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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Wistar Kyoto strain of spontaneously hypertensive rat (SHR) has been characterized as behaviorally hyperactive as well as hypertensive. The relationship between these two inbred traits remains uncertain, and their coexistence in the SHR has complicated studies of central nervous system mechanisms underlying the hypertensive process. A breeding program was initiated to examine the possible genetic linkage of these two traits which, if separable, would allow us to develop substrains of SHR that are hypertensive without being hyperactive, or hyperactive without being hypertensive. We crossed SHR males with Wistar Kyoto, normotensive (WKY) female rats and produced F1 hybrids which were then randomly inbred to produce an F2 population. When tested at 12 weeks of age, F2 rats exhibited the expected wide range of mean systolic blood pressures (BP), from 111 to 174 mm Hg, as determined using indirect tail plethysmography. The BP in the parental rats at the time of breeding (16 weeks) was 187 +/- 4.5 mm Hg (SHR males, n = 7) and 111 +/- 2.4 (WKY females, n = 7). Locomotor activity was determined in an automated activity cage in F1 and F2 rats at 12 weeks of age. These strains exhibited a wide range of phenotypic distribution of locomotor activity scores, and the mean scores were intermediary between those of SHR rats and WKY rats of the same age. Among individual rats of both the F1 and F2 hybrid strains, there was no correlation between the activity score and the level of the BP at 12 weeks of age. These findings indicated that the genes responsible for the hypertensive trait and those responsible for the hyperactivity trait were not tightly linked in the hybrid populations, suggesting that different genetic factors were involved in the transmission of each of these traits. Accordingly, it should be possible to separate the two traits by further selective, recombinant inbreeding procedures.
Hypertension
PMID:Dissociation of genetic hyperactivity and hypertension in SHR. 668 4

In spontaneously hypertensive and normal control rats in the conscious state, blood flow was observed in the carotid artery, superior mesenteric artery, renal artery, and terminal aorta with a chronically implanted electromagnetic flow probe. At rest, flow per body weight was not different between the two groups except at the terminal aorta where it was significantly smaller in hypertensive rats (P less than 0.05). Regional peripheral resistance was higher in hypertensive rats than in normal rats in all the four arteries, but its elevation in the former was not uniform but most marked in the hindquarter area supplied by the terminal aorta. Quantitatively, this area was estimated to contribute about 40% of the total conductance decrease in hypertensive rats in comparison with the control. This suggests the importance of elevation of resistance in muscle blood vessels in hypertension. The contributions from the superior mesenteric area and the bilateral kidneys were estimated to be about 15% each. In the transposition response induced by transposing rats from their home cage to a new cage, the increase in hindquarter flow was significantly greater in hypertensive rats than in normal rats (P less than 0.01). The sum of the mean flows of the four arteries, a measure of cardiac output, was not different between hypertensive and normal rats at rest but greater in the former during transposition response. Elevation of arterial pressure in the response in hypertensive rats but not in the normal rats was ascribable largely to a greater increase in cardiac output in the former than the latter.
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PMID:Regional blood flow in conscious spontaneously hypertensive rats. 668 14

Psychosocially stressed male mice competing in a Henry-Stephens complex population cage develop hypertension, cardiovascular damage, and chronic interstitial nephritis. Their plasma renin, noradrenaline, corticosterone, and adrenal-catecholamine synthetic enzymes are increased and they die prematurely. Adding 3.3 mg of caffeine a day per kilogram of mouse body weight (the equivalent of 20 micrograms/ml decaffeinated coffee) to their drinking water significantly intensifies most of these changes. A dose of 90 mg/kg of caffeine (the equivalent of 560 micrograms/ml, i.e., brewed tea or coffee) further increases the effects. The drug-induced enhancement of competitive social stimulation of the neuroendocrine system resulted in a further increase of plasma renin and corticosterone levels as well as blood pressure and adrenal weight. These effects together with accelerated mortality and increased pathology indicate that chronic consumption of caffeinated liquids adds to the risks of psychosocial stress.
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PMID:Caffeine as an intensifier of stress-induced hormonal and pathophysiologic changes in mice. 700

