Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male and female, normotensive, Sprague-Dawley (S-D) rats, and spontaneously hypertensive rats (SHR) were subjected to acute and massive myocardial infarction with isoproterenol. Some of the animals were pre-treated (7 days) with the prolactin-lowering drug, bromocryptine. SHR survived in greater numbers than S-D but developed massive congestive heart failure of late onset. The adrenal glands and hearts became greatly hypertrophied in parallel with severely involuted thymus glands. ECG tracings demonstrated intense tachycardia and myocardial ischaemia. Bromocryptine reduction of prolactin (PRL) showed no effect on ECG tracings but reduced triglyceride, free fatty acid, total cholesterol and glucose levels. Isoproterenol caused dynamic increase in glucose, free fatty acids and triglycerides. CPK levels demonstrated greater cardiac damage in S-D vs SHR; greatly elevated SGOT and SGPT levels confirmed the presence of fatty liver in S-D and SHR. Myocardial infarction caused marked increase in circulating PRL in females only and sustained increases in aldosterone and corticosterone. SHR survivors had a high incidence of atrial and ventricular thrombi, left ventricular aneurysms, and intense fibroplasia and cartilaginous metaplasia in areas adjacent to damaged myocardium. It is suggested that adrenal steroidogenesis during an acute myocardial infarct favours survival and more complete myocardial repair in females vs males, and preexisting hypertension in SHR is associated with hormonal and metabolic response patterns different from normotensive S-D rats.
 ...
PMID:Hormonal and metabolic changes during acute myocardial infarction in normotensive vs hypertensive rats. 684 10

Alterations in the number and reactivity of thymic and splenic lymphocytes were studied during the development of experimental renal hypertension in Sprague-Dawley rats. The mitotic responses of thymocytes and splenic T and B lymphocytes were tested by the T cell mitogen concanavalin A and the B cell mitogen dextran sulfate 3, 8, 12, and 36 days after the initiation of hypertension. At 3 days, hypertensive rats showed a fourfold increase in plasma corticosteroid levels, marked thymic atrophy, and a 50% reduction in the total number of thymocytes. The mitotic reactivity of the cells remaining in the organ was depressed 60% when compared to sham-operated controls. At 8 days a similar reduction in thymus size was accompanied by similarly decreased lymphocyte populations. Twelve days after initiation of hypertension structural recovery of the gland, lymphoid proliferation, and slightly increased thymocyte populations were observed. Differences with sham-operated controls were, however, still remarkable. Hypertensive rats sacrificed at 36 days showed thymus hypertrophy, and the thymocyte populations were larger than those of sham-operated animals. Despite the fluctuations in the number of thymocytes registered during the development of renal hypertension, the impaired mitotic reactivity of these cells to concanavalin A was sustained throughout the 36 days of the experiment. A similar reduction in the total number of cells and a similar depression in T lymphocyte reactivity was observed in the spleen between 8 and 36 days of hypertension. In contrast, after an initial depressed response, splenic B lymphocytes showed a slight but sustained increase in reactivity throughout the entire experimental period. These results indicate that with evolving renal hypertension there is a reduction in the number of lymphocytes as well as a depression in the ability of the remaining T lymphocytes to react with concanavalin A. Since T lymphocytes are important regulators of immunological homeostasis, this reduction in T cell reactivity may suggest the existence of an immunological imbalance accompanying the development of experimental renal hypertension.
 ...
PMID:Lymphoid alterations and impaired T lymphocyte reactivity in experimental renal hypertension. 698 32

