Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atrial natriuretic peptide (ANP) exerts hemodynamic effects by direct venodilation in the chick embryo. We hypothesized that ANP-induced venodilation affects ventricular diastolic filling resulting in reduced ventricular preload. Chick ANP (0.1 microgram in 10 microL of normal saline) was suffused onto the vitelline vascular bed in stage 21 (3 1/2 d) chick embryos. Equivalent aliquots of normal saline were suffused as sham controls, and normal embryos received no suffusion. We measured simultaneously dorsal aortic blood velocity and atrioventricular blood velocity with a 20-MHz pulsed-Doppler velocity meter. Analog wave forms were digitally sampled at 500 Hz, and the dorsal aortic cross-sectional area was used to calculate dorsal aortic blood flow. Passive ventricular filling volume equaled dorsal aortic stroke volume multiplied by the fraction of passive area; active filling volume equaled dorsal aortic stroke volume multiplied by the fraction of active area. Data were summarized as mean +/- SEM (n > or = 7 per group) and analyzed by analysis of variance. Cycle lengths were similar in ANP-suffused, sham control, and normal embryos. Dorsal aortic blood flow decreased from 0.49 +/- 0.04 mm3/S at baseline to 0.27 +/- 0.05 mm3/S at 4 min post-ANP suffusion (p < 0.05) and was unchanged in sham control and normal embryos (p > 0.05). Passive ventricular filling was reduced by ANP suffusion, whereas active filling was unaffected, resulting in a decreased passive/active filling ratio from 0.64 +/- 0.07 at baseline to 0.32 +/- 0.08 at 4 min in ANP-suffused embryos (p < 0.05). Passive/active ratio was unchanged in sham control and normal embryos. Thus, ANP-mediated vasodilation reduces cardiac output via decreased passive ventricular filling in the embryonic heart.
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PMID:Effect of atrial natriuretic peptide on diastolic filling in the stage 21 chick embryo. 759 86

We compared the effects of urodilatin (URO) and atrial natriuretic factor (ANF) in normal and hydronephrotic kidneys (HNK) of rats. Furthermore, the impact of blocking different vasoactive hormones on the action of natriuretic peptides on vessels of cortical (C) and juxtamedullary (JM) glomeruli was studied in HNK by using URO. In normal kidneys, effects of URO and ANF (1.2, 2.4, 4.8, 12, and 19.10(-11) mol.kg-1.min-1 i.v.) were not significantly different. At 12.10(-11) mol.kg-1.min-1, URO and ANF increased urine flow 5.4 +/- 1.7 and 3.0 +/- 0.8-fold, increased urinary sodium excretion 20.7 +/- 8.8 and 10.3 +/- 4.0-fold, and decreased blood pressure by 13 +/- 2% and 12 +/- 1%, respectively (mean +/- SEM). In HNK, URO and ANF (0.4, 0.9, and 2.0.10(-11) mol.kg-1.min-1 i.v. and local application of 0.5, 1.0, and 2.0.10(-9) M) dose-dependent dilated preglomerular vessels (max approximately 20%), constricted efferent arterioles (max approximately 15%), and increased glomerular blood flow of C glomeruli in an identical fashion. Comparing URO effects on C and JM arterioles (0.4 and 0.9.10(-11) mol.kg-1.min-1 i.v.), JM responses were about one third of C responses. Angiotensin converting enzyme inhibition (ACEI, 2.10(-6) mol.kg-1 quinapril i.v.), combined ACEI and cyclooxygenase inhibition (CYOI, 2.8.10(-5) M indomethacin), and endothelin (ET) receptor blockade (10(-6) M BQ 123 and IRL 1038) diminished preglomerular vasodilation (C and JM) caused by URO infusion. Efferent vasoconstriction (C and JM) caused by URO was exaggerated by blockade of nitric oxide synthesis (10(-5) M L-NAME) and abolished by combined ACEI and CYOI, by bradykinin receptor blockade (4.10(-8) M Hoe 140), and by ET blockade. CYOI attenuated only JM efferent constriction. Our results show that URO and ANF possess equipotent vascular and similar natriuretic effects in the rat kidney. The magnitude of preglomerular vasodilation, which is directly mediated by these peptides, depends on the basal level of endogenous vasoconstrictors, while efferent vasoconstriction may be mediated by the secondary release of ET.
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PMID:Effects of urodilatin in the rat kidney: comparison with ANF and interaction with vasoactive substances. 764 24

