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

Hypertension is a major cause in stroke mortality in Japan but is not the sole factor. This research, based on geographical comparisons between two selected towns of contrasted stroke experience, implicates a poor indoor thermal environment as having an important role, especially by sudden changes in temperature between rooms elevating blood pressure. High dietary salt is also an important contributory cause of stroke and is already the target of a public education campaign to encourage a reduced intake.
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PMID:Stroke mortality in Miyagi, Japan. 281 74

Isolate tail arteries from spontaneously hypertensive rats-stroke prone strain (SHRSP) display oscillatory contractile responses to norepinephrine. These oscillations are not observed in tail arteries from normotensive Wistar-Kyoto rats (WKY). The mechanism underlying these oscillatory contractions was investigated by simultaneous measurement of isometric force development and membrane potential (Em) from tail artery strips in vitro. After equilibration in physiological salt solution containing 1.6 mM calcium (37 degrees C), resting Em was not different between WKY (-52 +/- 1.1 mV) and SHRSP (-52 +/- 0.4 mV). Norepinephrine (3 x 10(-7) M) produced a similar degree of depolarization in tissues from the two strains (WKY = (-42.5 +/- 0.9, SHRSP = -41 +/- 0.8). However, while Em recordings from WKY arteries were quiescent, those from SHRSP displayed bursts of electrical spiking activity that were temporally associated with the rising phase of oscillations in contractile force. The frequency and duration of these bursts of action potentials increased with the concentration of norepinephrine. Action potentials were not observed in calcium-free solution or in presence of nifedipine (3 x 10(-7) M). Releasing the passive stretch on the tissues caused a decrease in the rate of spiking. These studies demonstrate catecholamine-induced regenerative electrical activity in tail arteries from SHRSP that is dependent on extracellular calcium. This activity is unique to tail arteries from this strain.
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PMID:Regenerative electrical activity and arterial contraction in hypertensive rats. 291 Aug 15

Hemodynamic responses to synthetic atrial natriuretic factor (ANF), were studied in renin-dependent two-kidney, one-clip (2K,1C) and deoxycorticosterone (DOC) salt-treated hypertensive rats as well as normotensive controls. ANF infusion (800 pmol/kg prime, 120 pmol X kg-1 X min-1 for 60 min) decreased blood pressure (BP) more in conscious 2K,1C (-24 +/- 4%) than in DOC salt-treated (-12 +/- 4%, P less than 0.05) or control rats. Hemodynamic parameters were also evaluated during graded infusion of three doses, each for 30 min. At 24 and 120 pmol X kg-1 X min-1, ANF lowered BP in 2K,1C rats, both conscious (from 156 +/- 6 to 144 +/- 7, P less than 0.05 and 135 +/- 5 mmHg, P less than 0.05) and anesthetized (from 148 +/- 7 to 138 +/- 7, P less than 0.05 and 128 +/- 7, P less than 0.05). In anesthetized 2K,1C, BP changes were associated with reduction in total peripheral resistance (TPR) that became significant at 120 pmol X kg-1 X min-1 (-10 +/- 2%), whereas cardiac output (CO) and stroke volume (SV) were unchanged. In DOC-salt-treated rats these doses did not lower BP despite progressive falls in CO (-7 +/- 3% and -24 +/- 5%, P less than 0.05) and SV (-8 +/- 2% and -23 +/- 5%, P less than 0.05), which were balanced by a simultaneous rise in TPR (+12 +/- 4% and +26 +/- 10%, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differing hemodynamic responses to atrial natriuretic factor in two models of hypertension. 293 31

Atrial natriuretic peptide ANP(1-23) reduced mean arterial pressure (MAP), cardiac output (CO), central blood volume (CBV) and stroke volume (SV) when given i.v. (100 pmol/min) to spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). In SHR, total peripheral resistance (TPR) was significantly lowered. The major cause of the fall in blood pressure in WKY was reduction in CO and in SHR reduction in TPR. Acute 20% volume expansion increased plasma immunoreactive ANP (IR-ANP) in WKY as well as in SHR. However, the ANP release in SHR was blunted compared with WKY. After chronic high salt intake, ANP release in SHR was even further reduced in relation to an acute volume load. We conclude that the release of ANP as well as the haemodynamic responses to exogenous ANP is altered in SHR.
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PMID:On the role of atrial natriuretic peptide in cardiovascular regulation in the spontaneously hypertensive rat. 294 31

