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Biomedical subjects

F Fyhrquist

Publications and source records attributed to F Fyhrquist.

At least 163 records · Page 9Linked to original sources
PubMed1985

Erythropoietin and renin substrate in cerebellar haemangioblastoma.

We examined eight cerebellar haemangioblastoma tumours from eight patients, aged 16-63 years, 5 females and 3 males. Preoperative haemoglobin values exceeded 180 g/l in four patients, and 150 g/l in four. All high Hb values were normalized upon surgical removal of the tumours. All tumours contained scattered cells which stained positively with antisera against pure human urinary erythropoietin and plasma renin substrate. We conclude that cerebellar haemangioblastomas produce immunoreactive erythropoietin, which shares common antigenic determinants with renin substrate.

Adolescent↗
PubMed1985

Angiotensin converting enzyme in cerebrospinal fluid: a new assay.

Serum and CSF angiotensin converting enzyme (ACE) were measured by a new inhibitor binding assay in 32 patients with sarcoidosis, 49 with neurologic diseases, and 38 controls. In neurosarcoidosis, 11 of 20 patients had high levels of CSF ACE. In systemic sarcoidosis without neurologic abnormality, only 1 of 12 patients had elevated CSF ACE. The highest value was observed in a patient with widespread meningeal sarcoidosis. High values were also observed in patients with bacterial meningitis or malignant tumors of the CNS. Fluctuation in successive analyses correlated to clinical course of neurosarcoidosis. CSF ACE analysis seems useful in diagnosis and follow-up of neurosarcoidosis.

Adolescent↗
PubMed1985

Effect of serial test meals on plasma immunoreactive GIP in non-insulin dependent diabetic patients and non-diabetic controls.

Previous reports have shown considerable variation in postprandial gastric inhibitory polypeptide (GIP) response in non-insulin-dependent diabetic (NIDD) patients. One reason for this may be the use of different GIP antisera. Employing antiserum R65, which specifically reacts with the 5000-dalton GIP, we investigated the plasma GIP response to serial test meals in 11 NIDD patients and 11 age- and weight-matched non-diabetic controls. The postprandial GIP response was lower in the NIDD patients than in the non-diabetic controls (p less than 0.05). Although the serum insulin concentrations did not differ between diabetic and non-diabetic subjects, the insulin to glucose ratio was lower in the diabetics than in the non-diabetic subjects (p less than 0.05) indicating some degree of relative insulin deficiency in the diabetic patients. The data suggest that the GIP secretory capacity may be impaired in NIDD patients. Whether the impairment of GIP secretion is associated with impaired insulin secretion requires further investigation.

Adult↗
PubMed1985

Radioimmunoassay of haemoglobin F in K 562 cells following induction with renin substrate and erythropoietin.

To test the hypothesis of renin substrate (RS; angiotensinogen) being a precursor of erythropoietin (EP), the capacity of RS and EP to induce Hb synthesis was compared in cultured human erythroid leukaemia cells of the K 562 line after prestimulation with haemin. For this purpose a radioimmunoassay for haemoglobin F (HbF) was developed. This assay was shown to be specific for HbF, reproducible, and sensitive for 0.1 ng of HbF. The cells were induced by RS and EP to increased HbF production. Cells stimulated with RS or EP showed increased benzidine staining. This data, corroborating our earlier observations on immunological similarities between RS and EP, supports the hypothesis that renin substrate is a likely precursor of erythropoietin.

Angiotensinogen↗
PubMed1985

Renin-aldosterone axis in ethanol intoxication: effect of A II infusion.

Plasma renin activity (PRA) is increased while plasma aldosterone is not, during moderate ethanol intoxication. To elucidate mechanisms behind this dissociation of renin-aldosterone nexus, six healthy males were given angiotensin II (4 ng kg-1 min-1) by i.v. infusion following ingestion of ethanol (1.2 g kg-1 body weight). Prior to angiotensin II (A II) infusion, PRA rose and plasma aldosterone declined. A II infusion caused a roughly 3-fold increase of plasma aldosterone both in ethanol intoxication and in control experiments, and a transient suppression of PRA. Plasma renin substrate, cortisol, and angiotensin converting enzyme (ACE) remained unchanged. The decrease of serum potassium or the rise of Na+/K+ ratio in ethanol intoxication may explain the failure of the adrenal cortex to respond with aldosterone release to endogenous angiotensin II. However, the pressor dose of A II infused obviously overcame the blunting effect of ethanol on aldosterone release previously reported by us. Blood pressure, both diastolic and systolic, increased similarly during ethanol and control experiments in response to A II infusion, except in one subject, who during ethanol intoxication experienced a paradoxical fall in blood pressure while reacting normally to A II infusion without ethanol.