Our objective in these experiments was to evaluate the effects of atrial natriuretic factor on the gain of the spontaneous baroreceptor-heart rate reflex in humans. On two separate study days, we gave either atrial natriuretic factor during supine rest (16 nmol over 3 minutes, then 16 pmol/kg per minute) or saline (as vehicle) to nine healthy men (age, 23 +/- 1 years; mean +/- SEM) according to a random, double-blind design. Beat-by-beat RR interval and systolic pressure were recorded noninvasively. Sequences during which systolic pressure and the RR interval of the following beat changed in parallel (either increasing [Up] or decreasing [Down]) over at least three consecutive beats were identified and classified as baroreceptor-heart rate reflex sequences. Regression lines relating RR interval to the preceding systolic pressure were derived for each individual sequence. The mean value of the slopes of these regression lines was calculated to obtain the mean spontaneous baroreflex sensitivity for heart rate for each subject. Saline infusion did not change RR interval, systolic pressure, or number of baroreflex sequences nor the slope of the mean spontaneous baroreflex sensitivity for heart rate or slopes of Up or Down sequences. Atrial natriuretic factor, at a dose that lowers central venous pressure, did not affect systolic pressure, respiratory rate, or the number of baroreflex sequences but reduced RR interval from 952 +/- 35 to 930 +/- 40 ms (P < .04) and the mean slope of spontaneous baroreflex sensitivity for heart rate from 32.7 +/- 4.8 to 23.1 +/- 2.8 ms.mm Hg-1 (P < .04).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of atrial natriuretic factor on spontaneous baroreflex sensitivity for heart rate in humans. 776 58

Atrial natriuretic peptide (ANP) response during acute saline loading and its relationship to changes in blood pressure (BP) and sodium excretion were studied in 21 patients with essential hypertension (EH) and nine normotensive volunteers. Following 2 liters of isotonic saline infusion at a rate of 500 mL/hour, plasma ANP concentrations in patients with EH increased significantly from 69.9 +/- 6.0 (mean +/- SEM) to 103.6 +/- 17.1 pg/mL (p < 0.05) in the first hour and peaked at the second hour. In normal subjects, the increase in plasma ANP was not significant until the third hour of infusion (64.6 +/- 6.2 to 82.0 +/- 7.5 pg/mL, p < 0.05). Mean BP (MBP) remained stable and the natriuretic responses were similar in the two groups. However, hypertensive patients with a prompt rise in ANP during the initial two hours of infusion (fast responders) maintained a BP balance more efficiently than those with a delayed rise in ANP (slow responders), as the latter displayed a significant increase in MBP two hours after saline loading (126 +/- 5 to 133 +/- 5 mmHg, p < 0.05). Fast responders also had a greater percent of suppression of plasma aldosterone (-49.7 +/- 9.2 vs 15.9 +/- 42.0%, p = 0.05) one hour after saline loading, and a higher increment of natriuresis (263.9 +/- 43.8 vs 97.5 +/- 27.4%, p < 0.025) in the second hour of infusion than slow responders. Our results indicate that during acute saline loading, patients with EH have a faster and greater rise in plasma ANP than normotensives.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic peptide and blood pressure responses during acute sodium loading in patients with essential hypertension. 790 59

