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

We investigated the influence of acute volume expansion on the hemodynamic and renal responses to the constant infusion of atrial natriuretic factor (ANF) (alpha-human ANP, 2 micrograms/kg bolus, 0.2 microgram.kg-1.min-1) in rabbits anesthetized with ketamine and acepromazine. The effects of the peptide were evaluated in 12 euvolemic rabbits and in 15 rabbits during the steady-state phase of volume expansion (0.9% NaCl 4.5 ml/min for 60 min). In the euvolemic animals, ANF caused an increase in natriuresis and a reduction in blood pressure (BP), which was associated with a decrease in cardiac output (CO), stroke volume (SV), and no significant changes in central venous pressure (CVP), peripheral hematocrit (Hct), and heart rate (HR). When the peptide was infused in the volume-expanded animals, the effects of ANF on BP and HR were comparable with those observed in the euvolemic animals. However, in these animals the ANF-induced changes in CO, SV, CVP, and Hct were significantly greater than those observed in the euvolemic group. In addition, the percent increases in diuresis and natriuresis were significantly smaller than those obtained in the euvolemic animals. In conclusion, volume expansion with saline potentiates the effects of ANF on systemic hemodynamics and blood volume.
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PMID:Influence of volume expansion on hemodynamic effects of atrial natriuretic factor in rabbits. 252 85

The chronotropic and inotropic effects of four atrial peptides (cardiodilatin 1-16, atrial natriuretic factor 8-33 and atriopeptin I and III) on the isolated systemic heart of Octopus vulgaris were studied. Using a preparation that produces a physiological stroke volume at physiological input pressures, it was found that ANF, atriopeptin I and atriopeptin III exerted both negative chronotropic and inotropic effects. In contrast, cardiodilatin produced a positive inotropic effect. A dose-response curve of ANF is reported, showing a threshold concentration of about 10(-12) M. The pharmacological and physiological implications of these results are discussed in relation to some characteristics of the cephalopod systemic heart.
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PMID:Chronotropic and inotropic effects of atrial peptides on the isolated systemic heart of Octopus vulgaris. 252 16

In order to investigate the interaction between atrial natriuretic factor (ANF) and arginine vasopressin (AVP) in the pathogenesis of essential hypertension, the effects of intravenous (iv) or intracerebroventricular (icv) injection of human ANF-(99-126) on plasma and brain AVP, as well as mean arterial pressure (MAP), urinary volume (UV) and sodium (UNaV) excretion in stroke-prone spontaneously hypertensive rats (SHRsp) and age-matched normotensive Wistar-Kyoto rats (WKY) were studied. The results showed that ten minutes after iv injection of ANF, MAP decreased by 9.4% and 12.2% (P less than 0.05), UV increased about 9 and 20 folds (P less than 0.01), UNaV increased about 16 and 29 folds (P less than 0.01) in SHRsp and WKY rats, respectively. No such significant changes in these parameters were found in the icv group. Although iv and icv injection of ANF caused significant decrease of plasma AVP in both strains, the decrease was less marked in SHRsp than in WKY rats, while the maximum decreases were 58% (iv) and 31% (icv) in SHRsp, the corresponding values were 80% (iv) and 65% (icv) in WKY. Intravenous and intracerebroventricular injection of ANF also induced significant increase of hypothalamic AVP in both SHRsp and WKY rats, but no significant change could be found in hypophyseal AVP content. The results suggest that decreased sensitivity of AVP inhibition as well as less marked hypotensive, diuretic and natriuretic effects to ANF in SHRsp might play a role in the pathogenesis of their hypertension.
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PMID:[Effects of human atrial natriuretic factor-(99-126) on plasma and brain vasopressin in stroke-prone spontaneously hypertensive rats]. 252 9