Male and female, normotensive, Sprague-Dawley (S-D), Wistar-Kyoto (WKy), and spontaneously hypertensive rats (SHR) were bred repeatedly until the females had given birth to and nursed 6 litters of pups. At the close of the 2nd, 4th and 6th breeding, breeder males and females, along with celibate males and females of equal age, were killed. S-D and WKy breeder rats manifested progressively increasing adiposity and high blood pressure with each successive breeding; breeder SHR showed mild exacerbation of their pre-existing high blood pressure. Adrenocortical hyperplasia and thymus-gland involution suggested increasing pituitary-adrenal activity in breeder rats. Circulating aldosterone levels decreased with repeated breeding in parallel with increased deoxycorticosterone and corticosterone secretion. The repeatedly bred normotensive rats manifested worsening aortic sclerosis as against little or no aortic sclerosis in the repeatedly bred SHR. Breeder SHR developed fibrinohyalin intimal lesions limited exclusively to the arterioles of the testis and ovary. Virgin rats did not develop any vascular disease. It is suggested that a diverse spectrum of adrenal steroids in breeder HSR combined with genetic direction control the morphogenesis of arterial disease in breeder SHR.
 ...
PMID:Genetically mediated resistance to naturally occurring aortic sclerosis in spontaneously hypertensive as against Sprague-Dawley and Wistar-Kyoto breeder rats. 706 85

Pituitary glands removed from adult female normotensive Sprague-Dawley (S-D) rats were implanted beneath the renal capsule of 100-day male S-D rats. Female neonatal S-D rats were given a single sc injection of 1.25 mg of testosterone proprionate (TP) suspended in sesame oil. Systolic blood pressure and blood samples were taken at various time intervals postimplantation and TP treatment prio to autopsy. Both the TP treatment and pituitary implants caused hyperprolactinemia, increased adrenal weight concomitant with thymus gland involution, hypersecretion of corticosterone, but no increase in systolic blood pressure. It is suggested that the failure of these hyperprolactinemic S-D rats to develop hypertension was due to the absence of a genetically mediated hypertensinogenic factor present in this normotensive strain which is activated by chronic hyperprolactinemia.
 ...
PMID:Hyperprolactinemia and hyperadrenocorticism accompanied by normal blood pressure in Sprague-Dawley rats. 732 61

Male spontaneously hypertensive rats (SHR) were gonadectomized at an age of 5 weeks. Systolic blood pressure and heart rate were measured up till an age of 12 weeks in trained unanesthetized rats. The development of the hypertension and heart rate were not significantly affected by removal of the testes and epididymis or removal of the testes only. Kidney, adrenal and thymus weight did differ from the values in sham-operated rats. After the administration of secobarbital sodium, however, a significant lower blood pressure had been observed in gonadectomized rats compared with sham-operated rats. Significantly higher levels of secobarbital were detected in plasma and brain of gonadectomized SHR. It is concluded that gonadectomy does not effect blood pressure of SHR and that the previously reported retardation of development of hypertension in gonadectomized SHR is caused by the different effect of anesthesia on blood pressure of gonadectomized and sham-operated rats.
 ...
PMID:Development of hypertension in spontaneously hypertensive rats after gonadectomy: effects of secobarbital anesthesia on the blood pressure. 733 98

Nonarteriosclerotic, virgin, Sprague-Dawley (SD), and spontaneously hypertensive (SHR) rats and arterio sclerotic breeder SD and SHR rats were subjected to adrenal regeneration-induced hypertension (ARH) with and without extra salt. ARH caused a marked increase in the blood pressure of SD rats and a mild increase in SHR rats; extra salt caused exacerbation of hypertension in SD rats only. Heart and kidney weights were greatly increased commensurate with blood pressure. Increased adrenal weight concomitant with thymus gland involution was considerable in SD and less marked in SHR rats. Testes and ovaries were involuted. Creatine phosphokinase and lactic dehydrogenase levels were abnormally high; blood triglycerides, FFA, glucose, and corticosterone decreased, and total cholesterol, glucose, and corticosterone increased in SD but decreased in SHR rats. Blood urea nitrogen levels were much more abnormally elevated in SD than in SHR rats. ARH did not induce arterial disease in the virgin SD or SHR rats, but it did produce a spectrum of arterial disease in SH breeders, e.g. aortic sclerosis, polyarteritis nodosa-like lesions, intimal cartilaginous metaplasia, and hyalin fibrosis. Altered adrenocortical steroidogenesis may have conditioned the arterial wall of SHR rats to develop diverse morphological changes, and extra salt is much more detrimental to normotensive rats (SD) than to genetically hypertensive rats.
 ...
PMID:Induction of diverse arterial and myocardial lesions by adrenal regeneration hypertension in Sprague-Dawley versus spontaneously hypertensive rats. 735 53

