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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Binding sites of atrial natriuretic peptide in the cerebral microvessels and choroid plexus of spontaneously hypertensive rats (SHR) and Wistar Kyoto control rats (WKY) were measured. In the microvessels, the number of ANP binding sites was lower in SHR than WKY, but there was no difference in affinity of binding sites for the ligand between SHR and WKY. In the choroid plexus, the number of ANP binding sites was lower and the affinity for the ligand was higher in SHR than in WKY. These results suggest that the physiological function regulated by the ANP receptors in the cerebral microvessels and choroid plexus were altered in hypertension and that ANP receptors in the cerebral microvessels and choroid plexus were differentially regulated.
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PMID:Atrial natriuretic peptide receptors in cerebral microvessels and choroid plexus of spontaneously hypertensive rats. 216 50

A monoclonal antibody to alpha-human atrial natriuretic polypeptide (alpha-hANP), KY-ANP-I, has been produced by fusion of a nonproducing mouse myeloma cell line, X63-Ag8.653, with spleen cells from BALB/c mice immunized with synthetic alpha-hANP conjugated to bovine thyroglobulin using the carbodiimide coupling procedure. Hybridomas were screened for antibody production by radioimmunoassay using culture media and 125I-alpha-hANP. They were cloned by the limiting dilution technique, expanded in culture, and injected intraperitoneally into BALB/c mice. The obtained antibody belonged to the immunoglobulin G1 subclass. Analysis by a Scatchard plot revealed a high affinity for alpha-hANP, with an association constant of 3.1 x 10(10) M-1. With this monoclonal antibody, a specific radioimmunoassay for alpha-hANP has been established. The antibody in mouse ascites was available for radioimmunoassay at a final dilution of 1:10(6). Values of IC10 and IC50 in this radioimmunoassay were 3 and 30 fmol/tube, respectively. The radioimmunoassay showed a cross-reactivity of 0.9% with alpha-rat ANP. alpha-hANP-(8-22) and alpha-ANP-(1-6) exhibited less cross-reactivity than alpha-rat ANP on a molar basis. There was no cross-reaction with alpha-ANP-(17-28). Thus, the recognized epitope must be located in the N-terminal half of the ring structure of alpha-hANP including Met12 residue. This radioimmunoassay could detect gamma-hANP and beta-hANP as well as alpha-hANP. The monoclonal antibody was also useful for immunohistochemical studies. ANP-positive cells were finely stained in the human atrium using the avidin-biotin-peroxidase complex technique.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1988 Aug
PMID:A monoclonal antibody to alpha-human atrial natriuretic polypeptide. 245 52

The role of human atrial natriuretic peptide (alpha-hANP) in the regulation of blood pressure (BP) and extracellular fluid volume (ECFV) remains elusive. This is of particular interest in chronic renal failure, in which first, increased sodium and water retention plays a major pathogenetic role in the development of hypertension, and second, altered secretion and/or metabolism of alpha-hANP may contribute to fluid volume and BP regulation. In the present study the relationship between renal function, BP, and circulating alpha-hANP was investigated in 16 non-dialyzed patients with stable chronic renal failure (CRF) without edema. Analysis of potential molecular heterogeneity of immunoreactive (ir) ANP was performed by gel permeation chromatography of plasma extracts from normotensive patients with CRF. Serum creatinine concentrations averaged 435 +/- 76 mumol/l ranging from 127 to 1187 mumol/l, systolic and diastolic BP averaged 158 +/- 4 and 94 +/- 2 mmHg, respectively. Plasma alpha-hANP concentrations ranged from 5 to 75 with a mean of 23 +/- 4 pmol/l as compared to a mean of 10 +/- 1 pmol/l in healthy volunteers (p less than 0.05). A significant linear correlation between plasma alpha-hANP and serum creatinine concentrations (r = 0.92) was observed; a weaker correlation was found between mean arterial pressure and alpha-hANP (r = 0.66). Chromatographic analysis revealed considerable amounts of higher molecular weight circulating ir-ANP, approximately 15,000 Da, in addition to the biologically active small mol wt ANP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human atrial natriuretic peptide in non-dialyzed patients with chronic renal failure. 252 67

Atrial natriuretic peptide is a recently discovered cardiac hormone with natriuretic, vasodilatory and hypotensive activities. The role of this hormone in the pathophysiology of hypertension is of particular interest. In contrast to an earlier concept, a deficiency of the atrial peptide could not be found in animal models of hypertension or in patients. ANP plasma levels were elevated in SHR with accelerated hypertension, in salt-sensitive Dahl rats, in rats with DOCA-salt-hypertension and in animals with renovascular hypertension. Elevated ANP levels under these conditions can be explained by an expansion of the intravascular volume or by an elevated atrial wall stretch induced by the hypertension itself. In patients with primary hypertension, plasma levels of the peptide are raised in some patients and are normal in others. Plasma ANP levels correlate with age, blood pressure and signs of left ventricular hypertrophy. A negative correlation is described between ANP and renin. Measurement of plasma ANP levels does not allow a differentiation between primary and secondary forms of hypertension. Elevated ANP levels are also found in primary hyperaldosteronism and in renal failure. Stimulation of ANP secretion by physical exercise and dietary salt loading is maintained in hypertension. Infusion of 1-28-hANP leads to a reduction in systemic arterial pressure in normotensives and hypertensives. The natriuresis induced by exogenous ANP is more pronounced in hypertensives. Stimulation of endogenous ANP secretion does not prevent the rise in blood pressure possibly due to a reduction in ANP receptors in target tissues.
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PMID:[Atrial natriuretic peptide and its significance for arterial hypertension]. 253 Dec 53