To assess the contribution of venous effects to the hemodynamic changes caused by atrial natriuretic factor (ANF), the cardiac and peripheral effects of ANF were compared with those induced by the venoarterial vasodilator sodium nitroprusside. On 3 different days, eight healthy subjects received 2-hour infusions of either ANF, sodium nitroprusside, or placebo, by a single-blind crossover design. ANF was administered at a rate of 15 ng/kg/min for hour 1 and 50 ng/kg/min for hour 2; each infusion rate was preceded by a 50-micrograms bolus. The lower ANF infusion rate increased plasma cGMP fourfold, but only modest cardiovascular effects (small decreases in left ventricular end-diastolic and end-systolic volumes) were noted. At the higher ANF infusion rate, left ventricular volumes and intravascular volume, as indirectly assessed by changes in hematocrit levels, decreased further, which resulted in decreases in stroke volume, cardiac index, and systolic blood pressure. No evidence for arterial vasodilation (no decrease in diastolic blood pressure, total peripheral resistance, or forearm resistance) was obtained, and no increase in sympathetic activity was noted. In contrast, sodium nitroprusside caused arterial vasodilation, an increase in cardiac index, and significant increases in sympathetic activity. We conclude that short-term increases in plasma ANF within the physiologic range primarily affect the venous vascular bed (by decreasing intravascular volume or by venodilation) without increasing sympathetic activity.
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PMID:Cardiac and vascular effects of atrial natriuretic factor and sodium nitroprusside in healthy men. 253 99

Atrial natriuretic factor lowers blood pressure in normotensive and hypertensive animal models. The present study examined the mechanism of the blood pressure-lowering effect in 10 normotensive dogs. Four awake dogs previously instrumented with electromagnetic flow probes for measurement of cardiac output and catheters for systemic hemodynamic and cardiac dynamic measurements were studied. After a 30-minute control period, a 3 micrograms/kg bolus followed by 0.3 micrograms/min/kg of a 24-residue synthetic atrial natriuretic factor was infused for 30 minutes, followed by a 1-hour recovery period. Mean arterial pressure fell significantly during infusion (control, 125 +/- 4; infusion, 108 +/- 5; recovery, 125 +/- 9 mm Hg; p less than 0.05) and was accompanied by a slight but significant bradycardia (control, 144 +/- 7; infusion, 134 +/- 5; recovery, 145 +/- 7 beats/min; p less than 0.05). Significant reductions in cardiac output (control, 2.66 +/- 0.60; infusion, 2.18 +/- 0.60; recovery, 2.74 +/- 0.60 L/min; p less than 0.05), stroke volume (control, 18.4 +/- 3.9; infusion, 16.0 +/- 4.2; recovery, 19.0 +/- 3.7 ml/beat; p less than 0.05), and maximum increase in rate of change of left ventricular systolic pressure (control, 2475 +/- 200; infusion, 2088 +/- 216; recovery, 2487 +/- 243 mm Hg/sec; p less than 0.05) were also observed during infusion. No significant changes in total peripheral resistance or central venous pressure were noted, although the latter tended to fall during infusion. A similar pattern was observed in six pentobarbital-anesthetized dogs, except that infusion of atrial natriuretic factor did not induce bradycardia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular effects of atrial natriuretic factor in anesthetized and conscious dogs. 293 24

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

To determine the hemodynamic effects of a hypotensive dose of atrial natriuretic factor (ANF), a synthetic peptide containing 26 amino acids of endogenous rat ANF (Arg-Arg-Ser-Ser-Cys-Phe-Gly-Gly-Arg-Ile-Asp-Arg-Ile-Gly-Ala-Gln-Ser-Gly -Leu-Gly-Cys-Asn-Ser-Phe-Arg-Tyr-COOH) was studied in two groups of barbiturate anesthetized rats. In the first experiment, a 20-minute infusion of a hypotensive dose, 95 pmole/min i.v., of the synthetic ANF decreased mean arterial pressure (MAP) by 40 +/- 3 mm Hg from a baseline of 128 +/- 5 mm Hg, and cardiac output (CO) (microsphere method) by 7.8 +/- 1.8 ml/min/100 gm from a baseline of 23.5 +/- 1.3 ml/min/100 gm. Synthetic ANF did not significantly affect the total peripheral resistance (TPR) measured at the end of the 20-minute infusion. Sodium nitroprusside (SNP), infused at an equihypotensive dose of 20 micrograms/kg/min i.v., produced the same hemodynamic profile in seven other animals; in contrast, 0.3 mg/kg i.v. of hydralazine (n = 7) lowered MAP by 56 +/- 6 mm Hg and reduced TPR index by 3.0 +/- 0.6 mm Hg/ml/min/100 gm, but did not change CO. Other than an increase in coronary blood during SNF infusion, there were no significant changes in the distribution of cardiac output. Infusion of the saline vehicle had no significant effects on any of these parameters. The results of the second experiment in anesthetized rats confirmed that hypotensive doses of 40 and 100 pmole/kg/min i.v. lowered CO (dye dilution method) from a baseline of 33 +/- 6 to a minimum of 24 +/- 2 ml/min/100 gm (p less than 0.05) without affecting TPR. In addition, synthetic ANF did not significantly affect heart rate (HR) but it slightly reduced cardiac contractility (dp/dt50). These results suggest that the hypotensive dose of synthetic ANF reduced cardiac output, partially by diminishing stroke volume, and perhaps contractility.
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PMID:Cardiac and hemodynamic responses to synthetic atrial natriuretic factor in rats. 294 28

