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

The effect of atrial natriuretic peptide (ANP), before and after converting enzyme (CE) inhibition, was investigated in six primary hypertensive patients taking a constant diet. In this placebo-controlled, single-blind, randomized study, the patients received, on three different days, i.v. infusions of (a) placebo, or (b) alpha-human ANP, 150 micrograms over 30 min, or (c) alpha-human ANP after acute CE inhibition by enalapril (EN) 20 mg P.O., 4 h before ANP infusion. ANP infusion increased urinary sodium (p less than 0.001) and volume excretion. Blood pressure (BP), heart rate, stroke volume and shortening fraction (echocardiography), plasma renin activity (PRA), and plasma aldosterone did not change significantly. Urinary norepinephrine and dopamine were significantly increased (p less than 0.05) after ANP infusion. BP was significantly reduced after EN in every patient (p less than 0.05). ANP infusion during CE inhibition induced a more sustained increase of sodium excretion and diuresis with respect to ANP infusion alone (p less than 0.05). PRA was significantly reduced while no further reduction of BP was observed. These data suggest that CE inhibition may increase the natriuretic and diuretic effect of ANP in hypertensive patients.
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PMID:Effects of infusing alpha-atrial natriuretic peptide in primary hypertension during converting enzyme inhibition. 248 53

22Na+ uptake into capillaries isolated from the cerebral cortex of adult (20- to 26-week-old) sustained-hypertensive spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) was compared with findings in age-matched Wistar Kyoto rats (WKY). In the presence of 1.0 mM ouabain, 1.0 mM furosemide and 2.0 mM LiCl, 22Na+ uptake into the isolated cerebral capillaries of WKY and SHR was significantly reduced to 38% and 65% of the control values, respectively, when 0.1 microM alpha-rat atrial natriuretic peptide (rANP) was added to the uptake buffer. The rANP-induced inhibition observed in SHR was significantly less, as compared with that in the WKY. Noteworthy was the observation that the Na+ uptake into the cerebral capillaries of SHRSP was not inhibited by rANP. As this peptide is thought to regulate amiloride-sensitive Na+ transport from the blood to brain by interacting with specific receptors, the present finding may relate to the etiology of dysfunction of the blood-brain barrier, in the presence of hypertension.
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PMID:Atrial natriuretic peptide-induced inhibition of amiloride-sensitive 22Na+ uptake into cerebral capillaries of spontaneously hypertensive rats. 252 19

The acute hemodynamic and humoral responses to intravenous dilevalol (10 to 390 mg) were evaluated in 10 patients with moderate hypertension. Dilevalol, in doses of 30 mg or more, decreased arterial pressure (p less than 0.0001) through a decrease in total peripheral resistance (p less than 0.0001) associated with an increase in stroke volume and cardiac output (p less than 0.0001). Heart rate increased moderately at doses above 190 mg. Plasma norepinephrine levels increased (p less than 0.05), but epinephrine levels remained unchanged. Plasma renin activity and level of atrial natriuretic peptide decreased (p less than 0.01 and p less than 0.01, respectively). The hypotensive and humoral changes persisted 3 hours after the last dose. Dilevalol modified the pattern of hemodynamic response to isometric stress, slightly enhancing the increases in peripheral resistance and blunting increases in cardiac output and heart rate. The response in arterial pressure during administration of dilevalol remained similar to that seen in the pretreatment phase. The results show that dilevalol, when given intravenously in a dose of 30 to 90 mg, reduces arterial pressure by reducing total peripheral resistance without acceleration in heart rate. On the basis of these hemodynamic effects, dilevalol should be further evaluated for treatment of hypertensive emergencies.
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PMID:Hemodynamic and humoral effects of intravenous dilevalol in patients with moderate hypertension. 252 58

A pituitary protein, designated 7B2, was demonstrated to be present in the cerebrospinal fluid (CSF) obtained from control subjects and patients with various cerebrovascular accidents (CVAs). Although there was not any significant difference in mean immunoreactive 7B2 concentrations among various CVA groups, the CSF immunoreactive 7B2 levels in control subjects were 10 to 100 times higher than those in control plasma samples. Immunoreactive calcitonin gene-related peptide (CGRP) and immunoreactive atrial natriuretic peptide (ANP) levels in the CSF were comparable to those in corresponding normal plasma samples. The CSF ANP concentrations in patients with cerebral bleeding and subarachnoid hemorrhage were significantly lower than those in control subjects. Gel chromatography or high-performance liquid chromatography indicated that the main immunoreactivities of 7B2, CGRP, and ANP coeluted with corresponding standard material. The high CSF concentrations of immunoreactive 7B2 observed might indicate a functional role of 7B2 in the central nervous system.
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PMID:Pituitary protein 7B2-like immunoreactivity in cerebrospinal fluid: comparison with other neuropeptides. 252 68

