Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was to investigate the relationship between circadian blood pressure (BP) variation and circadian variation of neurohumoral factors during the acute phase of stroke. We studied 17 patients with cerebral infarction in 16 and cerebral hemorrhage in one. We performed 24-hour ambulatory BP monitoring and examined plasma renin activity (PRA), catecholamine, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), endothelin 1 (ET1) and prothrombin fragment 1+2 (PT F1+2) and urinary catecholamine. Our result showed that the circadian variation of BP, neurohumoral and coagulation factors were diminished. There were significant relationships between BP levels and plasma BNP levels, nocturnal urinary adrenalines and ET1s. There were also significant relationships between night/day ratio of BP and plasma ET1 level. In conclusion the abnormal patterns of circadian BP rhythm were frequently observed during the acute phase of stroke. The cause of this abnormality may result from the diminished circadian rhythms of neurohumoral factors.
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PMID:Circadian variation of blood pressure and neurohumoral factors during the acute phase of stroke. 1184 63

The atrial natriuretic peptide (ANP) gene was, though inconclusive, implied to be etiologically related to stroke in rats and recently in humans. The present study tested the candidacy of ANP for stroke susceptibility by a combination of molecular genetic approaches. First, we undertook an association study using a reported ANP variant, G664A, in two case-control panels independently collected, which involved 970 Japanese subjects. Second, we compared the rat ANP gene sequences and neighboring marker alleles among stroke-prone SHR (SHRSP), normal SHR and WKY of an original inbred colony and we also compared brain ANP expression between SHRSP and normal SHR. In humans, we found no significant association between the 664A variant and stroke in the studied population. In rats, 21 polymorphic sites were identified by direct sequencing of 2170-bp ANP fragments, from which two distinct alleles, SHRSP- and WKY-types, were inferred. From a genealogical point of view, our data indicated that an SHRSP-type allele could not play a determinant role in stroke-proneness. Overall results did not support the disease relevance of ANP, disagreeing with previous reports. Thus, considerable caution should be taken when one attempts to transfer findings in the animal model to humans.
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PMID:Evaluation of the atrial natriuretic peptide gene in stroke. 1205 74

The hypothesis was tested that changing the direction of the transverse gravitational stress in horizontal humans modulates cardiovascular and renal variables. On different study days, 14 healthy males were placed for 6 h in either the horizontal supine or prone position following 3 h of being supine. Eight of the subjects were in addition investigated in the horizontal left lateral position. Compared with supine, the prone position slightly increased free water clearance (349 +/- 38 vs. 447 +/- 39 ml/6 h, P = 0.05) and urine output (1,387 +/- 55 vs. 1,533 +/- 52 ml/6 h, P = 0.06) with no statistically significant effect on renal sodium excretion (69 +/- 3 vs. 76 +/- 5 mmol/6 h, P = 0.21). Mean arterial pressure and left atrial diameter were similar comparing effects of supine with prone. The prone position induced an increase in heart rate (54 +/- 2 to 58 +/- 2 beats/min, P < 0.05), total peripheral vascular resistance (13 +/- 1 to 16 +/- 1 mmHg. min(-1). l(-1), P < 0.05), forearm venous plasma concentration of norepinephrine (97 +/- 9 to 123 +/- 16 pg/ml, P < 0.05), and atrial natriuretic peptide (49 +/- 4 to 79 +/- 12 pg/ml, P < 0.05), whereas stroke volume decreased (122 +/- 5 to 102 +/- 3 ml, P < 0.05, n = 6). The left lateral position had no effect on renal variables, whereas left atrial diameter increased (32 +/- 1 to 35 +/- 1 mm, P < 0.05) and mean arterial pressure decreased (90 +/- 2 to mean value of 85 +/- 2 mmHg, P < 0.05). In conclusion, the prone position reduced stroke volume and increased sympathetic nervous activity, possibly because of mechanical compression of the thorax with slight impediment of arterial filling. The mechanisms of the slightly augmented urine output in prone position require further experimentation.
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PMID:Effects of supine, prone, and lateral positions on cardiovascular and renal variables in humans. 1206 43