We examined the actions of potentially natriuretic autacoids in the isolated perfused cortical collecting duct (CCD) dissected from inbred Dahl (Rapp strain) salt-sensitive rats (SS). Atrial natriuretic peptide (ANP, 10 nM), bradykinin (BK, 10 nM), and clonidine (1 microM) were studied to determine their effects on the lumen-to-bath flux of 22Na+ (J1-->b, pmol min-1 mm-1), hydraulic conductivity (Pf, micron/s), and transepithelial voltage (VT, mV). ANP and BK have been shown by others to significantly reduce net Na+ reabsorption and hydraulic conductivity in the Sprague-Dawley (SD) rat CCD, but previous results from our laboratory showed no ANP or BK effect in the SD CCD. In the present study, we were also unable to observe any effect of either ANP or BK in the SS rat CCD. However, in the presence of AVP, clonidine (a partial alpha 2-adrenergic receptor agonist) significantly reduced J1-->b and Pf from 139 +/- 6 (SEM) to 88 +/- 7 and from 959 +/- 176 to 490 +/- 73, respectively. In addition, clonidine significantly depolarized VT from -14.5 +/- 2.8 to -11.2 +/- 1.8. However, unlike its effects in the SD rat CCD, yohimbine (300 nM, an alpha 2-adrenergic receptor antagonist) did not significantly reverse the effects of clonidine on J1-->b, Pf or VT in the SS rat CCD.
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PMID:Clonidine, but not bradykinin or ANP, inhibits Na+ and water transport in Dahl SS rat CCD. 835 63

Levels of calcitonin gene-related peptide (CGRP), a vasodilator peptide present in nerves and airway endocrine cells of the rat respiratory tract, are increased in hypoxic lung and decreased in plasma, suggesting impaired CGRP release. We wanted to determine whether there was an adaptive functional response to reduced CGRP levels in hypoxia. Density of binding sites for CGRP were compared with its vascular actions following hypoxia, and with binding following administration of the sensory neurotoxin capsaicin to deplete neural CGRP. Autoradiography of lung sections incubated with 125I-labelled CGRP and other vasoactive peptides was used to quantify their binding sites, in male Wistar rats exposed to periods of hypoxia (inspiratory oxygen fraction (FI,O2) = 0.1) ranging 0-10 days (n = 5 each), in controls, and in rats treated neonatally with capsaicin. Relaxation to CGRP was compared in pulmonary artery of control and hypoxic rats. CGRP binding was seen in the vascular endothelium and was significantly elevated after 5 days of hypoxia (mean +/- SEM: control 4.6 +/- 0.4 versus hypoxic 16.6 +/- 2.4 amol.mm-2). CGRP-induced (5 x 10(-7)M) relaxation of pulmonary artery was reduced, compared with controls, following 8 and 21 days of hypoxia (mean +/- SEM) percentage of relaxation to phenylephrine: 78 +/- 3, 36 +/- 5 and 32 +/- 3, respectively) and was abolished by removal of endothelium. Capsaicin treatment also significantly elevated vascular CGRP binding. Atrial natriuretic peptide (ANP) binding levels were decreased in smooth muscle of all blood vessels after 7 days of hypoxia, but endothelin-1 (ET-1) and vasoactive intestinal peptide (VIP) binding was unchanged. We conclude that the vasodilator effects of CGRP are endothelium-dependent and, whilst they are reduced in hypoxic lung, this is not due to reduction in receptors, thereby implicating alterations in the nitric oxide guanylyl cyclase system. Furthermore, adaptive responses in some peptide binding sites occur in hypoxia, which may be due to changes in endogenous peptide levels.
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PMID:Decreased endothelium-dependent pulmonary vasodilator effect of calcitonin gene-related peptide in hypoxic rats contrasts with increased binding sites. 866 97