1. The effects of low dose infusion of atrial natriuretic peptide (ANP) were observed in double-blind, placebo-controlled study in six fluid-loaded volunteers. After baseline observations, hourly increments of 0.4, 2 and 10 pmol min-1 kg-1 were infused with continuous observation of heart rate, blood pressure and cardiac output. Plasma ANP, aldosterone, and catecholamines, and urinary volume and sodium excretion, were estimated at half-hourly intervals. 2. ANP infusion resulted in an increase of 35, 98 and 207% in urinary sodium excretion and of 10, 20 and 71% in urinary volume when compared with placebo. Plasma ANP was markedly elevated above placebo levels only during infusion of 10 pmol of ANP min-1 kg-1. 3. No change in heart rate of blood pressure was noted during the study, but a significant fall in stroke volume index was observed during active treatment. Plasma levels of aldosterone and catecholamines were not significantly different on the 2 treatment days. 4. The potent natriuretic and diuretic effects of this peptide at plasma concentrations not significantly elevated from physiological suggest a hormonal role for ANP in the homoeostasis of salt and water balance.
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PMID:Low dose infusion of atrial natriuretic peptide causes salt and water excretion in normal man. 296 31

Hyponatremia is common following aneurysmal subarachnoid hemorrhage and has been linked to the syndrome of inappropriate secretion of antidiuretic hormone. However, the demonstration of volume depletion and natriuresis in some patients has suggested that salt wasting is a more likely etiology. Atrial natriuretic factor appears to play a role in both central and peripheral regulation of sodium homeostasis. To investigate the behavior of circulating atrial natriuretic factor following subarachnoid hemorrhage, we studied 25 patients with intracranial aneurysms: 21 after acute subarachnoid hemorrhage and four without evidence of recent rupture. Atrial natriuretic factor was measured by radioimmunoassay of extracted plasma (normal value, 20.8 +/- 24.6, mean +/- 3 SD). Mean +/- SEM plasma atrial natriuretic factor concentration was elevated to 84 +/- 25 pg/ml on Day 1, rose to 134 +/- 29 pg/ml on Day 3, and fell to 86 +/- 17 pg/ml by Day 7 after subarachnoid hemorrhage (p less than 0.01). In two patients (9.5%) who developed hyponatremia after aneurysm rupture, plasma concentrations were no different from that in the group as a whole; concentrations in patients with no evidence of recent subarachnoid hemorrhage were not elevated. Neither fluid administration nor timing of surgery could account for the elevated concentrations. We conclude that concentrations of circulating atrial natriuretic factor are elevated after subarachnoid hemorrhage but do not solely account for the accompanying hyponatremia.
Stroke 1988 Sep
PMID:Plasma atrial natriuretic factor and subarachnoid hemorrhage. 297 Jul 2

The effects of cicletanine were compared with those of four other antihypertensive drugs (prazosin, a highly selective alpha 1 antagonist; captopril, an angiotensin-converting enzyme inhibitor; indapamide, an antihypertensive diuretic; and hydrochlorothiazide, a purely diuretic agent) on young stroke-prone SHR rats with high-salt diet. All the drugs except hydrochlorothiazide prevented the onset of hypertension. The minimal effective dose on blood pressure was 1 mg/kg for both cicletanine and captopril, and 3 mg/kg for indapamide. The action on cardiac hypertrophy and diuresis occurs at a dose of cicletanine 10 to 30 times higher than that required to produce the antihypertensive effect. Renal hypertrophy was also decreased significantly by cicletanine at a dose of 100 mg/kg.
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PMID:Comparison of cicletanine with other antihypertensive drugs in SHR-SP models. 297 Sep 55

