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

Flavonoid, a plant extract, exhibits various biological actions. Dietary flavonoid intake is reported to reduce an elevated blood pressure, however the mechanism is unknown. The epithelial Na+ channel (ENaC) in the kidney plays a key role in the regulation of blood pressure by contributing to the Na+ reabsorption in renal tubules. Thus, we investigated the effect of quercetin, a flavonoid, on ENaC mRNA expression in the kidney of hypertensive Dahl salt-sensitive rats. Dahl salt-sensitive rats of 8 weeks were acclimated for 1 week in a metabolic cage and were subsequently kept for 4 weeks under four different conditions: (1) normal salt diet (0.3% NaCl), (2) normal salt diet with quercetin (10 mg/kg/day), (3) high-salt diet (8% NaCl), and (4) high-salt diet with quercetin. Quercetin diminished the alphaENaC mRNA expression in the kidney associated with reduction of the systolic blood pressure elevated by high-salt diet, suggesting that one of the mechanisms of the flavonoid's antihypertensive effect on salt-sensitive hypertension would be mediated through downregulation of ENaC expression in the kidney.
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PMID:Flavonoid-induced reduction of ENaC expression in the kidney of Dahl salt-sensitive hypertensive rat. 1498 96

This study tested the hypothesis that the inflammatory cytokine, interleukin-6, contributes to the hypertensive response to acute psychosocial stress, caused by switching male mice to a cage previously occupied by a different male mouse. Male C57BL6 (WT) and interleukin-6 (IL-6) knockout (KO) mice were implanted with biotelemetry devices to monitor mean arterial pressure, heart rate, and motor activity in the unrestrained state. Baseline mean arterial pressure was 98+/-1 and 103+/-1 for WT and IL-6 KO mice. Cage switch increased mean arterial pressure by 42+/-2 mm Hg in WT mice, but this was blunted significantly in KO mice (31+/-3 mm Hg peak increase). Area under the curve for the first 90 minutes also was significantly less. Heart rate and motor activity increased similarly, and there also were no differences in the increases in plasma renin activity or plasma norepinephrine concentration between WT and KO mice. Thus, the acute hypertensive response to psychosocial stress depends significantly on IL-6, and the effect appears to be specific for blood pressure rather than to a global impairment in the response to stress. However, because perfusion of the isolated mesenteric bed with phenylephrine and chronic infusion of angiotensin II caused similar responses in WT and IL-6 KO mice, it is clear that future studies are needed to determine to what extent the acute blood pressure effect of IL-6 is stress-specific.
Hypertension 2004 Sep
PMID:Hypertensive response to acute stress is attenuated in interleukin-6 knockout mice. 1528 66

It is well accepted that mortality in acromegaly is increased because of cardiovascular and respiratory diseases while neoplastic complications account less to mortality. Amongst different cardiovascular complications the most frequent is biventricular hypertrophy, which occurs independently of hypertension and metabolic complications that, in turn, aggravate the cardiomyopathy. Diastolic and systolic dysfunction develops in a variable number of patients, depending on age and disease duration. Other cardiac disorders, such as arrhythmias, valve disease, hypertension, atherosclerosis and endothelial dysfunction have been less characterized but all appear to be present in acromegaly, depicting the so called "acromegalic cardiomyopathy". The best characterized respiratory disease is the sleep apnea. Ventilatory dysfunction recognizes bony changes of thoracic cage and lung overgrowth as relevant pathogenetic factors. Earlier evidences that patients with acromegaly have an increased risk of developing malignancies have become more realistic in recent years. Most studies have reported an increased risk of colonic polyps, which more frequently recur in patients not controlled after treatment. Malignancies in other organs have also been described, but less convincingly than at the gastrointestinal level and are not a main cause of mortality. Bone changes are also feature of the disease. They involve theoretically all bones and, particularly, the appendicular and the axial skeleton. Patients with long-standing disease are more prone to develop degenerative changes. Control of acromegaly by surgery or pharmacotherapy, especially by somatostatin analogs, improves cardiovascular morbidity and sleep apnea. There is still no demonstration that improvement of different complications corresponds a reduction in mortality.
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PMID:Severe systemic complications of acromegaly. 1611 80

Genetic predisposition and psychosocial stress are known risk factors in the aetiology of hypertension. The aim of this study was to investigate the as yet unknown role of nitric oxide (NO) in mechanisms of social stress-induced hypertension in rats with a family history of hypertension. Male adult rats used in the study were offspring of normotensive (Wistar) dams and spontaneously hypertensive sires. The rats were exposed to 6-week crowding stress (5 rats/cage, 200 cm2/rat). Control rats were kept four per cage (480 cm2/rat). Blood pressure was determined non-invasively on the tail. Basal blood pressure of all rats was 131 +/- 2 mm Hg. Crowding stress increased significantly blood pressure (p < 0.02 vs. basal value). Crowding had no influence on NO synthase activity in the left ventricle, adrenal glands and kidney. However, crowding stress reduced significantly NO synthase activity in the aorta by 37% (p < 0.01 vs. control). Acetylcholine-induced relaxation and noradrenaline-induced vasoconstriction of the femoral artery were reduced in stressed rats by 58% (p < 0.001) and 41% (p < 0.003), respectively. On balance then, the results indicate that chronic social stress produced by crowding was associated with reduced vascular NO synthesis and altered vascular function in adult borderline hypertensive rats of normotensive mothers.
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PMID:Effect of chronic social stress on nitric oxide synthesis and vascular function in rats with family history of hypertension. 1625 77

