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Biomedical subjects

S Sen

Publications and source records attributed to S Sen.

At least 397 records · Page 22Linked to original sources
PubMed1986

Role of sodium in modulation of myocardial hypertrophy in renal hypertensive rats.

To evaluate the role of dietary sodium and antihypertensive drugs in the modulation of myocardial structure, especially myosin isozymic pattern, renal hypertensive rats (two-kidney, one clip) were treated with a sodium-deficient diet (7 mEq/kg), captopril, or atenolol. Native myosin was extracted under nondissociating conditions and separated by polyacrylamide gel electrophoresis. The percentage of myosin isozyme V1 was significantly decreased from 71.5 +/- 7.5 (Wistar controls) to 52.4 +/- 1.7% (p less than 0.05) in renal hypertensive rats and was associated with an increase in V3 component from 12.7 +/- 5.1 (Wistar controls) to 23.1 +/- 1.4% (renal hypertensive rats; p less than 0.05). There was a dramatic change in the myosin isozyme distribution pattern after treatment with low sodium and captopril. Six weeks of low sodium therapy in renal hypertensive rats resulted in an increase in V1 from 52.4 +/- 1.7 to 74.8 +/- 4.8% and a reduction in V3 from 23.1 +/- 1.4 to 9.5 +/- 2.4%. Normal rats treated with low sodium showed similar results. The percentage distribution of isozymes after low sodium therapy in the captopril-treated rats was not different from that in normal Wistar controls. Captopril therapy also caused an increase in V1 and a decrease in V3. Atenolol therapy, on the other hand, caused a significant increase in V3 and decrease in V1 with no change in blood pressure or heart weight. These data suggest that dietary sodium may play an important role in the modulation of myocardial mass and may modulate signals for synthesis of V1 or V3 myosin phenotypes.

Animals↗
PubMed1986

Dopamine inhibits the aldosterone response to upright posture.

Aldosterone secretion in man is stimulated by potassium, ACTH, and angiotensin II and is inhibited by dopamine (DA). In normal sodium-replete supine individuals, aldosterone secretion is under maximum tonic inhibition by DA. Dopaminergic control of aldosterone secretion is modified by dietary sodium depletion. To determine the physiological significance of dopaminergic inhibition of aldosterone secretion, we studied the effect of DA on the aldosterone response to upright posture. Twelve normal men were studied while eating an ad libitum sodium diet, and the effect of DA was determined in the supine and upright positions. Plasma aldosterone (PAC), plasma cortisol (F), plasma aldosterone-stimulating factor (ASF), PRA, and blood pressure were measured while the men were supine and after 4 h of upright posture during an infusion of 5% dextrose vehicle and during a DA infusion of 4.0 micrograms/kg X min. The men also were studied as a time control in the supine position while receiving vehicle or DA. PAC increased from a mean basal value of 20.4 +/- 3.2 ng/dl (+/- SE) by 25.9 +/- 5.1 ng/dl to a peak of 44.4 +/- 2.4 ng/dl in response to upright posture during vehicle infusion. The PAC response to upright posture was reduced to 7.4 +/- 1.8 ng/dl (P less than 0.05) when DA was infused. The increase in PRA with upright posture was 3.7 +/- 1.3 ng/ml X h during the vehicle infusion and 4.1 +/- 1.1 ng/ml X h (P = NS) during the DA infusion. ASF, F, and blood pressure were not altered by upright posture and DA. PAC did not change in the six men infused with DA while supine. Therefore, DA inhibits upright aldosterone responses without affecting PRA, ASF, or F.

Adult↗
PubMed1986

Cardiovascular hypertrophy in spontaneously hypertensive rats.

In 1974 we reported that left ventricular mass correlated poorly with blood pressure levels during both the development and the reversal of hypertensive cardiac hypertrophy. This study, which was confirmed by many, has since been extended along two main lines: investigation of the factors modulating left ventricular hypertrophy and of associated changes in contractile protein, and comparison of the left ventricular structural response to hypertension with those of the large and small resistance vessels. In addition to blood pressure control, two factors were identified as important modulators of left ventricular hypertrophy: the level of cardioadrenergic activity and a recently isolated myocardial factor in SHR which stimulates in vitro cardiac protein synthesis. Of greater importance haemodynamically are the structural changes in the small resistance vessels; these were estimated from resistance to constant flow during maximal vasodilatation (Folkow). Captopril-hydrochlorothiazide led to a significantly greater reduction in that index than hydralazine, although both led to equal blood pressure control. Despite some general parallelism, the structural cardiovascular responses to hypertension were not homogeneous; important differences were found among the heart, aorta and resistance vessels. The development and regression of cardiovascular hypertrophy are not dependent on mechanical load alone but seem to be modulated at three levels - increased pressure load, level of cardioadrenergic activity and local growth factor.

