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)

Macroscopic and light microscopic features of regional ischemic infarcts of retina in autopsy eyes are described. Lesions were found throughout life span, most patients having significant primary or secondary vascular disease (younger had systemic hypertension, rheumatic heart disease, vasculitis or sickle hemoglobinopathy; most older patients had arteriosclerosis). Diabetes mellitus and infarction of other organs (including brain) also were common. Topographically almost all lesions were found in posterior fundus; most were temporal and involved anatomical macula. Microscopically there was destruction of inner retinal layers with preservation of outermost cells of inner nuclear layer; occasionally ganglion cell layer was relatively spared.
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PMID:Regional ischemic infarcts of the retina. 108 10

Previous studies have suggested that some of the central nervous system (CNS) effects of interleukin-2 (IL-2) and perhaps other cytokines might be mediated through disruption of the blood-brain barrier (BBB). We investigated the ability of human IL-2 and, in selected studies, human IL-1 alpha and human IL-1 beta to disrupt the BBB to radioiodinated bovine serum albumin (RISA) after intravenous (i.v.) and intracerebroventricular (i.c.v.) injection. No disruption of the BBB occurred for up to 2 h after the i.v. injection of 2 micrograms/mouse of IL-2 (10(5) U/kg of body weight), 2 micrograms of IL-1 alpha (10(7) U/kg), or 2 micrograms of IL-1 beta (10(7) U/kg). This dose of i.v. IL-2 also did not affect BBB permeability to RISA in the brain to blood direction. Damage to the BBB induced by hypertension elicited by i.v. epinephrine was not enhanced or prolonged by IL-2. When given directly into the CNS by the i.c.v. route, 100 ng of IL-2 (2.2 x 10(5) U/kg of brain), 100 ng of IL-1 alpha (2.2 x 10(7) U/kg of brain), or 100 ng of IL-1 beta (2.2 x 10(7) U/kg of brain) had no effect on BBB integrity in either the blood to brain or the brain to blood direction. We conclude that the effects of IL-1 alpha, IL-1 beta, and IL-2 on the CNS, as studied under these conditions, are not due to disruption of the BBB but are mediated by other mechanisms including the ability of some interleukins to cross the BBB by a saturable transport system described previously.
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PMID:The interleukins-1 alpha, -1 beta, and -2 do not acutely disrupt the murine blood-brain barrier. 152 30

We previously demonstrated that dietary NaCl supplementation reduces endogenous norepinephrine stores and turnover in the anterior hypothalamic area (AHA) of male NaCl sensitive spontaneously hypertensive rats (SHR-S) but not in NaCl resistant control rats and have implicated this mechanism in the pathogenesis of NaCl sensitive hypertension. In the current study, we tested directly the hypothesis that dietary NaCl supplementation decreases the release of norepinephrine from nerve terminals in the AHA of SHR-S using the push-pull perfusion technique. Conscious, freely moving SHR-S and control Wistar-Kyoto (WKY) rats were studied after 2-3 weeks of 8% or 1% NaCl feeding. In the 1% NaCl fed SHR-S, 3-methoxy-4-hydroxyphenylglycol (MOPEG, the major metabolite of norepinephrine in brain) levels averaged 272 +/- 32 pg/10 min; norepinephrine levels, 17 +/- 2 pg/10 min; in the 8% NaCl fed SHR-S, MOPEG levels averaged 72 +/- 7 pg/10 min; norepinephrine levels were 6 +/- 1 pg/10 min. There was a positive linear correlation (r = 0.777; P less than 0.01) between MOPEG and norepinephrine levels in AHA perfusates, indicating that perfusate MOPEG levels provide a useful index of norepinephrine release from AHA nerve terminals. In contrast, MOPEG levels in AHA perfusates were not affected by dietary NaCl intake in control WKY, and in control posterior hypothalamic perfusates, were not affected by dietary NaCl intake in SHR-S.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased norepinephrine release in anterior hypothalamus of NaCl-sensitive spontaneously hypertensive rats during high NaCl intake. 172 21