The effects of chronic postweaning social isolation combined with subsequent resocialization on the sexual arousal were studied in male rats with inherited stress-induced arterial hypertension (ISIAH strain) and in Wistar rats. Young males were isolated on the Day 21 of postnatal life for 6 weeks. Then they were kept in groups of 5. 4-month males underwent the partition test: a receptive female was introduced into the male's cage, but the male and the female were separated by a transparent partition. The number of approaches to the partition and total time spent near the partition during the test served as an index of sexual motivation. Hormonal component of sexual arousal was estimated by measuring plasma testosterone level. No interstrain differences in magnitude of the sexual arousal were observed. However, chronic social isolation during juvenile period caused a genotype-dependent diminution of sexual motivation in the adult male rats of both strains. The decrease of sexual motivation in ISIAH rats was more pronounced as compared to Wistar rats. Moreover, the social isolation during the juvenile period completely abolished the female-induced rise in plasma testosterone in ISIAH and Wistar male rats. Plasma corticosterone level was increased during the period of sexual arousal, but this rise of corticosterone was not affected by the social conditions during postweaning period.
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PMID:[The effect of social isolation during juvenile period on the sexual arousal in adult rats]. 1640 45

Genetic predisposition and social stress may represent important risk factors in etiology of hypertension associated with endothelial dysfunction. Perturbations of endothelial structural integrity are also critical for the pathogenesis of vascular diseases. We examined effect of chronic social stress on structure of aortic endothelium in borderline hypertensive (BHR) and normotensive Wistar rats. Male BHR - offspring of Wistar mothers and SHR fathers and age-matched W were exposed to 6-week crowding stress (5 rats/cage, 200 cm2/rat). Aortic tissue was processed for electron microscopy and NO synthase activity measurement. Crowding stress significantly increased blood pressure in BHR compared to basal values (140+/-3 mm Hg vs. 130+/-3 mm Hg, p<0.05) and reduced enzyme activity by 37 % (p<0.01) in the aorta of BHR. Local slight structural alterations of endothelium were found in non-stressed BHR (p<0.001) when compared with Wistar rats. Chronic stress caused marked (p<0.005) subcellular injury of endothelial cells in aorta of BHR characterized by mitochondrial damage, presence of vacuoles, increased number of lysosomes, Weibel-Palade bodies, changes of intercellular connections and local disruption of endothelium, while only slight changes were seen in Wistar rats. Results suggest increased sensitivity of aortic endothelium of BHR to chronic crowding that may contribute to acceleration of arterial dysfunction.
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PMID:Ultrastructural characteristics of aortic endothelial cells in borderline hypertensive rats exposed to chronic social stress. 1837 95

The importance of dietary salt in the development of hypertension has long been a source of controversy. Recent studies suggest a combination of high-salt and ANG II infusion may increase sympathetic drive; however, the effect of a change in dietary salt alone is unclear. Using telemetry, we recorded renal sympathetic nerve activity (RSNA), arterial pressure (MAP), and heart rate (HR) in seven New Zealand white rabbits before and during a 6-day period of increased salt intake (normal NaCl 0.5 g x kg(-1) x day(-1), high NaCl 2.5 g x kg(-1) x day(-1)) and a second group of seven rabbits with normal salt intake throughout. The responses to stressful stimuli encountered in the laboratory were recorded and compared with rest in control and high-salt groups. Resting MAP, HR, and RSNA were not significantly altered with high salt intake [88 +/- 5 vs. 91 +/- 6 mmHg; 251 +/- 8 vs. 244 +/- 9 beats per minute (bpm); 9.7 +/- and 1.2 vs. 10.8 +/- 1.7 normalized units (nu)] despite significant reductions in plasma renin activity (1.88 +/- 0.18 vs. 1.27 +/- 0.15 nmol ANG I x l(-1) x h(-1); P < 0.05) and ANG II (7.5 +/- 1.2 vs. 4.3 +/- 0.8 pmol/l). Increasing levels of stressful stimuli (resting in home cage, containment in box, handling, and nasopharyngeal activation) in animals on a normal salt diet caused graded increases in MAP (89 +/- 2 mmHg, 95 +/- 2 mmHg, 107 +/- 4 mmHg, and 122 +/- 5 mmHg, respectively) and RSNA (9.7 +/- 0.9 nu; 11.8 +/- 2.7 nu; 31.4 +/- 3.7 nu; 100 nu) but not HR (245 +/- 8 bpm; 234 +/- 8 bpm; 262 +/- 9 bpm; 36 +/- 5 bpm). High dietary salt did not significantly alter the responses to stress. We conclude that a 6-day period of high salt intake does not alter the level of RSNA, with non-neural mechanisms primarily responsible for the observed renin-angiotensin system suppression.
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PMID:A high-salt diet does not influence renal sympathetic nerve activity: a direct telemetric investigation. 1949 74