Previous studies have shown that exercise-induced changes in muscle antioxidant status occur shortly after exercise. The present studies were designed to determine if longer-term exercise-related changes in antioxidant enzyme activities in both normotensive (WKY) and hypertensive rats (SHR) occurred, and if these changes were related to the levels of lipid peroxidation. WKY and SHR rats were exercised over a 10-week period using a progressive treadmill regimen. After a 1-week detraining period, the animals were euthanized and measurements of tissue antioxidant enzyme activities and lipid peroxide levels were determined in both exercised and cage-sedentary groups. Decreases in antioxidant activities (particularly glutathione peroxidase and catalase) in liver, kidney, skeletal and cardiac were associated with exercise training in both WKy and SHR rats (e.g. left ventricular glutathione peroxidase specific activity in WKY rats was decreased from 234 +/- 25 [SD, n = 12] to 187 +/- 17 [SD, n = 11] units/mg protein). Elevations in activities of antioxidant enzymes were generally associated with hypertension in these tissues (e.g. left ventricular glutathione peroxidase specific activity in SHR rats was 275 +/- 30 [SD, n = 12] units/mg protein), but changes in activities were more variable than those seen in response to exercise. Exercise-related changes in tissue levels of thiobarbituric acid-reactive substances (an indirect measure of tissue lipid peroxide levels) generally did not correlate with exercise-related antioxidant enzyme activity changes, and hypertension had no effect on these levels except in liver.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antioxidant enzyme activities and lipid peroxidation levels in exercised and hypertensive rat tissues. 758 28

The aim of this study was to investigate the effects of recombinant human erythropoietin (rh-EPO) in patients with cancer-related anaemia. Thirty-six ambulatory patients who had malignant neoplasms and haemoglobin (Hb) values of < 11 g/dl (Pretoria is 1,310 m above sea level) entered the study. Patients with renal insufficiency or anaemia caused by bleeding or haemolysis, and patients with iron deficiency or megaloblastic anaemia, were not entered in the study. 22 IU/kg rh-EPO was given subcutaneously 3 times/week. The dose was escalated if Hb values did not rise after 4 weeks. All 36 patients were evaluable for toxicity. Side effects ascribed to rh-EPO were pain or discomfort at the site of injection (12 patients), heart palpitations (3 patients), skin rash (2 patients) and hypertension, deep vein thrombosis, and myalgia in 1 patient each. Thirty of the 36 patients who entered the study were evaluable for response. There were 16 females and 14 males among the evaluable patients. Median age was 64.5 years. Response, defined as an increase of Hb of at least 2 g/dl or to 12.5 g/dl, for at least 1 month, was documented in 12 patients. This was accompanied by an improvement in performance status and occurred within 1 month in 5 of the 12 patients who responded. rh-EPO has a limited but measurable therapeutic value for patients with cancer-associated anaemia.
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PMID:Recombinant human erythropoietin in the treatment of cancer-related anaemia. 797 Apr 93

Reduction of renal mass (RRM) combined with a high-salt diet results in volume retention, a rise of cardiac output, and hypertension. The present studies were designed to determine whether prevention of volume retention would alter the rise of mean arterial pressure (MAP) in RRM rats given high salt. Rats were studied in a modified metabolic cage to permit continuous determination of total body weight (TBW). In group 1, NaCl was increased from 1 to 14.5 meq/day and delivered isotonically. In group 2, NaCl was increased while TBW was servo-controlled to a constant level. Group 3 was also servo-controlled, but rats received an intravenous infusion of an arginine vasopressin V1 antagonist throughout the study. MAP in group 1 rose 24 mmHg by day 4 of high salt with a parallel increase of TBW of 26 g. In group 2, MAP rose 48 mmHg by day 4 of high salt, while TBW was controlled to within 0.6% of control body weight. With inhibition of vasopressin V1 receptors (group 3), MAP rose 39 mmHg. Nearly equivalent amounts of NaCl were retained in all groups, which was associated with no change of plasma Na in group 1 but an increase of nearly 7 meq/ml in groups 2 and 3. Hematocrit fell nearly 9% in groups 2 and 3 compared with a 4% reduction in group 1. The results suggest that under conditions where net retention cannot occur, high salt intake increases MAP by an osmotically driven fluid transfer from cells, which results in an even greater expansion of blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertension induced by high salt intake in absence of volume retention in reduced renal mass rats. 797 2