Adrenal Cortex↗
PubMed1985

Comparison of C-terminal and N-terminal PTH in secondary hyperparathyroidism in renal failure.

In 89 patients with disorders in calcium regulation either C-terminal or N-terminal PTH or both, were elevated. In haemodialysis patients the results of C-terminal and N-terminal PTH measurements showed the same trend in 10 patients; in 30 patients only C-terminal and in four patients only N-terminal PTH was elevated. In patients with renal failure, creatinine clearance less than 30 ml/min, both C-terminal and N-terminal PTH were elevated in five patients, C-terminal PTH in 12 patients and N-terminal PTH in none of the patients studied. Fourteen patients with primary hyperparathyroidism were studied; in ten both C-terminal and N-terminal PTH were elevated, in two only C-terminal PTH and in another two only N-terminal PTH was elevated. The results show that there seems to be a better clinical correlation for hyperparathyroidism, in haemodialysis patients and patients with renal failure, using N-terminal PTH determinations rather than C-terminal PTH determinations, because in haemodialysis patients and patients with renal failure split products of the C-terminal region of PTH give unrealistically high PTH results.

Humans↗
PubMed1985

Evidence that renin substrate (angiotensinogen) may be a precursor of erythropoietin.

We suggested a role for renin substrate (RS, angiotensinogen) in the biogenesis of erythropoietin (EP) (Nature 308:649-652, 1984). Purified RS was prepared from pooled plasma of healthy adult subjects, or from plasma of pregnant, healthy females. Antisera against human RS were shown to cross-react with purified human urinary EP, using a haemagglutination technique. On the other hand, antisera generated against highly purified human urinary EP showed strong cross-reaction with purified human plasma RS, by agglutinating erythrocytes covered with glutaraldehyde-coupled human RS. Moreover, using antisera generated against RS or EP, we have demonstrated monocytoid cells staining positive for both EP and RS in cerebellar haemangioblastoma tumors from 8 patients. Taken together, these observations point to a close relation between RS and EP. One interesting explanation is that renin substrate may be a precursor of erythropoietin.

Adult↗
PubMed1985

Hypertension and progression of experimental nephritis. Interaction between immunological and haemodynamic factors.

Hypertension has been shown to accelerate the course of experimental nephritis. On the other hand, Heymann nephritic rats undergoing long-term DOCA-NaCl treatment develop hypertension with a malignant course. The present study examined the effect of a short-term DOCA-NaCl load on the development of hypertension and progression of nephritis. Heymann nephritic rats were treated with DOCA-NaCl between weeks 2 and 6 after the first immunization with brush border antigen. Within six weeks, hypertension developed in Heymann nephritis-DOCA-NaCl rats but not in Heymann nephritic rats without DOCA-NaCl treatment whereas DOCA-NaCl-treated rats developed a moderate elevation of blood pressure. During that time, anti-brush border antibodies and immune deposits typical of membranous nephropathy ensued, preceding appearance of proteinuria or histopathologically detectable renal changes in the immunized rats. After discontinuation of DOCA-NaCl treatments at week 6, blood pressure nearly normalized in DOCA-NaCl-treated rats. Within one year, however, blood pressure rose most markedly in nephritic rats treated initially with DOCA-NaCl. The rise in blood pressure at that time correlated with glomerular sclerosis, tubulo-interstitial changes and proteinuria. It is concluded that, during acute nephritis, immunological and hypertensinogenic mechanisms interact, leading to hypertension and aggravated course of nephritis. These experimental observations on nephritis-associated hypertension may have important bearings on human hypertension as well.

Animals↗
PubMed1984

Effect of beta-blocking drugs on beta-cell function and insulin sensitivity in hypertensive non-diabetic patients.

The effects of two beta-blocking drugs on endogenous insulin secretion and insulin sensitivity were investigated in a double-blind cross-over study in 13 hypertensive patients. The patients were randomly allocated to each of three 2-week treatment periods with propranolol 80 mg b.i.d., atenolol 50 mg b.i.d. and placebo b.i.d. Endogenous insulin secretion was assessed by measuring serum insulin and C-peptide before and 6 min after iv administration of glucagon; insulin sensitivity was determined by measuring insulin binding to erythrocytes, and as the glucose disappearance rate (KITT) after i.v. insulin. Fasting concentrations of serum free fatty acids (S-FFA) and plasma gastric inhibitory polypeptide (P-GIP) were also recorded during the three study periods. Both propranolol and atenolol reduced blood pressure, heart rate and S-FFA concentrations compared to placebo, and all patients showed measurable plasma concentrations of propranolol and atenolol. The results can be considered representative, therefore, of clinical beta-blockade. The two drugs did not significantly influence the fasting blood glucose level. There was an increase in fasting and glucagon-stimulated serum C-peptide concentration during propranolol therapy compared with placebo (p = 0.037 and p = 0.030, respectively), although this was not reflected by a significant change in serum insulin. Propranolol and atenolol did not significantly influence insulin binding to erythrocytes, but they clearly reduced the glucose disappearance rate KITT was compared to placebo (p = 0.0036 and p = 0.0003), respectively). The findings support the view that beta-blocking drugs can influence glucose metabolism by mechanisms other than inhibition of endogenous insulin secretion.