Because changes in extracellular volume during dialysis cause reflex neurohonnonal changes that may influence parathyroid hormone (PTH) release independently of calcium, the influence of isotonic volume depletion (by isolated ultrafiltration) and central hypovolemia (70 degrees tilt) on serum PTH1-84 was studied in 16 hemodialysis patients. Tilting was performed in volume depleted state, i.e., immediately after hemodialysis. In the control study, patients underwent sham ultrafiltration (UF = 0) and after dialysis maintained the supine position for the same length of time they remained in the tilt position in the active experiment. Isolated ultrafiltration (-2.3 +/- SEM 0.3 L) caused a 21% fall in mean arterial pressure (from 101 +/- 6 to 80 +/- 6 mmHg, P < 0.01), a fall that was accompanied by a marked increase in plasma catecholamine levels (norepinephrine P < 0.001, epinephrine P < 0.025), in plasma renin activity (P < 0.001) and in plasma arginine vasopressin (P < O.001). Atrial natriuretic factor showed a slight reduction, whereas the plasma endothelin-1 level did not change. Serum Ca showed the expected, hemoconcentration-dependent rise (from 4.1 +/- 0.1 to 4.4 +/- 0.1 meq/L, P < 0.01). Interestingly, UF caused a marked rise in plasma PTH1-84 concentration (from 252 +/- 62 to 335 +/- 72 pg/ml, P < 0.01). UF-induced changes in serum PTH1-84 were related to norepinephrine changes (r = 0.57) as well as to plasma renin activity (r = 0.50). After hemodialysis, tilting induced a pronounced rise in serum PTH1-84 (from 102 +/- 29 to 200 +/- 55 pg/ml), and these changes were slightly related to plasma epinephrine (r = 0.49) but independent of other parameters. In the control experiment, neither sham UF nor recumbency modified serum PTH. In hemodialysis patients, serum PTH is sensitive to changes in extracellular and central blood volume of magnitude sufficient to decrease arterial pressure. Avoiding marked volume stimuli might help to refine the interpretation of the Ca/PTH curves during hemodialysis in these patients.
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PMID:The influence of volume depletion and central hypovolemia on the plasma concentration of parathyroid hormone in dialysis patients. 933 86

Atrial natriuretic peptide (ANP) is synthesized in the kidney but its physiologic significance there is unclear. To determine whether renal expression of the ANP gene is regulated, renal ANP mRNA expression was assessed in remnant kidneys after 5/6 nephrectomy in Munich-Wistar rats. In normal sodium intake groups, ANP mRNA expression in the remnant kidney was significantly increased by 5.0 +/- 0.8-fold (n = 7, mean +/- SEM) at 4 d when compared with sham-operated controls (n = 6, all sham-operated groups) (*P < 0.001 by Scheffe's test) and by 28.3 +/- 5.1-fold at 14 d. This latter response was markedly diminished to 7.6 +/- 2.1-fold (n = 7, versus sham) in rats maintained on a low sodium diet. At 4 d, on the other hand, no significant downregulation was observed with dietary sodium restriction. Because natriuretic peptides have previously been shown by us to play a major role in the adaptive responses of remnant nephrons to renal mass ablation, these data suggest that ANP of renal origin may contribute to the overall mechanism for enhancing sodium excretion in the face of declining nephron number.
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PMID:Upregulation of atrial natriuretic peptide gene expression in remnant kidney of rats with reduced renal mass. 972 69

Abstract Experiments examined release of atrial natriuretic factor (ANF), measured by radioimmunoassay, from acutely prepared explants of rat hypothalamus maintained in vitro by intra-arterial perfusion of artificial cerebrospinal fluid. Perfusates collected from intact preparations contained 6.1 +/- 0.6 pg (mean +/- SEM) of ANF per 2-min sample. Following a 3-min infusion of noradrenaline (60 muM), ANF release increased significantly (P<0.05) to 11.4+/-1.4 pg/sample. Media collected from hypophysectomized preparations showed the same basal ANF release (6.8 +/- 0.9 pg/sample) as intact preparations, but demonstrated no significant increase after noradrenaline infusions. Levels of spontaneous ANF release were not appreciably affected by the absence of the paraventricular nuclei and/or the anteroventral third ventricle area. Extracted material from the perfusate by reverse-phase high performance liquid chromatography revealed two main peaks of immunoreactive ANF: a small molecular weight form that coeluted with synthetic ANF (99-126) and with similar biological activity in a radioreceptor assay, and a larger molecular weight form with the same elution profile as the ANF (1-126) prohormone. These observations indicate that the ANF released from perfused rat hypothalamic explants contains distinct contributions from the hypothalamus (sites undetermined) and the neurointermediate lobe.
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PMID:Release of atrial natriuretic factor from intact and hypophysectomized rat hypothalamic expiants. 1921 Apr 46


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