Cross-fostering of litters was used to determine the timing of preweanling maternal influences on the development of high blood pressure in spontaneously hypertensive (SHR) rats. The SHR litters were either reared by their natural mothers or reciprocally cross-fostered to normotensive Wistar-Kyoto (WKY) mothers for postnatal days 1-7, 1-14, 1-21, 8-21, or 15-21. All SHR litters were weaned at 21 days of age and males were housed in groups of two to three per cage until physiological measures were obtained at 100 days of age. At 100 days of age, all rats were surgically prepared with tail artery catheters and, on the day after surgery, direct measures of mean arterial pressure (MAP, mmHg) and heart rate (HR, bpm) were obtained while rats were resting and undisturbed in their individual home cages. Our findings indicate that cross-fostering SHR pups to WKY foster mothers was attended by significant effects on body weights at weaning and on adult MAPs. Compared to control SHRs, cross-fostered SHRs, with the exception of the 15-21-day group, were significantly heavier at weaning. By 100 days of age, body weights of SHRs were similar across treatment groups. Basal MAPs of SHRs cross-fostered for days 1-7, 1-14, 1-21, and 8-21, but not days 15-21, were reduced significantly compared to SHR controls reared by their natural mothers. In contrast, basal HRs were not affected in any of the cross-fostered SHR groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Timing of preweanling maternal effects on development of hypertension in SHR rats. 802 3

We investigated the role of central corticotropin-releasing factor (CRF) in the development of cardiovascular and thermal responses induced by stress or by interleukin-1 beta (IL-1 beta) in free-moving rats. Intracerebroventricular (icv) injection of alpha-helical CRF9-41 (10 micrograms), a CRF receptor antagonist, significantly attenuated hypertension, tachycardia, and a rise in body temperature induced by cage-switch stress, a mild stress. However, icv injection of alpha-helical CRF9-41 (10 micrograms) had no effect on hypertension, tachycardia, or fever induced by intraperitoneal (ip) injection of IL-1 beta (2 micrograms/kg) or icv prostaglandin E2 (PGE2, 100 ng). In contrast, icv injection of alpha-helical CRF9-41 (10 micrograms) significantly attenuated hypertension, tachycardia, or fever induced by icv injection of IL-1 beta (20 ng). The present results suggest that central CRF has an important role in the development of the cage-switch stress-induced responses, but it does not seem to contribute to the hypertension, tachycardia, and fever induced by ip IL-1 beta or by central PGE2. However, it is possible that when IL-1 beta directly acts on the central nervous system, some of its actions are mediated by central CRF.
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PMID:Effect of a central CRF antagonist on cardiovascular and thermoregulatory responses induced by stress or IL-1 beta. 823 54

1. We investigated the central role of corticotrophin-releasing factor (CRF-41) in psychological stress-induced responses, including cardiovascular, thermoregulatory and locomotive activity in free-moving rats. 2. Psychological stress was induced by cage-switch stress. After rats were placed in the novel environment, blood pressure, heart rate, body temperature and locomotive activity significantly increased. The intracerebroventricular (I.C.V.) injection of alpha-helical CRF(9-41), a CRF-41 receptor antagonist, significantly attenuated the stress-induced hypertension, tachycardia, hyperthermia and increase in locomotive activity. However, in unstressed rats, the I.C.V. injection of alpha-helical CRF(9-41) had no effect on physiological parameters measured in this study. 3. In unstressed rats, the I.C.V. injection of CRF-41 (1 microgram and 10 micrograms) increased blood pressure, heart rate, body temperature and locomotive activity in a dose-dependent manner. The changes in these responses were quite similar to those observed during cage-switch stress. 4. The results suggest that central CRF-41 plays an important role in psychological stress-induced hypertension, hyperthermia, tachycardia and increase in locomotive activity. However, it is likely that central CRF-41 does not contribute to normal cardiovascular and body temperature regulation when rats are free from stress.
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PMID:The central role of corticotrophin-releasing factor (CRF-41) in psychological stress in rats. 848 93

Blood pressure and circulating catecholamines were evaluated in borderline hypertensive rats (BHR) that were exposed to daily sessions of either short (20 min) or long (120 min) duration air-jet stimulation. Indirect measures of systolic blood pressure indicated that within 2 weeks both experimental groups developed stress-induced hypertension in comparison to home cage controls. Animals exposed to 120 min stress sessions had significantly higher systolic blood pressure relative to the 20 min group. However, direct measures of blood pressure taken after 5 weeks of daily stress did not reveal any differences between the stress groups. Daily measurements indicated that acute changes in blood pressure during stress were modest and transient, suggesting little contribution to the chronic elevation in blood pressure observed as a consequence of stress. Circulating catecholamines were significantly increased by the stressor. Epinephrine returned to baseline within 60 min, although norepinephrine remained elevated throughout the 120 min session. The results indicate that increasing the duration of daily air jet stimulation did not impact the development of stress-induced hypertension over the 5-week measurement period.
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PMID:Stress-induced hypertension in the borderline hypertensive rat: stimulus duration. 851 Nov 66


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