Actomyosin↗
PubMed1986

Tumor growth enhancement and systemic responses of Ehrlich ascites carcinoma following intermittent whole body hyperthermia.

Intermittent whole body hyperthermia 42 degrees C (WBH(I) administered for 30 min daily during 7 days caused significant enhancement of the growth of Ehrlich ascites carcinoma. The tumoricidal effects of hyperthermia were evident from the cytological picture as well as from the increased activity of lysosomal enzyme of the tumor cells. Elevated plasma corticosteroid levels, adrenal hypertrophy, thymus involution and lymphocytopenia were observed in both normal and tumor bearing mice exposed to hyperthermia. The alterations were more marked in the tumor bearing groups. Withdrawal of treatment caused gradual restoration of stress effects. It appears that the tumoricidal effects of WBH(I) were counteracted and surpassed by the growth stimulatory effects induced probably by hormone mediated immunosuppression.

Adrenal Glands↗
PubMed1986

Probable occurrence of brain basic protein factor I, an activator of phosphoprotein phosphatases.

Basic protein factor I (BPFI was purified to homogeneity from bovine brain by boiling and trichloroacetic acid-precipitation of tissue homogenate, followed by DEAE-cellulose, Sephadex G-150, Affi-Gel-phenothiazine, and Bio-Gel P-6DG chromatographic procedures. The preparation appeared as a single protein band in the SDS-polyacrylamide gel electrophoresis with a minimal Mr of 13,200. The factor was a basic protein as indicated by an estimated isoelectric point of pH 8.3 and a high content of amino acids including arginine, histidine, lysine and others. In the absence of Mn2+, the factor stimulated the phosphoprotein phosphatases (PPase) from rabbit brains. Unlike histones or protamine, the factor was a poor substrate for megamodulin-dependent protein kinase. In addition, the factor did not interact significantly with E. coli megamodulin.

Amino Acids↗
PubMed1986

Modulation of the catalytic subunit of cyclic AMP-dependent protein kinase by calmodulin, S-100 protein, parvalbumin and troponin.

The activity of the catalytic subunit of cyclic AMP-dependent protein kinase (A-PK), utilizing type II-S, III-S histone or protamine (free base) as a substrate, was augmented in the presence of regulatory protein including calmodulin, S-100 protein, parvalbumin, or troponin. However, inhibition by calmodulin or S-100 but stimulation by parvalbumin or troponin on this A-PK subunit was observed when II-S histone was replaced by V-S, VI-S, VII-S, or VIII-S histone. In addition, the stimulatory effect of calmodulin or S-100 on this A-PK subunit utilizing III-S histone was greatly diminished when half the dose of III-S was replaced by other histones in a bi-mixed form.

Animals↗
PubMed1986

[Diseases of the central nervous system and cardiac arrhythmias].

Diseases of the central nervous system can result in various cardiac arrhythmias. In some neuromuscular disorders, a distinctive morphologic correlate of such arrhythmias can be found as a secondary cardiomyopathy. In other intracranial diseases, in particular subarachnoid and intracerebral hemorrhages, the lack of gross alterations of cardiac morphology suggests some "functional" nature of rhythm disturbances. Lesions of the autonomic regulatory centres frequently cause (unilateral) autonomic imbalance that is projected to the heart according to its asymmetric peripheral sympathetic innervation. The resultant propensity for sympathetically mediated arrhythmias is frequently reflected in prolongation of the QT interval and can be accentuated by simultaneous vagal discharge as well as catecholamine-mediated disseminated myocardial necroses. It is, however, unlikely that such neurogenic arrhythmias bear any independent prognostic significance; on the contrary, prognosis is usually determined by the severity of the underlying neurologic disease and its complications.

Arrhythmias, Cardiac↗
PubMed1985

The expression and chromatin structure of the chicken glyceraldehyde-3-phosphate dehydrogenase gene in mouse cells.