The ability to monitor and record precise blood pressure fluctuations in research animals is vital to research for human hypertension. Direct measurement of blood pressure via implantable radio telemetry devices is the preferred method for automatic collection of chronic, continuous blood pressure data. Two surgical techniques are described for instrumenting the two most commonly used laboratory rodent species with radiotelemetry devices. The basic rat procedure involves advancing a blood pressure catheter into the abdominal aorta and placing a radio transmitting device in the peritoneal cavity. The mouse technique involves advancing a thin, flexible catheter from the left carotid artery into the aortic arch and placing the telemetry device under the skin along the animal's flank. Both procedures yield a chronically instrumented model to provide accurate blood pressure data from an unrestrained animal in its home cage.
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PMID:Direct blood pressure monitoring in laboratory rodents via implantable radio telemetry. 1976 22

We determined whether genetic deficiency of angiotensin II Type 1A (AT(1A)) receptors in mice results in altered neuronal responsiveness and reduced cardiovascular reactivity to stress. Telemetry devices were used to measure mean arterial pressure, heart rate, and activity. Before stress, lower resting mean arterial pressure was recorded in AT(1A)(-/-) (85+/-2 mm Hg) than in AT(1A)(+/+) (112+/-2 mm Hg) mice; heart rate was not different between groups. Cage-switch stress for 90 minutes elevated blood pressure by +24+/-2 mm Hg in AT(1A)(+/+) and +17+/-2 mm Hg in AT(1A)(-/-) mice (P<0.01), and heart rate increased by +203+/-9 bpm in AT(1A)(+/+) and +121+/-9 bpm in AT(1A)(-/-) mice (P<0.001). Locomotor activation was less in AT(1A)(-/-) (3.0+/-0.4 U) than in AT(1A)(+/+) animals (6.0+/-0.4 U), but differences in blood pressure and heart rate persisted during nonactive periods. In contrast to wild-type mice, spontaneous baroreflex sensitivity was not inhibited by stress in AT(1A)(-/-) mice. After cage-switch stress, c-Fos immunoreactivity was less in the paraventricular (P<0.001) and dorsomedial (P=0.001) nuclei of the hypothalamus and rostral ventrolateral medulla (P<0.001) in AT(1A)(-/-) compared with AT(1A)(+/+) mice. Conversely, greater c-Fos immunoreactivity was observed in the medial nucleus of the amygdala, caudal ventrolateral medulla, and nucleus of the solitary tract (P<0.001) of AT(1A)(-/-) compared with AT(1A)(+/+) mice. Greater activation of the amygdala suggests that AT(1A) receptors normally inhibit the degree of stress-induced anxiety, whereas the lesser activation of the hypothalamus and rostral ventrolateral medulla suggests that AT(1A) receptors play a key role in autonomic cardiovascular reactions to acute aversive stress, as well as for stress-induced inhibition of the baroreflex.
Hypertension 2009 Dec
PMID:Role of angiotensin II Type 1A receptors in cardiovascular reactivity and neuronal activation after aversive stress in mice. 1988 64

1. The amygdala is a part of the limbic system that is associated with mediating the emotional and hormonal response to stress and although studies have focused on the central amygdala, there is increasing evidence that the medial amygdala is a major region activated by stressful stimuli. 2. Neuroanatomical studies in rats have shown greater activation in the medial amygdala following aversive stresses compared with other brain regions, including the central amygdala. Inhibition of the medial, but not the central, amygdala attenuates the development of hypertension in spontaneously hypertensive rats. 3. Schlager (BPH/2J) mice have a neurogenic form of hypertension that is most evident during the night when the mice are most active and is closely correlated with the level of activation of neurons in the medial, but not the central, amygdala. Pressor responses to aversive stimuli, such as restraint and cage-switch stress, are much greater in BPH/2J hypertensive than BPN/3J normotensive mice, but appetitive arousal produces normal increases in blood pressure. The degree of activation in the medial amygdala in BPH/2J hypertensive mice during aversive stress closely correlates with the increased blood pressure. 4. Thus, the inappropriate activation of the medial amygdala evoked by specific fear or aversive stimuli may be key to the neurogenic hypertension.
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PMID:Role of the medial amygdala in mediating responses to aversive stimuli leading to hypertension. 2052 79


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