Adrenergic beta-Antagonists↗
PubMed1984

Plasma vasopressin levels after I.C.V. infusion of histamine agonists in the conscious goat.

Histamine H1-agonists 2-pyridylethylamine (2-PEA) and 2-methylhistamine and H2-agonists 4-methylhistamine, dimaprit and impromidine were given i.c.v. to conscious goats and the release of arginine vasopressin (AVP) was measured. 2-PEA at very low doses (9 and 27 mumoles/animal, equivalent to H1-activity of about 0.5 and 1.5 mumoles histamine, resp.) significantly increased plasma AVP. The H2-agonists did not cause consistent changes in AVP even if their relative doses were higher. It is concluded that the vasopressin releasing effect of histamine is due to H1-receptor activation.

Animals↗
PubMed1984

Homeostatic responses to water deprivation or hemorrhage in lactating and non-lactating Bedouin goats.

Three lactating and three non-lactating black Bedouin goats were subjected to four days of water deprivation or to hemorrhage. Four days of water deprivation caused body wt losses of 32 and 23% and plasma volume losses of 30 and 34% in lactating and non-lactating goats respectively. Plasma osmolality increased 17 and 15% in lactating and non-lactating goats. Plasma arginine vasopressin concentration rose from about 5 pg/ml to a mean of 36 pg/ml. Plasma renin activity increased from about 0.7 ng/ml/hr to a mean of 3.45 ng/ml/hr in lactating and to 3.15 ng/ml/hr in non-lactating goats. At 4.5 hr post-rehydration plasma osmolality and plasma vasopressin concentration were back to normal in non-lactating, but still elevated in lactating goats. Plasma renin activity increased after rehydration. Rapid blood volume loss of 21-28% increased plasma vasopressin concentration to 16-35 pg/ml in non-lactating and to 70 or greater than 500 pg/ml in lactating goats. It is concluded that black Bedouin goats are well adapted to endure severe dehydration and rapid rehydration, but that they (especially lactating animals) react strongly to rapid volume depletion.

Animals↗
PubMed1984

Inhibitor binding assay of rat serum angiotensin converting enzyme.

Based on a specific binding of labelled inhibitor to the enzyme active centre, a new principle of enzyme assay, inhibitor binding assay (IBA), was developed and applied to measurement of rat serum angiotensin converting enzyme (ACE). Serum diluted 1:50 was incubated with 125I-labelled ACE inhibitor, 351A, at pH 7.0, 37 degrees C, for 2 h. Inhibitor bound to ACE was separated with coated charcoal and results were calculated from a standard curve. The advantages offered by the novel inhibitor binding assay include simplicity, specificity, absence of interference by other enzymes or immunological cross-reactions, and great sensitivity enabling measurement of ACE in concentrations less than 0.1 units/ml. This principle of enzyme assay will not only have potential new applications for research involving ACE but may also be extended to other enzymes.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

A long-term follow-up of patients with essential hypertension treated with captopril.

Seventy-four patients from four short-term studies of captopril in mild-moderate essential hypertension continued in a cooperative long-term efficacy and tolerance program. The duration of observation is 2- greater than 4 years, the total treatment time being 2434 months. No development of resistance to therapy was observed. The total daily dose of captopril has been gradually decreased and in 20 patients changed from t.i.d. to b.i.d. regime. The drug has been well tolerated and only few and mild side-effects have been observed after the initial titration period. The drop-outs (n = 19) were mostly due to non-medical causes (n = 14). Except for one case of proteinuria, no laboratory abnormalities were detected and there were no signs of long-term toxicity.

Adult↗
PubMed1984

Tissue distribution of angiotensin converting enzyme in the rat: effect of captopril treatment.

Effect on different tissues with regard to angiotensin converting enzyme during captopril treatment in the rat was studied. Male Wistar-Kyoto rats (n = 9) were treated during four weeks with captopril dissolved into the drinking water at the dose 30 mg/kg/day. Control rats (n = 9) had water only. Serum angiotensin converting enzyme (ACE) activity increased three-fold during captopril treatment, and ACE of purified pulmonary plasma membranes increased about 64% (P less than 0.001) compared to untreated rats. ACE activity of membrane fractions of other tissues studied i.e. testicles, epididymes, kidneys, and small intestine brush border did not increase similarly during captopril treatment. The highest amounts of ACE was demonstrated in epididymes, but captopril did not produce increased amounts of ACE in the epididymes. The main source of increased serum ACE activity during captopril treatment appeared to be in the pulmonary tissue.