Imidapril hydrochloride (imidapril) is a long-acting, non-sulfhydryl angiotensin-converting enzyme (ACE) inhibitor, which has been used clinically in the treatment of hypertension, chronic congestive heart failure (CHF), acute myocardial infarction (AMI), and diabetic nephropathy. It has the unique advantage over other ACE inhibitors in causing a lower incidence of dry cough. After oral administration, imidapril is rapidly converted in the liver to its active metabolite imidaprilat. The plasma levels of imidaprilat gradually increase in proportion to the dose, and decline slowly. The time to reach the maximum plasma concentration (T(max)) is 2.0 h for imidapril and 9.3 h for imidaprilat. The elimination half-lives (t(1/2)) of imidapril and imidaprilat is 1.7 and 14.8 h, respectively. Imidapril and its metabolites are excreted chiefly in the urine. As an ACE inhibitor, imidaprilat is as potent as enalaprilat, an active metabolite of enalapril, and about twice as potent as captopril. In patients with hypertension, blood pressure was still decreased at 24 h after imidapril administration. The antihypertensive effect of imidapril was dose-dependent. The maximal reduction of blood pressure and plasma ACE was achieved with imidapril, 10 mg once daily, and the additional effect was not prominent with higher doses. When administered to patients with AMI, imidapril improved left ventricular ejection fraction and reduced plasma brain natriuretic peptide (BNP) levels. In patients with mild-to-moderate CHF [New York Heart Association (NYHA) functional class II-III], imidapril increased exercise time and physical working capacity and decreased plasma atrial natriuretic peptide (ANP) and BNP levels in a dose-related manner. In patients with diabetic nephropathy, imidapril decreased urinary albumin excretion. Interestingly, imidapril improved asymptomatic dysphagia in patients with a history of stroke. In the same patients it increased serum substance P levels, while the angiotensin II receptor antagonist losartan was ineffective. These studies indicate that imidapril is a versatile ACE inhibitor. In addition to its effectiveness in the treatment of hypertension, CHF, and AMI, imidapril has beneficial effects in the treatment of diabetic nephropathy and asymptomatic dysphagia. Good tissue penetration and inhibition of tissue ACE by imidapril contributes to its effectiveness in preventing cardiovascular complications of hypertension. The major advantages of imidapril are its activity in the treatment of various cardiovascular diseases and lower incidence of cough compared with some of the older ACE inhibitors.
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PMID:Protection of the cardiovascular system by imidapril, a versatile angiotensin-converting enzyme inhibitor. 1217 88

The myocardial interstitium is important in regulating cardiac function. Between the atrial lumen and the pericardial space are transmural pathways, and movement of interstitial fluid (ISF) through these pathways is one of the main driving forces regulating translocation of substances from the interstitium into the blood. To define how ISF translocation from the interstitial space into the luminal space is regulated by each component of atrial hemodynamics, we devised a new rabbit atrial model in which each physical parameter could be controlled independently. Using this system, we also defined the physiological role of the cardiac Na(+)/Ca(2+) exchanger on secretion of atrial natriuretic peptide (ANP) by depletion of extracellular Na(+) ([Na(+)](o)). Increases in stroke volume and atrial end-systolic volume increased ISF translocation and ANP secretion. However, an increase in atrial rate did not influence ISF translocation but, rather, increased ANP secretion. Gradual depletion of [Na(+)](o) caused gradual increases in ANP secretion and intracellular Ca(2+) ([Ca(2+)](i)), which were blocked in the presence of Ca(2+)-free buffer and Ni(2+), but not in the presence of KB-R7943, diltiazem, mibefradil, caffeine, or monensin. Amiloride and its analog blocked an increase in ANP secretion but not an increase in [Ca(2+)](i) by [Na(+)](o) depletion. Therefore, we suggest that ANP secretion and ISF translocation may be differently controlled by each physical factor. These results also suggest that the increase in ANP secretion in response to [Na(+)](o) depletion may involve inhibition of Na(+)/Ca(2+) and Na(+)/H(+) exchangers but not an increase in [Ca(2+)](i).
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PMID:Regulation of ANP secretion by cardiac Na+/Ca2+ exchanger using a new controlled atrial model. 1238 35