The effects of cicletanine were compared with those of three other antihypertensive drugs: prazosin, a highly selective alpha 1 antagonist, captopril an angiotensin converting enzyme inhibitor and indapamide a diuretic antihypertensive agent, on young stroke-prone SHR rats with high salt diet; furthermore, vascular reactivity to cicletanine was studied on isolated rat aorta. At an equal dose (30 mg/kg per os) all the drugs prevent the onset of hypertension with the same intensity. The minimal effective dose on blood pressure was 1 mg/kg for both cicletanine and captopril, and 3 mg/kg for indapamide. The action on diuresis and electrolyte excretion occurs at a dose of cicletanine 10 to 30 times higher than that required to produce the anti-hypertensive effect. One of the possible mechanisms of the antihypertensive effects of cicletanine could be due to a direct action of the drug on the vascular wall. This vascular impact could be an interaction with the alpha-adrenoceptor system (apparent pA2 cicletanine = 5.12) or a decrease in the vascular spasmogenic response whatever agonist was studied.
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PMID:Antihypertensive profile of cicletanine, a furopyridine derivative: comparison with captopril, indapamide and prazosin. 297 70

Ten obese men (20-40% overweight) with previously untreated arterial hypertension (WHO stages I and II) were examined before and during sodium-restricted isocaloric diets. The mean (+/- s.d.) daily sodium excretion was reduced from 199 +/- 65 to +/- 25 mmol/24 h. Intra-arterial blood pressure (BP), cardiac output (CO), plasma volume, circulating and urinary noradrenaline (NA), plasma renin activity (PRA) and urinary aldosterone were measured. Vascular reactivity was assessed with intravenous bolus injections of 50, 100 and 200 micrograms phenylephrine, and baroreflex sensitivity was assessed with the R-R interval response to pressure elevations on electrocardiogram. Significant reductions in systolic BP from 163 +/- 18 to 147 +/- 17 mmHg and in diastolic BP from 97 +/- 7 to 88 +/- 9 mmHg occurred during salt restriction. Blood pressure reductions were correlated with changes of urinary sodium excretion (r = 0.71; P less than 0.05). No significant changes in CO, heart rate (HR) or stroke volume (SV) were observed; therefore, BP reduction was secondary to the fall in total peripheral resistance (TPR) from 21.8 +/- 4.1 to 19.0 +/- 4.1 units (P = 0.05). Plasma volume, as well as total blood volume, was not affected by the moderate sodium restriction, but PRA rose from 0.71 +/- 0.1 to 0.87 +/- 0.1 micrograms angiotensin 1/ml per h (P less than 0.05). Urinary aldosterone was increased from 32 +/- 12 to 54 +/- 9 nmol/24 h. No change in venous or arterial concentrations of NA or of urinary NA was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Central haemodynamics, baroreceptor sensitivity and alpha 1-adrenoceptor-mediated vascular reactivity during weight-stable sodium restriction in obese men with hypertension. 300 1

The role of sodium and its accompanying anion for the development of DOCA-salt hypertension was studied in uninephrectomized DOCA-treated weanling Wistar rats which were fed a diet containing either sodium chloride or sodium bicarbonate (170 mmol/kg). The blood pressure was increased in both groups of rats with sodium overload as compared to rats fed a low-salt diet only. A decreased cardiac output and substantially elevated systemic resistance were demonstrated in both groups of rats with high sodium intake in comparison with rats kept on a low-salt diet. However, these haemodynamic changes were more pronounced in rats with sodium chloride overload than in animals with a high sodium bicarbonate intake. On the other hand, the rigidity of major arteries which was estimated as the pulse pressure/stroke volume ratio, was increased only in rats fed a diet with sodium chloride but not in rats with sodium bicarbonate overload. Thus high sodium intake was responsible for the changes of systemic resistance in DOCA-treated animals and its action was only slightly augmented by a high chloride intake. In contrast to this, the chloride overload seemed to be essential for the induction of increased arterial rigidity.
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PMID:The importance of sodium and chloride ions for the development of DOCA-NaCl hypertension: a haemodynamic study. 302 Jun 2


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