Animals↗
PubMed1984

Effects of captopril on arterial blood pressure, plasma renin activity and vasopressin concentration in sodium-repleted and sodium-deficient goats. A serial study during pregnancy, lactation and anestrus.

The effects of captopril (intravenous loading dose of 20 mg, 1 h later followed by 10 mg infused during the next h) on arterial blood pressure and plasma renin activity were followed in 4 goats during the last months of pregnancy, during lactation and during anestrus. Experiments were made both when the animals were sodium-repleted and sodium-deficient. Furosemide and dietary restriction were used to deprive the animals of sodium. In sodium-replete animals, captopril caused a more pronounced fall in mean arterial blood pressure and a larger increase in plasma renin activity (PRA) when the animals were pregnant than when they were lactating or in anestrus. During sodium-deficient conditions the response was similar as during sodium repletion in pregnant goats. In anestral goats, PRA rose in response to captopril, but the blood pressure fall was similar as when the goats were sodium-replete. In lactating sodium-deficient goats, captopril caused a marked fall in mean arterial blood pressure concomitant with a 2-3 times higher rise in PRA than during corresponding sodium-repletion experiments. The respiratory rate was elevated in pregnant animals and increased further during captopril. The plasma vasopressin concentration did not change during captopril-induced hypotension. If the blood pressure fell greater than or equal to 10 mmHg the animals became very quiet and occasionally they fell asleep. All goats delivered healthy kids. The fact that the blood pressure fall was marked and consistent in all animals during pregnancy, but less and more variable during anestrus indicates that the activity of the renin-angiotensin system is of greater importance for blood pressure maintenance during pregnancy than during anestrus.(ABSTRACT TRUNCATED AT 250 WORDS)

Anestrus↗
PubMed1984

Enalapril and lisinopril in renovascular hypertension--antihypertensive and hormonal effects of two new angiotensin-converting-enzyme (ACE) inhibitors. A preliminary report.

We assessed the antihypertensive and hormonal effects of two new angiotensin converting enzyme (ACE) inhibitors, enalapril (MK-421) and lisinopril (MK-521) in 22 patients with renovascular hypertension. All patients had angiographically verified renal artery lesions, 3 had bilateral renal artery stenosis and one a stenosis in a single kidney, and the rest had unilateral renal artery stenosis. After placebo treatment for 3 days in hospital, increasing doses from 5 to 40 mg daily, of both ACE-inhibitors were given. Both drugs induced a significant fall in blood pressure (BP). Significant BP reductions were seen after 2 h with a maximum fall for the enalapril group at a dose of 40 mg 4 h after drug intake (mean supine BP decrease - 31/24 mm Hg, standing - 29/16 mmHg). The corresponding maximal BP reductions were for the lisinopril group at a dose of 40 mg o.d. at 6 h: mean supine BP fall - 25/28 mmHg and standing - 33/31 mm Hg. Both drugs significantly inhibited serum ACE to about 5 to 10% of initial values and with a duration for more than 24 h. Both drugs also caused a decrease in plasma-AII levels and also in plasma aldosterone concentrations. There were not toxic effects and no serious side effects. Careful monitoring of biochemical variables showed no significant changes. We conclude that both enalapril and lisinopril are effective and very safe agents for the treatment of renovascular hypertension and with a long duration of action and with very good tolerance.

Adult↗
PubMed1984

Angiotensin I-converting enzyme inhibition after renal transplantation.

The angiotensin I-converting enzyme inhibitor captopril was administrated to 15 renal transplant patients for a minimum period of 14 weeks after transplantation. The object was to decrease ischaemic damage caused by secondary activation of the renal renin-angiotensin system after rejection and associated vascular damage. Captopril patients had lower s-creatinine values than controls in the immediate phase after rejection. On the other hand, after 14 weeks renal perfusion was better, but glomerular filtration rate lower in the captopril group than in the control group. However, none of the differences were significant. Renal function was examined during captopril administration, which may have affected the results. Final evaluation of this trial requires extended follow-up. Captopril was well tolerated in the low doses used (37.5-75 mg daily) in spite of varying degrees of renal failure and concomitant azathioprine administration. Only one case of mild leukopenia was recorded, which improved immediately after captopril interruption. No other serious side effects were observed. Captopril may be safely administered to renal transplant patients, if monitoring of renal function and possible side effects is carried through.

Adult↗