Chicken glyceraldehyde-3-phosphate dehydrogenase gene (GAPD) and thymidine kinase gene (TK) were co-transfected into mouse LMTK- cells by the calcium phosphate precipitation technique. Four of the eight hypoxanthine/aminopterin/thymidine-containing medium-resistant, TK+ transfectants were shown to produce different amounts of chicken glyceraldehyde-3-phosphate dehydrogenase by zymogram analysis. Subcloning and further analysis revealed that the chicken GAPD was stably inherited and that its enzyme subunits randomly combined with mouse subunits in heterotetramers. Although the contribution of chicken enzyme varied from approximately 30 to approximately 90% of the total glyceraldehyde-3-phosphate dehydrogenase activity with a proportional increase in total activity in the different subclones, it did not appear to affect the expression of mouse endogenous glycolytic enzymes since there was no distinct change in the levels of either mouse glyceraldehyde-3-phosphate dehydrogenase mRNA nor mouse phosphoglycerate kinase enzyme activity. The levels of chicken GAPD copy number, mRNA, and enzyme apparently were generally correlated in the different subclones, suggesting that the chicken GAPD in the mouse cells were expressed constitutively. In situ hybridization revealed that the transfected genes were integrated into mouse chromosomes in one cluster, and the locations of these clusters were different in different clones. Chromatin structure analyses of the chicken GAPD in four different transfectants revealed three DNase I-hypersensitive sites located around 0.2, 2.0, and 3.4 kilobases upstream from the 5' side of the gene. These sites are also present in the same locations in chicken lymphoblastoid cells (Kuo, M. T., Iyer, B., and Schwartz, R. J. (1982) Nucleic Acids Res 10, 4565-4579), indicating the dominant transmission of DNase I-hypersensitive cleavage sites in the transfected gene.

Animals↗
PubMed1985

Antimyotonic therapy with tocainide under ECG control in the myotonic dystrophy of Curschmann-Steinert.

Ten patients suffering from advanced myotonic dystrophy with severe myotonic symptoms were treated with 800-1200 mg/day of the anti-arrhythmic drug tocainide (Xylotocan). All patients reported a marked subjective improvement of myotonia, which was confirmed by objective tests. Except for a slight QT-prolongation in one patient, the ECG was not significantly altered by the treatment. Twenty-four-hour ECG after treatment disclosed that pre-existing ventricular arrhythmia disappeared in three cases. The occurrence of complex ventricular arrhythmia in two patients under treatment was not necessarily due to specific effects of the drug but might be explained by the high spontaneous variability of rhythm disorders. In these patients suffering from myotonic dystrophy with typical cardiomyopathy no deleterious effects of the drug were observed, especially no cardiac arrhythmias which would have necessitated interruption of treatment. Therefore, the authors recommend symptomatic therapy with tocainide for myotonia and paramyotonia congenita, as well as in myotonic dystrophy patients suffering from marked myotonic stiffness. ECG and 24-h ECG should be carefully recorded as necessary in any treatment with anti-arrhythmic drugs.

Adult↗
PubMed1985

Direct evidence of hypertension and the possible role of post-menopause oestrogen deficiency in the pathogenesis of berry aneurysms.

To determine the significance of hypertension in the pathogenesis of berry aneurysms, 113 patients with subarachnoid haemorrhage (SAH) and verified aneurysm and 63 patients with SAH without aneurysm were compared. Of those patients with angiographically verified aneurysms, 61.9% were found to have elevated blood pressure (greater than 160/95 mmHg) and 19.5% showed electrocardiographic signs of left ventricular hypertrophy (SV1 + RV5 (6) greater than 3.5 mV). The percentages for patients without aneurysm were 36.5% and 6.4% respectively. A significant correlation was found between anterior aneurysms and left ventricular hypertrophy (P less than 0.01). The mean Sokolow index values were also significantly elevated in cases of aneurysm (P less than 0.01). There was a complementary relationship between the extent of left ventricular hypertrophy and the percentage of females with regard to localization of an aneurysm and age group. The predominance of females in the total aneurysm population, in the 50- to 59-year-old age group, and among patients with internal carotid aneurysms indicates that a sex-specific hormonal factor may also play a role in the pathogenesis of aneurysms in addition to hypertension. The collagen wasting commonly observed in bone and skin in the post-menopausal period due to decreased oestrogen levels could possibly be responsible for the formation of aneurysms in the proximal segments of the cerebral arteries, as occurs in various connective tissue diseases.

Adult↗