We investigated the possible relation between neuropeptides and cerebral vasoconstriction in samples of ventricular or cisternal cerebrospinal fluid from 14 patients with subarachnoid hemorrhage. Neuropeptide Y, calcitonin gene-related peptide, atrial natriuretic peptide, and pituitary polypeptide 7B2 were present in the cerebrospinal fluid of these patients. Concentrations of calcitonin gene-related peptide and 7B2 were not significantly different from those in control subjects, but that of atrial natriuretic peptide was significantly lower. Although the mean concentration of neuropeptide Y was not significantly higher than control, consecutive determinations showed an increase 6-11 days after the onset of subarachnoid hemorrhage. An initially high 7B2 concentration decreased gradually, although half the patients showed a second increase greater than 10 days after the onset. Considering the well-recognized vasoconstrictive effect of neuropeptide Y, it is possible that this increase in its concentration in the cerebrospinal fluid plays a role in the pathogenesis of the cerebral vasospasm that is often seen after subarachnoid hemorrhage.
Stroke 1989 Dec
PMID:Increased neuropeptide Y concentrations in cerebrospinal fluid from patients with aneurysmal subarachnoid hemorrhage. 253 45

1. A biventricular, low-output congestive cardiomyopathy was induced in 19 rabbits by administering adriamycin (16 mg/kg). The effects of alpha-rat atrial natriuretic peptide (ANP) infused at 0.1, 0.2 and 0.4 micrograms/kg per min, were then examined in terms of (i) central haemodynamics (ii) regional blood flow (iii) renal function and (iv) plasma norepinephrine and plasma renin. 2. In this dose range, ANP produced progressive and significant falls in stroke volume, cardiac output and mean arterial pressure, owing to a fall in venous return. The heart rate response to this was blunted. 3. Using radiolabelled microspheres, significant falls in the perfusion of cutaneous, gastrointestinal and musculoskeletal tissues were observed, due to reduced vascular conductances in these beds. These changes were accompanied by activation of the sympathetic nervous system as evidenced by a progressive rise in plasma norepinephrine. A significant increase in plasma renin was only observed with the highest infusion of ANP. 4. Renal blood flow was maintained in the face of a falling mean arterial pressure and cardiac output, but diuretic and natriuretic effects were absent. 5. It was concluded that the dominant influence of ANP infusion in this model of heart failure appeared to be a reduction in cardiac preload with detrimental overall haemodynamic consequences.
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PMID:Regional distribution of the cardiac output and renal responses to atrial natriuretic peptide infusion in rabbits with congestive heart failure. 253 97

The non-osmotic stimulation of release of arginine vasopressin (AVP) seems to be the main determinant of the impaired water excretion and hyponatraemia in patients with cardiac failure. This non-osmotic stimulation of AVP release could be secondary to a decrease in stroke volume to which the ventricular receptors respond by decreasing the vagal afferent input to the hypothalamus via the mid-brain. Improvement of cardiac stroke volume would then decrease AVP release and improve water excretion. In cardiac failure, the non-osmotic stimulation of AVP release is not clearly modulated by the renin-angiotensin system or by the atrial natriuretic peptide plasma concentration. Nevertheless, physiological concentrations of atrial natriuretic peptide could inhibit the renal epithelial water transport at the collecting duct level. Water-loading and osmotic-loading experiments in patients with cardiac failure indicated that the release of AVP is still under osmotic control and favoured the concept that volume depletion in general and cardiac failure in particular may lower the osmotic threshold and increase the osmotic sensitivity to vasopressin release. Experiments using a specific vasopressin antagonist rarely indicated a vasoconstrictor role for endogenous AVP in either experimental or clinical cardiac failure. Intrarenal factors also contributed to the impaired water excretion observed in patients with cardiac failure: increased central sympathetic efferent discharge and stimulation of the renin-angiotensin-aldosterone system would be expected as a consequence of the decreased effective arterial blood volume. These effects could then decrease maximal reabsorption of solute further impairing the ability of the kidney to excrete free water. The impaired water excretion is correlated with the severity of the cardiac deterioration and thus has prognostic implications.
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PMID:Water disturbances in cardiac failure. 253 70