Recent studies have suggested a differential influence of mean pressure and pulse pressure on myocardial infarction and stroke, and differences among the major drugs in their efficacy at preventing these individual endpoints. We hypothesized that antihypertensive drugs have differing influences upon the pulse wave even when their effects on blood pressure are the same. We studied 30 untreated hypertensive patients, aged 28-55 years, who were rotated through six 6-week periods of daily treatment with amlodipine 5 mg, doxazosin 4 mg, lisinopril 10 mg, bisoprolol 5 mg, bendrofluazide 2.5 mg or placebo. The best drug was repeated at the end of the rotation. Blood pressure readings and radial pulse tonometry (by Sphygmocor) were performed at each visit, and blood was taken for measurement of levels of atrial natriuretic peptide and brain natriuretic peptide (BNP). The Sphygmocor derivation of the central aortic pulse wave was used to measure time for transmission of the reflected wave (T(R)) and the augmentation index (AI), which is the proportional increase in systolic pressure due to the reflected wave. There was a dissociation between the effects of the drugs on blood pressure and pulse wave analysis. Bisoprolol caused the greatest falls in blood pressure and T(R), but was the only drug to increase AI. This paradoxical response to bisoprolol was associated with a 3-fold increase in plasma BNP levels. There was a smaller elevation of BNP in women compared with men, as described previously, and this elevation also was associated with significantly higher values of AI. Other drugs reduced AI, and this was associated with a significant decrease in BNP by amlodipine. In conclusion, antihypertensive drugs differ in their short-term effects on augmentation of the systolic pulse wave and secretion of BNP from the heart, regarded as a sensitive measure of strain on cardiomyocytes. These differences may help to explain cause-specific differences in outcome in recent trials.
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PMID:Influence of drugs and gender on the arterial pulse wave and natriuretic peptide secretion in untreated patients with essential hypertension. 1240 Nov 23

To elucidate the role of atrial natriuretic peptides (NPs) in the amphibian heart, the myotropic effects and the cardiac distribution of frog atrial natriuretic factor (fANF) have been studied in Rana esculenta. Spontaneously, beating in vitro isolated working heart preparations were treated with increased concentrations (10(-11)-10(-8) M) of fANF-(1-24). The peptide at 10(-9) and 10(-8) M significantly reduced heart rate (HR) and, on the electrically paced preparations, decreased cardiac output (CO), stroke volume (SV) and work. Such negative inotropism was abolished by pretreatment with the pertussis toxin or by blocking the particulate guanylate cyclase (GC) with anantin while it was independent both from the functional impairment of the endocardium-endothelium by Triton X-100 and the inhibition of the soluble guanylate cyclase by 1 H-(1,2,4,) oxadiazolo-(4,3-a) quinoxalin-1-one (ODQ). By autoradiography, two classes of high and low affinity NPs binding sites were detected in the ventricular endocardium and myocardium and in the bulbus arteriosus. The analysis of displacement binding data using the radioligand [125I]-rat atrial natriuretic peptide [125I-rANP-(1-28)], its cold counterpart and the fANF-(1-24) showed that in the ventricular myocardium, the low affinity NPs sites bound both the heterologous and the homologous ligands at a concentration close to that responsible for the negative inotropism and chronotropism.
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PMID:Cardiac role of frog ANF: negative inotropism and binding sites in Rana esculenta. 1283 96

1. Homozygous deletion of the pro-atrial natriuretic peptide (Nppa) gene (ANP-/-) has been associated with both cardiac hypertrophy and salt-sensitive hypertension in mice, suggesting that cardiac hypertrophy in ANP-/- mice may be related, at least in part, to increased afterload. 2. To test the hypothesis that cardiac hypertrophy in ANP-/- mice is independent of blood pressure, male ANP-/- and wild-type ANP+/+ mice were fed a low (0.05%) or basal (0.55%) NaCl diet. Five weeks later, mean arterial pressure (MAP) was measured in conscious mice; the whole heart, atria, left and right ventricles (LV and RV, respectively), brain, lung, kidney, liver and spleen were weighed and fixed for histological analysis. Separate groups of mice were subjected to echocardiographic examination under tribromoethanol anaesthesia. 3. Mean arterial pressure and atrial, LV and RV mass were greater in ANP-/- mice than in ANP+/+ mice fed the basal salt diet. Salt depletion equalized MAP in the two genotypes, but did not alter the relative cardiac hypertrophy in ANP-/- mice. The ANP-/- mice had significant LV cardiomyocyte hypertrophy when fed either basal or low-salt diets. 4. Left ventricle chamber dimensions did not differ between genotypes, but were significantly reduced in mice fed the low-salt diet; LV posterior wall and septal thickness were greater in ANP-/- than ANP+/+ mice and were not altered by diet, indicating a concentric pattern of LV hypertrophy in ANP-/- mice. Left ventricle function (cardiac output, stroke volume, ejection fraction, circumferential wall stress and velocity of circumferential wall shortening) did not differ between strains on either diet; circumferential wall stress was reduced in the low-salt groups; other functional parameters were not altered by diet. 5. These findings indicate that ANP deletion results in cardiomyocyte hypertrophy and biventricular hypertrophy independent of blood pressure, supporting the concept that ANP has direct antihypertrophic effects in the heart.
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PMID:Pressure-independent enhancement of cardiac hypertrophy in atrial natriuretic peptide-deficient mice. 1285 24

