declined to interictal or even lower level later (4 to 6 h) in the course of an attack. The local vasoconstriction at the beginning of a migraine attack might be ET-mediated secondarily to serotonin activation.

Adult↗
PubMedDate not supplied

Downregulation of angiotensin-converting enzyme by tumor necrosis factor-alpha and interleukin-1beta in cultured human endothelial cells.

Angiotensin-converting enzyme (ACE) and cytokines are considered to play an important role in the pathophysiology of cardiovascular diseases such as atherosclerosis. In the present study, the effects of the cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) on ACE in cultured human umbilical vein endothelial cells (HUVECs) was studied. TNF-alpha (0.1-10 ng/ml) and IL-1beta (0.1-10 ng/ml) caused a dose- and time-dependent decrease in the amount of ACE in intact endothelial cell membranes and decreased levels of ACE mRNA. TNF-alpha and IL-1beta activated p44/42 and p38 mitogen-activated protein kinases (MAPKs) in HUVECs; this was inhibited by the specific inhibitors of these kinases, PD98059 and SB202190, respectively. Pretreatment of endothelial cells with the specific p38 MAPK inhibitor SB202190 (5 microM) or hydrocortisone (5 microM) partly reversed the suppression of ACE by TNF-alpha or IL-1beta, whereas the specific p44/42 MAPK inhibitor PD98059 (40 microM) was without effect. Vascular endothelial growth factor (1 ng/ml) caused an increase in membrane-bound ACE and ACE mRNA levels which was inhibited by pretreatment of the cells with TNF-alpha (1 ng/ml) or IL-1beta (1 ng/ml). In summary, the cytokines TNF-alpha and IL-1beta downregulated ACE in cultured human endothelial cells, which effect was probably mediated by the p38 MAPK pathway. Downregulation of ACE by TNF-alpha and IL-1beta locally in the vascular wall may be a counterbalancing mechanism in inflammatory processes such as atherosclerosis, leading to decreased production of angiotensin II and accumulation of bradykinin.

Cells, Cultured↗
PubMedDate not supplied

Comparison of pharmacokinetics, metabolic effects and mechanisms of action of glyburide and glipizide during long-term treatment.

Fourteen non-insulin-dependent diabetic (NIDDM) patients continued their previous medication (7 on glyburide, 7 on glipizide) for 6 mo, after which they switched to the alternate treatment for another 6 mo. The treatment periods were followed by 1 mo of placebo. The sulfonylurea dose was increased to achieve fasting plasma glucose levels less than 9 mM or to a total maximum daily dose of 25 mg. The mean final doses of glyburide (14.7 +/- 2.4 mg/day) and glipizide (15.2 +/- 2.2 mg/day) were similar. Postprandial (postdose) glipizide levels were higher than those of glyburide, whereas fasting (predose) glyburide concentrations were higher than those of glipizide. Both treatments improved glucose control by 25% compared with placebo. Glipizide therapy evoked higher postprandial insulin concentrations than did glyburide, whereas basal insulin concentrations were higher during glyburide. Insulin sensitivity, assessed by an insulin tolerance test, was more improved with glyburide than with glipizide. In conclusion, overall glucose control is similarly improved by glyburide and glipizide. However, glipizide amplifies the plasma insulin response to meals more than glyburide, whereas glyburide enhances basal insulin secretion more than glipizide. Both pharmacokinetic and pharmacodynamic factors may contribute to these differences.

Blood Glucose↗
PubMedDate not supplied

Plasma atrial natriuretic factor concentration in a heart-lung transplant recipient.

Plasma concentration of atrial natriuretic factor, a polypeptide secreted by the heart, was measured in a heart-lung transplant recipient before operation and for 8 days after operation, until the patient died. Plasma atrial natriuretic factor level decreased in combination with the transplantation; after transplantation the peptide level varied within a wide range, correlating with diastolic pulmonary artery pressure (r = 0.93, p less than 0.01). The physiologic atrial natriuretic factor response to changes in right ventricular afterload thus seems to be preserved in the denervated heart.

Adult↗
PubMedDate not supplied

Erythropoietin and renin after renal transplantation.

Serum concentration of erythropoietin (EP) was measured with a hemagglutination inhibition technique and plasma renin activity (PRA) with a radioimmunoassay for angiotensin I in 26 renal transplant recipients 2-54 months after renal transplantation. In all patients, the EP values were significantly correlated with the levels of PRA (r = 0.76 p less than 0.001) and hematocrit values (r = 0.72, p less than 0.001). In one patient, erythrocytosis and high blood pressure associated with high EP and PRA levels disappeared after bilateral nephrectomy of his own kidneys. The results indicate an as yet unidentified relationship between the production of EP and renin.

Erythropoiesis↗