The 5-HT2 antagonist ketanserin inhibited salt appetite induced by subchronic deoxycorticosterone acetate (DOCA) treatment, as well as salt appetite induced by sodium depletion (which is governed by the synergy of aldosterone and angiotensin in the brain). The effect of ketanserin was more evident following intraperitoneal than intracerebroventricular injection. On the other hand, ketanserin did not inhibit either salt intake induced by intracranial renin injection, or the need-free salt intake of the multidepleted female rat, which is not dependent on the renin-angiotensin-aldosterone system. These findings suggest that the antinatriorexic action of ketanserin is selective for the mineralcorticoid mechanisms controlling salt appetite. Ritanserin, too, a potent 5-HT2 antagonist showing a different receptor selectivity profile from that of ketanserin, suppressed DOCA-induced salt appetite, thus supporting the involvement of 5-HT receptors in the antinatriorexic action. DOCA treatment alters serotonin metabolism in the central nervous system and it has been proposed that changes in 5-HT metabolism may be important in the genesis of DOCA-induced hypertension. The present results indicate that ketanserin inhibits DOCA-induced salt appetite and suggest that serotoninergic mechanisms might be involved in the elicitation of mineralocorticoid-induced salt appetite.
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PMID:Effect of the 5-HT2 antagonist ketanserin on salt appetite in the rat. 192

Intravenous injection of prostaglandin (PG) E2 (0.01-1.0 mg/kg) induced a dose-dependent increase in the rectal temperature of urethane-anesthetized rats; the maximum change attained was 0.14 +/- 0.08 to 1.38 +/- 0.16 degrees C at 23 to 51 min after injection. The i.v. injection of PGE2 methyl ester (PGE2-Me), a lipophilic derivative of PGE2, resulted in hyperthermia 1.5-fold higher than that by PGE2 injection over the same dose range. The hyperthermia was associated with tachycardia, hypertension, cutaneous vasodilation and a rise in abdominal skin temperature. Using [3H]PGE2 and radioimmunoassay, we showed PGE2 to be transported into the brain immediately (15 sec) after the i.v. injection of the PG; the PGE2 content ranged from 2.3 +/- 0.5 to 102.6 +/- 5.5 ng/g of brain when given at 0.01 to 1.0 mg/kg, which was 0.07 to 0.13% of the administered dose. When [3H]PGE2-Me was used, the radioactivity in the brain at 15 sec after injection was 1.3- to 2.9-fold higher than that after [3H]PGE2 injection. However, 80% or more of PGE2-Me was hydrolyzed rapidly and recovered as PGE2 in the brain within 15 sec post-injection. PGE2-Me disappeared within 5 min. When PGE2 or PGE2-Me administered i.v. was followed in terms of PGE2, it decreased gradually in the brain with a half-life of 9.0 to 9.5 min in both cases, and was almost undetectable (less than 0.7 ng/g of brain) at the time when rectal temperature reached a peak. The maximum change and duration of hyperthermia were correlated closely with the PGE2 content in the brain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Central action of prostaglandin E2 and its methyl ester in the induction of hyperthermia after their systemic administration in urethane-anesthetized rats. 318 62

Rats were subjected to adrenaline-induced acute hypertension during either the day or night. Albumin leakage into the brain was studied with Evans blue and 125I labeled serum albumin. The leakage was significantly lower during the night than during the day (P less than 0.001). d,1-propranolol had a protective effect (P less than 0.001) during the day and a slight reduction of the radioactivity (P less than 0.05 in some parts of the brain) was obtained by metoprolol (10 mg/kg) but not by butoxamine (10 mg/kg). None of the drugs reduced the tracer leakage during the night. The results suggest that the degree of alertness is of importance for the function of the blood-brain barrier in acute hypertension. However, the present experimental situation does not allow a separation of the effect of alertness per se and dark/light cycles. The changed vulnerability during the night could be related to enhanced neuronal activity, altered beta-adrenoreceptor sensitivity or to hormonal factors.
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PMID:The blood-brain barrier in adrenaline-induced hypertension. Circadian variations and modification by beta-adrenoreceptor antagonists. 611 Nov 72

Retinal blood vessels differ from most other vessels in the body (with the exception of those in the brain) in two important respects. The first is the presence of blood-retinal barriers, best illustrated by fluorescein angiography. The second important difference is that retinal vessels do not have sympathetic innervation and blood flow is modulated by autoregulation mechanisms. In 1939 Keith, Wagener and Barker proposed a classification system for hypertensive retinopathy which was innovative and of prognostic importance at that time. However, the different features of hypertensive and arteriosclerotic vasculopathies are not adequately distinguished by this classification system. Clinical features of accelerated hypertension are retinal haemorrhages, cotton wool-spots, hard exudates, papilloedema and increased vascular permeability. These must be differentiated from features associated with arteriosclerosis which are arteriovenous crossing changes and arterial constriction. The advantages of the Hogan classification system, based up on histopathologic and pathogenetic considerations are discussed. Other retinal vascular diseases associated with hypertension are also mentioned. Such as toxaemia of pregnancy, arterial macroaneurysm and anterior ischaemic optic neuropathy. Retinal branch vein occlusion is rather associated with arteriosclerosis than with hypertension.
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PMID:[Hypertensive retinopathy]. 667 24

