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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effects of long-term treatment with the angiotensin I converting-enzyme inhibitor YS 980 were examined in stroke-prone spontaneously hypertensive (sp-SH) rats. Development of hypertension was markedly blunted in the YS 980-treated animals. 2. Effective converting-enzyme inhibition was confirmed by significant increases in plasma angiotensin I (ANG I) and plasma renin concentration, inhibition of the pressor responses to intravenous ANG I and potentiation of the depressor responses to intravenous bradykinin. 3. Urinary free aldosterone excretion was decreased but no changes in urinary sodium and potassium excretion were observed. 4. The pressor responses to intravenous leucine-enkephalin were reduced. 5. The pressor responses to injection of ANG I and bradykinin into the lateral brain ventricle were unaltered. 6. We conclude that the antihypertensive action of YS 980 in sp-SH rats cannot be explained by the inhibition of the plasma renin-angiotensin system alone. Effects on other peptide systems must be considered.
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PMID:A novel orally active converting-enzyme inhibitor YS 980: effects on blood pressure in spontaneously hypertensive rats. 23 20

1. The angiotensin converting enzyme (ACE) activity of spontaneously hypertensive (SHR) and spontaneously hypertensive stroke-prone (SHRSP) rats was compared to the ACE activity of normotensive Wistar-Kyoto rats (WKY). 2. ACE activity was assessed indirectly in conscious unrestrained rats using the equipressor response end point to simultaneously calculate the extent of conversion of angiotensin I (AI) to angiotensin II (AII) and the pulmonary degradation of bradykinin (BK). 3. The pulmonary degradation of BK was significantly elevated (99.4%) in SHR rats whereas the elevation was not significant in SHRSP rats (99.2%) compared to WKY rats, even though the pulmonary inactivation of BK in WKY rats was higher (98.6%) than in normotensive Wistar rats (95.6% and 97.5%) previously studied. 4. Blood pressure responsiveness to intra-aortically injected BK (bolus injection and infusion) was markedly increased in SHR and SHRSP rats with no change in reactivity to sodium nitroprusside. 5. Conversion of AI to AII assessed by the equipressor doses of the hormones which produced a 20-mmHg rise in blood pressure was markedly elevated in SHR (86 +/- 4%) and SHRSP (80 +/- 7%) rats when compared to WKY rats (38 +/- 4%). 6. The marked increase in conversion of AI to AII in hypertensive animals, accompanied by an increased pulmonary degradation of BK in SHR rats, suggests that ACE activity is increased in conscious SHR and SHRSP rats and may participate in the genesis of hypertension in this model of genetic hypertension.
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PMID:Angiotensin converting activity assessed in vivo is increased in hereditary hypertensive rats. 134 16

Vasodilatory responses to bradykinin (BK) and acetylcholine (ACh) were compared in phenylephrine preconstricted perfused kidneys from 30-week-old male stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY). Responses to ACh did not differ between kidneys from SHRSP and WHY. BK-induced dilatation was greater in kidneys from SHRSP relative to WHY and was not affected by indomethacin or captopril. These results indicate that renal vasodilatory responsiveness to bradykinin is enhanced in SHRSP with established hypertension.
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PMID:Enhanced vasodilatory responses to bradykinin in stroke-prone spontaneously hypertensive rats. 160 Oct 60

To identify those vascular beds that contribute to the elevated peripheral resistance (TPR) seen in spontaneously hypertensive rats (SHR) as compared to Wistar-Kyoto rats (WKY), the distribution of cardiac output, organ blood flow, and regional vascular resistance were measured using radiolabelled microspheres. WKY and SHR had similar heart rates, cardiac outputs, and cardiac stroke volumes, whereas SHR had significantly elevated TPR. This increased TPR was the cumulative effect of significant elevations in vascular resistance in the brain, testes, epididymides, gastrointestinal tract, pancreas/mesentery, skin, kidneys, and skeletal muscle. Only in the renal and skeletal muscle vasculature was this elevation in resistance associated with reduced blood flow. Haemodynamic responses to bradykinin [thought to act through a release of endothelium-derived relaxing factor (EDRF)] were similar in both WKY and SHR with the exception of the liver where no reduction of hepatic arterial resistance was seen in the SHR. We suggest that the increase in resistance in the renal and skeletal muscle vasculature is due to active vasoconstriction in these beds. This vasoconstriction diverts a significant proportion of the cardiac output through other vascular beds, especially the brain, liver, and coronary circulation. This will result in increased shear-stress and consequent damage to endothelial cells.
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PMID:Regional vascular resistance and haemodynamics in the spontaneously hypertensive rat: the effects of bradykinin. 168 15