Eels seem to be a suitable model system for analysing regulatory mechanisms of drinking behavior in vertebrates, since most dipsogens and antidipsogens in mammals influence the drinking rate in the seawater eels similarly. The drinking behavior in fishes consists of swallowing alone, since they live in water and water is constantly held in the mouth for respiration. Therefore, contraction of the upper esophageal sphincter (UES) muscle limits the drinking rate in fishes. The UES of the eel was innervated by the glossopharyngeal-vagal motor complex (GVC) in the medulla oblongata (MO). The GVC neurons were immunoreactive to an antibody raised against choline acetyltransferase (ChAT), an acetylcholine (ACh) synthesizing enzyme, indicating that the eel UES muscle is controlled cholinergically by the GVC. The neuronal activity of the GVC was inhibited by adrenaline or dopamine, suggesting catecholaminergic innervation to the GVC. The AP and the commissural nucleus of Cajal (NCC) in the MO projected to the GVC and were immunoreactive to an antibody raised against tyrosine hydroxylase (TH), rate limiting enzyme to produce catecholamines from tyrosine. Therefore, it is likely that activation in the AP or the NCC may inhibit the GVC and thus relaxes the UES muscle, which allows for water to enter into the esophagus. During passing through the esophagus, the imbibed sea water (SW) was desalted to approximately 1/2 SW, which was further diluted in the stomach and arrived at the intestine as approximately 1/3 SW, almost isotonic to the plasma. Finally, from the diluted SW, the eel intestine absorbed water following the Na(+)-K(+)-2Cl(-) cotransport (NKCC2) system. The NaCl and water absorption across the intestine was regulated by various factors, especially by peptides such as atrial natriuretic peptide (ANP) and somatostatin (SS-25 II). During desalination in the esophagus, however, excess salt enters into the blood circulation, which is liable to raise the plasma osmolarity. However, the eel heart was constricted powerfully by the hyperosmolarity, suggesting that the hyperosmolarity enhances the stroke volume to the gill, where excess salt was extruded powerfully via Na(+)-K(+)-2Cl(-) cotransport (NKCC1) system.
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PMID:Water metabolism in the eel acclimated to sea water: from mouth to intestine. 1466 89

Bone marrow stromal cells (BMSC) have been shown to generate neural cells under experimental conditions in vitro and following transplantation into animal models of stroke and traumatic CNS injury. Hastened recovery from the neurological deficit has not correlated with structural repair of the lesion in the stroke model. Secretory functions of BMSC, such as the elaboration of growth factors and cytokines, have been hypothesized to play a role in the enhanced recovery of neurological function. Using gene expression arrays, real time RT-PCR and radioimmunoassay, we have found that brain natriuretic peptide (BNP) is synthesized and released by BMSC at physiologically relevant levels in vitro. BNP, like its close homolog atrial natriuretic peptide (ANP), exerts powerful natriuretic, diuretic and vasodilatory effects. We speculate that transplanted BMSCs facilitate recovery from brain and spinal cord lesions by releasing BNP and other vasoactive factors that reduce edema, decrease intracranial pressure and improve cerebral perfusion.
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PMID:Expression of brain natriuretic peptide by human bone marrow stromal cells. 1469 30


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