This study examined the role of the thymus in hypertension. Seven to eight week old, normotensive Wistar-Kyoto rats (WKYs) (systolic blood pressure 138 +/- 7 mm Hg) received a bolus injection of (1) WKY thymic extract (control), (2) spontaneously hypertensive rat (SHR) thymic extract, (3) SHR liver extract or (4) normotensive Sprague-Dawley rat (SD) thymic extract. Blood pressures of WKYs receiving SHR thymic rose significantly (p < 0.01) over an eight week period (168 +/- 6 mm Hg), while WKYs injected with WKY thymic extract (143 +/- 10), SHR liver extract (144 +/- 5) or SD thymic extract (138 +/- 4) showed no change in blood pressure. Thymuses from WKYs injected with SHR extract were significantly (p < 0.01) smaller than thymuses from WKYs injected with WKY extract. Aorta from WKYs administered SHR extract were significantly (p < 0.01) hyperresponsive to contractile agents, suggesting that immune dysfunction may lead to vascular damage as seen in several hypertensive models. The results suggest that hypertension can be transferred via an endogenous thymic factor, possibly a viral pathogen.
 ...
PMID:Cell-free thymic extract from hypertensive rats induces hypertension in normotensive rats. 775 67

We have determined the effects of bilateral electrolytic lesions of the ventromedial hypothalamus (VMH) on activity in the hypothalamo-pituitary-adrenal (HPA) system. Acutely, during the first 5 days, lesions of the anterior-medial VMH caused loss of the diurnal rhythms in food intake and plasma corticosterone (B) levels. Plasma B concentrations were elevated during the time of the normal trough of the basal diurnal rhythm in HPA axis activity and the diurnal rhythm in food intake was abolished, in agreement with the results of others. Consistent with hyperactivity in the HPA axis, lesioned rats had increased adrenal weight, decreased thymus and body weights and decreased plasma transcortin concentrations. To determine how lesions of the VMH provoke these increases in activity of the HPA system, the sensitivity of ACTH in adrenalectomized, lesioned rats to replacement with exogenous B was determined under basal conditions during the trough (morning-AM) and peak (evening-PM) of the diurnal rhythm in HPA axis activity. ACTH in lesioned rats in the AM was insensitive to feedback over the very low range of plasma B of 1-4 micrograms/dl, whereas sham-lesioned controls exhibited the normal, high sensitivity of ACTH to B at this time of day. There was no difference between the sensitivity of ACTH to this low range of B in the PM in VMH- and sham-lesioned rats. Two to 5 weeks after VMH lesions, as found by others, mean daily plasma B levels did not differ from sham-lesioned controls; however, plasma B during the AM was still mildly elevated in these rats. Inhibition of plasma B in the PM by dexamethasone was less effective in lesioned rats. Although HPA system responses to hypoglycemia, corticotropin-releasing factor and ACTH were normal, the lesioned rats exhibited obesity, hyperinsulinemia, hyperglycemia, hypertension and tachycardia, all signs consistent with mild hyperactivity of the PHA axis. Occupancy of type I, high-affinity corticosteroid receptors is known to control basal activity of the HPA system during the trough of the diurnal rhythm and to interact with glucocorticoid receptors to affect basal activity during the peak of the diurnal rhythm and during AM stress. We conclude that VMH lesions disrupt transmission of inhibitory signals, mediated by occupancy of type I corticosteroid receptors, that are initiated by a B feed-back site.
 ...
PMID:Ventromedial hypothalamic lesions inhibit corticosteroid feedback regulation of basal ACTH during the trough of the circadian rhythm. 778 59