Acetylcholine produces less dilatation of pial arterioles in stroke-prone spontaneously hypertensive rats (SHRSP) than in normotensive (WKY) rats. Responses of cerebral vessels to acetylcholine and bradykinin appear to involve different mechanisms. Our first goal was to determine whether responses of pial arterioles to bradykinin are impaired in SHRSP. Diameter of pial arterioles (20-60 microns) was measured using intravital microscopy in WKY rats and SHRSP (9-12 months old). Superfusion of bradykinin (3 x 10(-7) M) dilated pial arterioles by 35 +/- 6% (mean +/- SEM) in WKY rats, but only 21 +/- 3% in SHRSP (p less than 0.05 versus WKY rats). Both nitric oxide (5 x 10(-7) M) and nitroglycerin (10(-5) M) produced similar vasodilatation in WKY rats and SHRSP. Our second goal was to determine whether alteration of postreceptor mechanisms contributes to impairment of endothelium-dependent cerebral vasodilatation in SHRSP. Calcium ionophore A23187 (10(-5) M) produced more vasodilatation in WKY rats than in SHRSP (32 +/- 8% versus 9 +/- 4%, p less than 0.05). Responses to A23187 (10(-5) M) were inhibited by indomethacin (46 +/- 13% versus 15 +/- 5%, p less than 0.05) in WKY rats, whereas responses to A23187 (10(-6) M) were potentiated modestly by indomethacin (-3 +/- 2% versus 4 +/- 2%, p less than 0.05) in SHRSP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelium-dependent responses of cerebral blood vessels during chronic hypertension. 190 37

Bradykinin produces less dilatation of pial arterioles in stroke-prone spontaneously hypertensive rats than in normotensive Wistar-Kyoto rats. The goals of this study were to determine the mediator of bradykinin-induced dilatation in cerebral arterioles of rats and to determine whether responses to this mediator are altered in hypertensive rats. Diameter of pial arterioles (20-65 microns) was measured using intravital microscopy in 18 normotensive and 17 hypertensive rats. Superfusion of 3 x 10(-7) M bradykinin dilated pial arterioles by 53 +/- 4% (mean +/- SEM) in normotensive rats but only 33 +/- 6% in hypertensive rats (p less than 0.05 versus normotensive rats). Vasodilatation in response to bradykinin was almost completely inhibited by 280 units/ml catalase in both normotensive and hypertensive rats (n = 7 and n = 7, respectively) whereas 150 units/ml superoxide dismutase (n = 6 and n = 5, respectively) and 1 mM deferoxamine (n = 5 and n = 5, respectively) did not attenuate bradykinin-induced vasodilatation. These findings suggest that hydrogen peroxide is the mediator of bradykinin-induced dilatation in cerebral arterioles of rats. We also examined responses of cerebral arterioles to hydrogen peroxide in five normotensive and six hypertensive rats. Dilator responses of cerebral arterioles to 3.2 x 10(-5) M to 1.6 x 10(-4) M hydrogen peroxide did not differ in normotensive and hypertensive rats, which suggests that impaired dilatation of cerebral arterioles in response to bradykinin is not related to altered responsiveness of smooth muscle to an endothelium-derived relaxing factor.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1991 Sep
PMID:Mechanisms of impaired endothelium-dependent cerebral vasodilatation in response to bradykinin in hypertensive rats. 192 61

Four fatal cases following scorpion sting in children are presented. Two victims had rectal temperature above 41 degrees C, the third exhibited a temperature of 40.9 degrees C from the combined effects of scorpion sting and heat stroke, while the fourth was hypothermic. All victims developed hypothermia 48 hr following the sting. The hyperthermia was effectively treated by acetaminophen suppositories, ice packs and water sponges. All victims showed late hypotension that was refractory to dopamine infusion. This was explained by bradykinin released by the venom blocking the dopaminergic receptors. Deterioration of the cortical activity of the victims maintained on mechanical ventilation before the incidence of asystole suggests a central component in the cardiovascular manifestations of envenomation. A. amoreuxi venom was selected as a model for the pharmacokinetic and quantitative toxicological studies since it has no effect on body temperature. In hyperthermic rabbits injected with labelled lethal fraction of A. amoreuxi venom, there was a significant decrease in the elimination half-life, t1/2 beta, the apparent volume of the tissue compartment, Vt, the apparent volume of distribution, Vdss, and the intercompartmental rate constant, kCT. Hypothermic rabbits showed a significant decrease in the apparent first-order elimination rate constant, kd, and a significant increase in the elimination half-life. In both states a higher concentration of the lethal fraction in the blood was calculated. This would explain the rapidity of onset of the electrocardiographic effects and the decreased survival time in both the hyperthermic and hypothermic rabbits injected with venom when compared to normothermic animals. The s.c. LD50 in mice and the i.v. MLD in rats were significantly reduced in the hypothermic mice and hypothermic and hyperthermic rats.
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PMID:Do changes in body temperature following envenomation by the scorpion Leiurus quinquestriatus influence the course of toxicity? 208 94