A randomized, double-blind, placebo-controlled, multicenter trial was performed to assess the safety and efficacy of subcutaneous recombinant erythropoietin (EPO) in peritoneal dialysis patients. Seventy-eight patients were randomized to receive EPO and 74 received placebo during the first 12 wk. After this, placebo patients with hematocrit less than 32% entered the EPO maintenance phase along with the initial EPO patients. Hematocrit rose significantly in the EPO group from 23.8 to 32% after 6 wk, and this was sustained at 33.7% at 12 wk. In the placebo group, the prestudy hematocrit was 23.8% as well, and no significant change in hematocrit occurred over 12 wk. Concomitant with the rise in hematocrit, transfusion requirements fell only in the EPO group. Eighty-eight percent of patients receiving EPO had their anemia ameliorated by Week 12 of the study. There was a wide range of dosage requirements during the maintenance phase, ranging from 8,000 U thrice weekly to 4,000 U every other week. Adverse events after EPO were similar to those seen in hemodialysis patients given this agent, with hypertension developing or worsening in 55% of EPO patients during the initial 12 wk of therapy. Blood pressure was more likely to rise in patients with hypertension before receiving EPO. EPO is safe and effective in peritoneal dialysis patients, as it is in hemodialysis patients. Other than a rise in blood pressure, which is manageable with antihypertensives and ultrafiltration with dialysis, no serious side effects are seen. The optimal target hematocrit, effects of anemia improvement on quality of life, and end-organ (heart, brain) effects of anemia improvement in this patient population require further study.
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PMID:Multicenter trial of erythropoietin in patients on peritoneal dialysis. 770 90

The transgenic TGR(mRen-2)27 rat, in which the Ren-2 mouse renin gene is transfected into the genome of the Sprague-Dawley rat, develops severe hypertension at a young age that responds to inhibitors of angiotensin-converting enzyme and to antagonists of the type 1 angiotensin II (Ang II) receptor. Despite this evidence that the hypertension is Ang II dependent, TGR(mRen-2)27 rats have suppressed renal renin and renin mRNA content, and there is controversy concerning the plasma levels of renin and Ang II in these rats. We investigated the effect of the transgene on circulating and tissue levels of angiotensin and bradykinin peptides in 6-week-old male homozygous TGR(mRen-2)27 rats. Systolic blood pressure of TGR(mRen-2)27 rats was 212 +/- 4 mm Hg (mean +/- SEM, n = 25) compared with 108 +/- 2 mm Hg (n = 29) for age- and sex-matched Sprague-Dawley rats. Compared with control rats, TGR(mRen-2)27 rats had increased plasma levels of active renin (4.5-fold), prorenin (300-fold), and Ang II (fourfold) as well as tissue levels of Ang II (twofold to fourfold in kidney, adrenal, heart, aorta, brown adipose tissue, and lung and 18-fold in brain). Plasma angiotensinogen levels were reduced to 73% of control, and plasma aldosterone levels were increased fourfold. Plasma angiotensin-converting enzyme was reduced to 64% of control. Compared with control rats, TGR(mRen-2)27 rats had increased bradykinin levels in brown adipose tissue (1.9-fold) and lung (1.6-fold).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 May
PMID:Angiotensin and bradykinin peptides in the TGR(mRen-2)27 rat. 759 Oct 27

The state of peripheral and central hemodynamics was examined in 603 workers engaged into shifted duty expeditions in West Siberia, considering the length of service in the shifted duty cycle. The examination revealed high occurrence of cardiovascular diseases with prevalent hypertension. Rheographic findings proved that in 5 years of the shifted duty work high blood pressure develops with increased peripheral vascular tone (especially in brain) and enhanced contractility of left ventricle. Important role in the high blood pressure formation is played by changes of hemodynamics in first days after the duty shift.
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PMID:[Etiology of hypertensive states in workers engaged in expedition shifted-duty brigades]. 775 84


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