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Biomedical subjects

F Fyhrquist

Publications and source records attributed to F Fyhrquist.

At least 217 records · Page 12Linked to original sources
PubMed1980

Efficacy of captopril in experimental low renin hypertension.

Captopril (SQ 14225) had a clear antihypertensive effect in rat Heymann nephritis-DOCA-NaCl hypertension, a low renin model introduced recently, but was ineffective in 1-kidney-DOCA-NaCl hypertension although plasma renin activity (PRA) was suppressed similarly in both. Thus, the antihypertensive effect of captopril was independent of circulating renin. This result also suggests different pathogenetic mechanisms of hypertension in these two DOCA-NaCl models.

Animals↗
PubMed1980

Induction of angiotensin I-converting enzyme rat lung with Captopril (SQ 14225).

Angiotensin I-converting enzyme (ACE, EC 2.4.15.1.) was measured in serum and in pulmonary plasma membranes of 40 spontaneously hypertensive rats (SHR, Okamoto Aoki strain), divided into 4 groups, and treated with SQ 14225 (Captopril), 0.2 mg . ml-1 in drinking water, for 0-24 weeks. Serum ACE activity increased 2.5-3 fold after 12-24 weeks of SQ 14225 treatment, paralleled by an increase of ACE concentration in purified pulmonary plasma membranes (25-52%), and in ACE concentration upon solubilization with Triton X-100 from such plasma membranes (96-120%). We conclude that the ACE inhibitor, SQ 14225, causes marked induction of pulmonary ACE biosynthesis. High serum ACE activity probably reflects increased total biosynthesis of the enzyme.

Animals↗
PubMed1980

Vasopressin release by histamine in the conscious goat.

The vasopressin releasing activity of histamine was studied in conscious goats. Histamine was infused into the brain ventricles or intravenously and serial blood samples were taken from the jugular vein. Plasma vasopressin was assayed by a radioimmunoassay for arginine vasopressin (AVP). After i.v. infusions of 300 micrograms and 1 mg of histamine, a pronounced increase in plasma AVP up to greater than 100 pg/ml occurred. This was considered secondary to hypotension, since it only occurred with doses that markedly decreased arterial blood pressure. When given i.c.v. even smaller doses of histamine increased plasma AVP without any concomitant decrease in blood pressure. There was a simultaneous decrease in renal free water clearance in hydrated animals. Up to the dose of 300 microgramshistamine, the increase in AVP was modest. Histamine 1 mg i.c.v., given to either hydrated or non-hydrated animals, increased plasma AVP about tenfold, up to 38.3 +/- 23.3 pg/ml and 56.7 +/- 19.0 pg/ml, respectively. In individual experiments the correlation between the AVP level and the degree of antidiuresis was less apparent, since the kidney seemed to be very sensitive even to small changes in plasma AVP. It is concluded that histamine releases vasopressin through a central mechanism and it is reasonable to suppose that histamine may act as a neurotransmitter in the vasopressin releasing system.

Animals↗
PubMed1980

Renin, water drinking, walt preference and blood pressure in alcohol preferring and alcohol avoiding rats.

Mechanisms controlling fluid volume were studied in alcohol preferring AA (Alko, Alcohol) and alcohol avoiding ANA (Alko, Non-Alcohol) rats. Hypertonic sodium chloride solution (5%) given orally caused a higher dipsogenic response in AA rats than in the ANA's. One hour after ethanol loading (4.8 g/kg, by stomach tube), plasma renin activity of AA rats was four times as high as in ANA rats. ANA rats had higher degree of sodium chloride (0.9%) preference and higher blood pressure. The strain differences in voluntary salt intake and salt metabolism may modulate the consumption of calories and water as well as blood pressure and different reactivity of the renin system in AA and ANA rats.

Alcohol Drinking↗
PubMed1980

Hemodynamic significance of vasopressin in the newborn infant.

In 21 normal deliveries, high concentrations of arginine vasopressin in cord arterial blood were associated with higher blood pressure and lower skin temperatures, indicating peripheral vasoconstriction. Following cesarean section after the onset of labor, cord AVP concentrations and blood pressures were lower than after normal delivery, but higher than after elective cesarean section. Maternal AVP concentrations at delivery were normal, as were plasma AVP concentrations in all infants three days after delivery. We conclude that the massive release of vasopressin is associated with normal delivery, and with peripheral vasoconstriction. These findings reflect favorable hemodynamic adaptation to the hypoxia and stress of delivery, intended to redistribute cardiac output to vital organs.

Arginine Vasopressin↗
PubMed1980

Enzyme inhibitors for renin assay in rat plasma.