Using strips of human basilar arteries mounted in organ chambers to record isometric tension, we investigated vascular reactivity to thrombin and bradykinin. Both agents produced endothelium-dependent relaxation of basilar artery strips precontracted with phenylephrine but had no effect on resting tension in strips with or without endothelium. The relaxations caused by thrombin were abolished by antithrombin III/heparin, hirudin, and MD805. Thrombin but not bradykinin caused complete tachyphylaxis toward a second exposure. Indomethacin did not inhibit the relaxations induced by thrombin or bradykinin, whereas bromophenacyl bromide and methylene blue did. Aging decreased the relaxation induced by thrombin but did not affect the concentration needed to reach 50% maximal relaxation, nor did it affect the maximal relaxation in response to bradykinin, calcium ionophore A23187, and sodium nitroprusside. Our results suggest that thrombin and bradykinin produce endothelium-dependent relaxations mediated by an endothelium-derived relaxing substance and that the relaxation caused by thrombin is mediated by a proteolytic action on endothelial cells. The decrease in relaxations in response to thrombin with increasing age might be due to a decrease in the number or sensitivity of thrombin receptors on endothelial cells.
Stroke 1990 Jul
PMID:Effect of aging on endothelium-dependent vascular relaxation of isolated human basilar artery to thrombin and bradykinin. 211 73

The haemodynamic and neurohormonal responses to the angiotensin converting enzyme (ACE) inhibitor captopril were studied in 12 patients with primary autonomic failure; seven had multiple system atrophy and five had pure autonomic failure. Basal supine mean arterial blood pressure was higher in the patients with multiple system atrophy than in those with pure autonomic failure and the normal subjects. Basal plasma noradrenaline levels were normal in the patients with multiple system atrophy, but lower in those with pure autonomic failure. Captopril lowered the mean arterial pressure in the patients with multiple system atrophy and pure autonomic failure but not in the normal subjects. In the patients with multiple system atrophy and pure autonomic failure, captopril lowered the cardiac output and the stroke volume. Forearm vascular resistance was unchanged. No significant changes occurred in the normal subjects. Plasma renin activity was unchanged after captopril in the patients with autonomic failure, but rose in the normal subjects. Plasma noradrenaline was unchanged in all groups after the administration of captopril. We conclude that captopril lowers the mean arterial pressure in patients with multiple system atrophy and pure autonomic failure. After the administration of captopril there is a reduction in cardiac output, secondary to a fall in stroke volume. The vasodepressor response to captopril in patients with autonomic failure is not related to the basal level of plasma renin activity or sympathetic nervous activity, indicating that the hypotensive effects of bradykinin or prostaglandins, or both, may contribute.
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PMID:Angiotensin converting enzyme inhibition lowers blood pressure in patients with primary autonomic failure independently of plasma renin levels and sympathetic nervous activity. 269 48

We studied pial vessels in vivo in mice, examining under mercury light the permeability of these vessels to sodium fluorescein. Topical application of hypertonic solutions of NaCl caused leakage of fluorescein. However, putative chemical mediators of leakage, such as histamine, serotonin, arachidonic acid, and bradykinin, all failed to increase permeability to the dye. Apparent increases in permeability only accompanied endothelial damage caused by the dye + light combination, as indicated by production of local platelet aggregates. The technique is useful, provided inadvertent endothelial injury is recognized and avoided. The data in mice suggest that pial vessels may not participate in the permeability changes reportedly produced in parenchymal brain vessels by several of the mediators we tested. Therefore, studies of pial vascular permeability are not expected to provide reliable data concerning the actions of agents that might mediate cerebral edema.
Stroke
PMID:In vivo studies of pial vascular permeability to sodium fluorescein: absence of alterations by bradykinin, histamine, serotonin, or arachidonic acid. 312 Mar 61


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