To study the factors controlling the release of atrial natriuretic factor (ANF), we analyzed the peripheral plasma ANF concentration in 34 patients with heart disease who underwent cardiac catheterization. A significant positive correlation between plasma ANF concentration and pulmonary arterial pressure (systolic, r = 0.87; diastolic, r = 0.75; mean, r = 0.85; each p less than 0.001) was found in all the patients examined. There were significant positive correlations between plasma ANF concentration and systolic right ventricular pressure (r = 0.86, p less than 0.001), pulmonary capillary wedge pressure (r = 0.50, p less than 0.01) and mean right atrial pressure (r = 0.39, p less than 0.05). A weak but significant negative correlation was found between plasma ANF concentration and stroke volume index (r = -0.43, p less than 0.05). The correlation coefficient between plasma ANF concentration and mean pulmonary arterial pressure was significantly stronger than those between plasma ANF concentration and pulmonary capillary wedge pressure, and between plasma ANF concentration and mean right atrial pressure (p less than 0.05 and p less than 0.01, respectively). In 10 patients with mitral valvular disease, significant correlations with plasma ANF concentration were also found for pulmonary arterial pressure (systolic, r = 0.80; diastolic, r = 0.82; mean, r = 0.82; each p less than 0.01). These findings suggest that pulmonary arterial pressure may play an important role in the mechanism of release of ANF from atrial cardiocytes.
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PMID:Pulmonary arterial pressure and plasma concentration of atrial natriuretic factor (ANF) in patients with heart disease. 295 17

Hemodynamic and hormonal effects of two graded infusions of alpha-human-(1-28)-atrial natriuretic factor (0.5 microgram/kg prime followed by 0.05 microgram/kg per min for 20 minutes and by 0.1 microgram/kg per min for 20 minutes) were evaluated in 13 patients with mild to moderate essential hypertension. The lower dose of atrial natriuretic factor did not change significantly any of the considered variables, although it tended to reduce aortic mean blood pressure (from 132.6 +/- 5.3 to 125.5 +/- 4.6 mm Hg), cardiac index (from 3.67 +/- 0.2 to 3.54 +/- 0.18 liters/min per m2) and forearm vascular resistance (from 178.6 +/- 15 to 148.3 +/- 10 mm Hg/ml per s). The higher dose of atrial natriuretic factor significantly reduced mean aortic pressure (118.6 +/- 5 mm Hg), cardiac index (3.29 +/- 0.16 liters/min per m2) and stroke volume index (from 45.9 +/- 2.6 to 38.9 +/- 3 ml/m2) and slightly decreased pulmonary wedge pressure, whereas both total peripheral resistance and forearm vascular resistance were not modified. With this latter dose a reduction in aortic pressure was observed in all patients at the steady state, and this was associated with a fall in stroke volume index in 10 of the 13 patients and with a reduction in total peripheral resistance in only 6 patients. Heart rate and right atrial and pulmonary pressures did not change during infusion of atrial natriuretic factor. Plasma renin activity was only slightly reduced by atrial natriuretic factor, whereas plasma norepinephrine rose significantly (from 233 +/- 34 to 330 +/- 58 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and hormonal effects of atrial natriuretic factor in patients with essential hypertension. 295 31


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