1. Degradation of 125I-labelled [Ile5]-angiotensin I and unlabelled angiotensin I was studied during incubation of rat plasma treated with disodium ethylenediaminetetra-acetate (disodium EDTA) at 37 degrees C, pH 6.5, for 1 h with 8-hydroxyquinoline, phenylmethylsulphonyl fluoride or di-isopropyl fluorophosphate. 2. Isoelectric focusing showed approximately 100, 59--66 and 10--31% preservation of 125I-labelled angiotensin I during incubation with 8-hydroxyquinoline (5.0 mmol/l), phenylmethylsulphonyl fluoride (15 mmol/l) and di-isopropyl fluorophosphate (1.09 mmol/l) respectively. Mean recovery of unlabelled angiotensin I was 102, 77 and 32% with 8-hydroxyquinoline, phenylmethylsulphonyl fluoride and di-isopropyl fluorophosphate respectively. 3. 8-Hydroxyquinoline appears the preferable enzyme inhibitor for renin assay in rat plasma.

Angiotensin I↗
PubMed1980

Autologous immune complex nephritis and DOCA-NaCl load: a new model of hypertension.

In order to explore immunological features of hypertension, we studied autologous immune complex nephritis (Heymann nephritis) combined with DOCA-NaCl treatment. This combination resulted in hypertension and increased heart weight whereas DOCA-NaCl treatment alone induced only a slight elevation of blood pressure and a moderate increase in heart weight. Nephritic rats without DOCA-NaCl load remained normotensive, their heart weights being comparable to those of controls. This new model of hypertension was neither characterized by azotemia nor by reduced renal excretory capacity. Hypertension was not renin-angiotensin-dependent. DOCA-NaCl treatment accelerated the development of proteinuria. In the hypertensive rats, systolic blood pressure to daily urinary protein excretion. Renal histopathology revealed changes resembling those of malignant nephrosclerosis. Immunohistology and electron microscopy showed a typical membranous glomerulonephritis in all immunized animals. It was concluded that immune complex disease of the Heymann nephritis type may interfere with normal hemodynamic adaptation to hypervolemic sodium load, resulting in hypertension.

Animals↗
PubMed1980

Transient vasopressin release and thirst in response to prolonged intracerebroventricular infusions of hypertonic mannitol in saline.

In the conscious goat infusions of 0.4 M mannitol in 0.15 M NaCl into the lateral cerebral ventricle (40 or 100 min, 0.02 ml/min) caused slight, transient vasopressin release and temporary thirst, whereas infusions or pure, hypertonic (0.7 M) mannitol did not elicit thirst and inhibited the basic vasopressin release in the nonhydrated animal. In contrast, infusions of equiosmolal (0.35 M) NaCl induced persistent thirst and pronounced elevation of the plasma vasopressin concentration throughout the infusion period. The cerebrospinal fluid (CSF) osmolality was raised by the same order of magnitude (= 13%) after the mannitol/NaCl and the hypertonic NaCl infusions. The CSF Na+ concentration was elevated by greater than 10% at 5 min after hypertonic NaCl infusions, but it was reduced by approximately 10% at 5 min after the mannitol/NaCl infusions. There was no appreciable difference in the CSF K+ concentration after the infusions. The results are discussed with regard to the possible importance of CSF Na+-concentration as opposed to strict osmotic factors for the excitation of receptors involved in the control of water balance.

Animals↗
PubMed1980

Marathon run: effects on blood cortisol -- ACTH, iodothyronines -- TSH and vasopressin.

Blood cortisol, ACTH, thyroxine, triiodothyronine, reverse triiodothyronine, thyroid stimulating hormone (TSH) and vasopressin concentrations were determined in 9 runners (29-56 years old) and one 80 year old man taking part in a non-competitive Marathon in Athens, Greece on October 1976. After the run the mean concentrations of cortisol, ACTH and vasopressin showed a significant rise. The thyroid function variables and TSH did not differ from the control values. There was a significant correlation between the cortisol and ACTH levels after the race and also between their increments from the corresponding base values. A significant correlation was found between the physical fitness (as measured by indirect determination of VO2max) and the post-race cortisol levels. One of the well trained runners with a fairly good running time had the highest post-race values for 6 of 7 hormones studied.

Adrenocorticotropic Hormone↗
PubMed1980

Purification of human lung angiotensin-converting enzyme.

Angiotensin-converting enzyme (ACE) was purified about 7000 times from human lung tissue obtained at thoracotomy. After solubilization with Triton X-100 and sonication, ion exchange DEAE cellulose chromatography and Sepharose 4B gel filtration were performed. After gel filtration a 5-6 fold increase in purity was achieved by neuraminidase treatment of the protein and recycling over DEAE cellulose. Purity was established in SDS electrophoresis and on electrofocusing 125I-labelled purified protein and these procedures indicated a molecular weight of about 150,000 and pI value of 4.5, respectively. The purified protein split Angiotensin I and this action was inhibited by Captopril (Squibb 14,225), specific inhibitor of ACE (kininase II). The Km value for the synthetic substrate hippuryl-histidyl-leucine was 3.7 X 10(-4) mol/l. The IC50 of Captopril when inhibiting human lung ACE action on the same substrate, was 4.5 X 10(-9) mol/l.

Chromatography, Gel↗
PubMed1980

Late results of surgical treatment for renovascular hypertension.