Previous studies that have evaluated the Na(+)-H+ antiporter in cells from hypertensive subjects were generally performed under conditions in which HCO3-CO2, the physiological buffer system, was absent from the assay media. The objective of this study was to evaluate the activity of the Na(+)-H+ antiporter and that of the Na(+)-dependent and Na(+)-independent Cl(-)-HCO3- exchangers in cells assayed in the presence of HCO3-CO2 in the media. Lymphocytes from 6- to 8-week-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) rats were obtained from the thymus gland and assayed immediately after isolation. The activity of the Na(+)-H+ antiporter after stimulation by cell acidification (pHi approximately 6.4) was similar in SHR and WKY rats (18.67 +/- 1.03 and 16.12 +/- 0.92 mmol H+/L per minute, respectively). Recovery from cell alkalinization was effected by an Na(+)-independent Cl(-)-HCO3- exchanger, with maximal activity at an alkaline pHi (approximately 7.7). The stimulated activity of this Na(+)-independent Cl(-)-HCO3- exchanger was also not different between SHR and WKY cells (2.65 +/- 0.25 and 2.55 +/- 0.32 mmol H+/L per minute, respectively). Acute chloride removal produced a rise in pHi that was Na(+)-dependent and sensitive to 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) but resistant to ethylisopropylamiloride (EIPA), reflecting the activity of an Na(+)-dependent Cl(-)-HCO3- exchanger. Unlike the Na(+)-H+ exchanger and the Na(+)-independent Cl(-)-HCO3- exchanger, which had their highest activities at extremes of pHi (low pHi, Na(+)-H+ exchanger, and high pHi, Na(+)-independent Cl(-)-HCO3- exchanger), the Na(+)-dependent Cl(-)-HCO3- exchanger had its maximal activity near steady-state pHi (approximately 7.1). No significant differences were found in the stimulated activity of this exchanger between cells from SHR and WKY rats (2.23 +/- 0.26 and 2.50 +/- 0.43 mmol H+/L per minute, respectively). The kinetic properties of the Na(+)-dependent and Na(+)-independent Cl(-)-HCO3- exchanger, examined as a function of external Cl-, were also virtually identical in cells from SHR and WKY rats. We conclude that in lymphocytes from SHR and WKY rats, the activity of the two Cl(-)-HCO3- exchangers, like that of the Na(+)-H+ exchanger, is dependent on the prevailing pHi. The Na(+)-dependent Cl(-)-HCO3- exchanger has its highest activity near steady-state pHi, suggesting an important role in the cell defense against intracellular acidosis under physiological conditions.(ABSTRACT TRUNCATED AT 400 WORDS)
Hypertension 1994 Apr
PMID:Regulation of intracellular pH in the spontaneously hypertensive rat. Role of bicarbonate-dependent transporters. 814 20

The spontaneously hypertensive rat (SHR) is a stress-sensitive animal which exhibits moderate immune dysfunction that has been implicated in the onset of hypertension. In this study, we examined the morphology of SHR thymus and spleen and further characterized the immune deficiency using Wistar-Kyoto (WKY) and Fisher 344 (F-344) rats for comparison. The adult SHR thymus does not display the increase in medullary volume typically noted with aging and the volume density of the marginal zone is decreased in the spleen. In vivo tritiated-thymidine incorporation is also decreased in the spleen of unstimulated SHR. In mixed lymphocyte reactions (MLR), the proliferative response of SHR splenocytes is significantly decreased relative to controls, WKY and F-344. Addition of interleukin-1 (IL-1), interleukin-2 (IL-2), or indomethacin to the MLR cultures does not increase proliferation. The proliferative response to T cell receptor monoclonal antibody (mAb-TCR) or interleukin-2 (IL-2) are similarly impaired in the SHR. The depressed proliferative T cell response is reversed by prolactin. It is suggested that the SHR is a valuable model for the study of immune deficiency.
 ...
PMID:Immune system of the spontaneously hypertensive rat: II. Morphology and function. 823 75


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>