The sequential effects of an increased daily NaCl intake on hemodynamics, fluid electrolyte balances, and hormonal responses were evaluated in dogs (n = 7) with fixed circulating levels of angiotensin II (ANG II). During the control period, ANG II was infused at 3 ng.kg-1.min-1 while dogs were maintained on an 8 meq NaCl/day diet. Water intake was fixed at 700 ml/day. Continuously recorded (24 h/day) changes of total body weight (TBW) were used as an index of total body water. Cardiac stroke volume and arterial pressure were recorded, and each beat was digitized to provide hourly and 24-h average cardiac output (CO), mean arterial pressure (MAP), and total peripheral resistance (TPR). After three stable control days, daily salt intake was increased to 120 meq for 7 days. TBW increased gradually to 448 +/- 111 g (2.9%, P less than 0.05) above control by day 3. An 11% expansion of blood volume (P less than 0.05) was found (51CR-labeled red blood cells) on day 2 of high NaCl. CO rose 12% and MAP 20% (P less than 0.05) in parallel with TBW by day 4. By day 7, CO remained only 5% elevated, whereas MAP had stabilized at 20% above control levels. TPR remained significantly elevated from days 3 through 7. A positive Na balance averaging 91 +/- 8 meq (P less than 0.05) occurred on day 1. Plasma Na concentration was increased 2-3 meq/l above control throughout the period of high-salt intake. Plasma renin activity and aldosterone levels decreased to nearly undetectable levels, vasopressin rose slightly, and atrial natriuretic peptide levels increased significantly. Dogs maintained at 8 meq/day NaCl during the same infusion of ANG II showed no changes in MAP, CO, TPR, or TBW. In summary, the salt-induced hypertension was consistently related to small but significant fluid retention, blood volume expansion, elevations of cardiac output, and a gradual increase in TPR.
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PMID:Hemodynamics and blood volume in angiotensin II salt-dependent hypertension in dogs. 258 96

1. To test the hypothesis that NaCl increases blood pressure, while NaHCO3 does not, we measured the effect of an NaHCO3-containing mineral water on blood pressure in stroke-prone spontaneously hypertensive (SHR-SP) and Wistar-Kyoto (WKY) rats. We compared mineral water with equimolar amounts of NaCl and demineralized drinking water in six groups of 20 rats each over 24 weeks. 2. NaCl consistently increased blood pressure in both SHR-SP and WKY compared with demineralized water, while mineral water did not. 3. We studied the possible role of sodium-regulating hormones. Sodium, potassium-dependent adenosine triphosphatase activity was decreased by NaCl and by age, but not by mineral water. The concentration of atrial natriuretic peptide was greater in SHR-SP, but was not influenced by the two regimens. Components of the renin-angiotensin-aldosterone system and 18-hydroxydeoxycorticosterone tended to decrease with NaCl, but not with mineral water. 4. Plasma pH values in the six groups of rats were not different; however, SHR-SP had consistently lower PCO2 and HCO3- values and higher anion gap values than WKY rats. These values were not influence by the two regimens. 5. NaCl elevates blood pressure in SHR-SP while NaHCO3 does not. The changes in hormones regulating sodium homoeostasis suggest that NaCl induces volume expansion while NaHCO3 does not. The effect may be related to influences on renal sodium reabsorption by chloride and bicarbonate. The possible role of increased proton excretory activity in SHR-SP remains to be determined.
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PMID:Effect of sodium chloride and sodium bicarbonate on blood pressure in stroke-prone spontaneously hypertensive rats. 284 Feb 35

1. The haemodynamic and renal effects of short-term infusion of human atrial natriuretic peptide (ANP) (1-28) were examined in sheep treated with ACTH and compared with the responses previously observed in normotensive sheep. 2. Infusion of ANP at 100 micrograms/h for 60 min in ACTH-treated sheep (5 micrograms/kg per day for 5 days) decreased blood pressure and produced a fall in both cardiac output and stroke volume. No changes were seen in heart rate and total peripheral resistance. 3. ANP produced large increases in urine volume, urinary sodium and chloride excretion, and further decreased plasma potassium concentration in the ACTH-treated sheep. Compared with normal sheep studied previously under the same conditions, the ACTH-treated sheep showed a much greater diuretic and natriuretic response to ANP, although the blood pressure response to ANP was similar in both states. 4. The change in renal responsiveness to ANP in sheep may be related to the increased blood volume of the ACTH-treated animals because volume expansion is known to enhance the renal effects of ANP.
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PMID:Enhancement of renal but not haemodynamic effects of atrial natriuretic peptide (1-28) in sheep treated with ACTH. 285 18


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