Over a 4-year period, 32 patients, 11 females and 21 males between 18 to 62 years of age (mean age 39 years) were operated on because of renovascular hypertension. Three patients were operated on bilaterally. The most common type of arterial reconstruction was aortorenal venous bypass. Early nephrectomy was performed in two patients, and secondary nephrectomy due to graft occlusion in four patients. There was no operative mortality. Seven patients died during follow-up, five of them of cardiovascular causes. The proportion of patients who were cured or improved by surgery throughout a follow-up of two to 72 months (mean 24 months) exceeded 87%. Nine of these 28 patients were normotensive, the other 19 were improved with less need of drugs following surgery. Four patients were failures. Lateralizing renal venous renin activity was found to be the best single criterion for prediction of improvement following surgery. In the majority of the patients who were cured after surgery, there was no preoperative heart hypertrophy and fundoscopic findings were normal or mildly pathological. A higher incidence of hypertensive changes in the target organs was observed preoperatively in the improved patients than in the cured ones.

Adolescent↗
PubMed1979

The syndrome of inappropriate secretion of antidiuretic hormone. A case report.

A 72-year-old woman with the syndrome of inappropriate secretion of antidiuretic hormone of unknown cause during more than one year of observation is reported. Plasma vasopressin levels were excessively elevated, even during a water load test. Her serum electrolyte abnormalities and general state were ameliorated after fluid restriction. During treatment with demeclocycline the patient was able to increase fluid without deterioration.

Aged↗
PubMed1979

Renin, aldosterone and cortisol during ethanol intoxication and hangover.

The effect of ethanol intoxication and hangover on plasma renin activity (PRA), plasma aldosterone (PA) and plasma cortisol (PC) concentrations was studied in 7 healthy supine men in controlled clinical conditions during 18 h beginning at 6 p.m. Large individual variation was observed in the response of PRA, PA and PC to ethanol. Following ethanol, stimulation of PRA was observed at the 14th and the 16th hour (P less than 0.05), of PA at the 4th and the 6th hour (P less than 0.01 and P less than 0.05, respectively) and of PC at the 4th and the 14th hour (P less than 0.01 and P less than 0.05, respectively). Ethanol ingestion suppressed PC during the first hour (P less than 0.02). Water ingestion at 8 a.m. suppressed PA between the 14th and the 16th hour (8-10 a.m.) in control and ethanol experiment (P less than 0.01 and P less than 0.005, respectively). There was a dissociation between PRA and PA, but intra-individually PRA and PA correlated fairly or well. Plasma arginine vasopressin (AVP) and PC were also significantly correlated. The results suggest that changes in PA and PC as well as the dissociation of PRA and PA after ethanol ingestion might be partly related to dehydration and to the increased secretion of hypothalamic and pituitary hormones as well as to sodium and potassium balance. There was a biphasic effect of ethanol, including an inital suppression of PC and a subsequent increase of PC, PRA and PA. Upright posture appears to exaggerate the stimulating effect of ethanol on PRA, PA and PC.

Adult↗
PubMed1979

Adenosine 3',5' cyclic monophosphate, calcium and magnesium excretion in ethanol intoxication and hangover.

Effect of ethanol on adenosine 3', 5' cyclic monophosphate (cAMP), calcium (Ca) and magnesium (Mg) excretion was studied in controlled clinical conditions in man. Seven male volunteers served as their own controls. In 5 subjects cAMP excretion was primarily suppressed by ethanol. Ethanol appeared to have a biphasic effect on Ca excretion, an initial stimulation followed by a conservation phase. Mg excretion was stimulated by ethanol in 5 subjects. Subjects having nausea and vomitus and the most severe hangover symptoms had the lowest urinary Ca excretion and the lowest imitial cAMP excretion. Ca and Mg metabolism and the susceptibility of the body to the toxic effects of ethanol appeared to be interrelated.

Adult↗
PubMed1979

Plasma vasopressin in conscious goats after cerebroventricular infusions of angiotensins, sodium chloride, and fructose.

Using a sensitive RIA, the levels of plasma arginine vasopressin (pAVP) were determined from jugular venous blood of conscious goats given cerebroventricular (c.v.) infusions of angiotensins, saralasin, NaCl, and fructose. In hydrated goats, c.v. angiotensin II (0.1--1.0 microgram) caused a dose-dependent rise of pAVP, drinking, and antidiuresis. The same responses were obtained after angiotensin III (1.8 microgram) and hypertonic NaCl (0.5 M), but the effect on water intake was less striking. [des1,2]Angiotensin II hexapeptide and isotonic NaCl (0.15 M) failed to affect these variables. In nonhydrated goats, there were no changes in drinking, diuresis, or pAVP after c.v. infusions of saralasin (5.0 microgram) and isotonic NaCl (0.15 M). Fructose (0.3 M) infusions lowered the pAVP, apparently by reducing the cerebrospinal fluid (CSF) Na+ concentration, while the renal free water clearance turned positive. Angiotensin III thus carries the minimal structural requirements for pAVP release via central nervous receptors in the goat. Lack of a saralasin effect suggests that, in the nonhydrated goat, angiotensin II may not regulate pAVP via receptors accessible to the CSF. Sodium-sensitive cells monitoring the Na+ concentration of the CSF seem to control the pAVP.

Angiotensin II↗