In the first part of this study we selected 24 hypertensive subjects (11 males, 13 females, mean age 55.4 +/- 10.2 years) affected by essential arterial hypertension (EAH). Eleven people (5 males, 6 females, mean age 21.6 +/- 9.5 years) had one or two hypertensive parents. Seventeen subjects (8 males, 9 females, mean age 56.4 +/- 5.9 years) were the control group. Plasmatic ANP was measured using the RIA method, after extracting the peptide on Sep-Pak C18 cartridges. The results show the following ANP values: healthy control subjects 27.6 +/- 8.6 pg/ml; offspring of essentially hypertensive subjects 25.6 +/- 7.7 pg/ml; essentially hypertensive subjects 45.5 +/- 24.9* pg/ml* (P less than 0.005). In the second part of our study, we evaluated the plasma levels of this hormone in a group of subjects undergoing dialysis. The group consisted of 21 subjects (12 males, 9 females, mean age 63.1 +/- 10.5 years), 11 of whom were affected by EAH. ANP evaluation was done during the dialysis after a "long" dialytic interval of three days. Both groups showed a noticeable increase in ANP levels, even if the hypertensive group had overall higher values (254.5 +/- 134.9 pg/ml, vs. 188.7 +/- 113.7 pg/ml). All subjects, after dialysis, had ANP values significantly lower than the initial ones.
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PMID:Evaluation of plasmatic ANP levels in subjects affected by essential arterial hypertension and in a group of patients undergoing dialysis. 253 81

The study included 15 healthy individuals aged 37.3 +/- 7.7 years and 27 patients with the primary uncomplicated blood hypertension (stages I and II according to WHO classification) of the comparable age, untreated and given a diet containing 100-120 nM Na+ daily. Plasma ANP concentrations were measured prior to and after 30, 60, and 90 minutes following 40 mg furosemide intravenously. An increase in 1-minute urine output and 1-minute Na+ excretion in the urine were determined during 90 minutes following furosemide administration. A significant decrease in ANP plasma levels was noted in all examined individuals following furosemide administration in all time intervals comparing with baseline values. An increase in 1-minute urine output and 1-minute sodium excretion with the urine significantly correlated with plasma ANP decrease during 90 minutes following furosemide administration. The obtained results suggest that furosemide inhibits ANP secretion in the patients with uncomplicated primary hypertension similarly to healthy individuals.
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PMID:[Effect of furosemide on the plasma level of atrial natriuretic peptide (ANP) in healthy persons and in patients with uncomplicated primary arterial hypertension]. 253 30

High concentration of atrial natriuretic peptide (99-126) (ANP) receptors were localized by quantitative autoradiography in superior cervical and stellate ganglia from young and adult Wistar Kyoto (WKY) rats. ANP increased cyclic GMP formation in stellate ganglia from adult rats. Both young and adult spontaneously hypertensive rats (SHR) had a much lower number of ANP receptors in the sympathetic ganglia. In spite of low receptor concentration, the cyclic GMP response to ANP in SHR was unchanged. These results suggest the existence of physiologically active ANP receptors in the rat sympathetic ganglia. These receptors may also be involved in the pathophysiology of spontaneous hypertension.
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PMID:Atrial natriuretic peptide receptors in sympathetic ganglia: biochemical response and alterations in genetically hypertensive rats. 282 2

The influence of a 6-week treatment of female Wistar rats with one-kidney, one clip (1-K, 1 C) renal hypertension, with the calcium antagonist nifedipine on plasma volume, red cell Na+ handling and plasma atrial natriuretic peptide immunoreactivity (ANP-IR) was studied. Measurements were performed at 2 and 6 weeks after surgery. In 1-K, 1 C rats plasma volume was increased and red cell Na+ pump activity was reduced only after 2 weeks. Blood pressure, heart weights and plasma ANP were massively increased after both 2 and 6 weeks. 1-K, 1 C-rats treated with nifedipine had normal plasma volume, plasma ANP, and red cell Na+ pump activity in comparison with sham-operated rats. Increases in blood pressure and heart weights were attenuated. It is concluded that 1-K, 1 C hypertension in the rat is associated with cardiomegaly, rise in plasma ANP, initial hypervolemia and depression of the membrane Na+ pump. Nifedipine prevents the occurrence of hypervolemia and secondary phenomena such as rises in plasma ANP and cardiomegaly. This may play an important contributory role in the prevention of pathological sequelae.
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PMID:Modulation by chronic nifedipine of plasma atrial natriuretic peptide, cell Na+ transport and plasma volume in rats with renal hypertension. 284 89

The effects of acute volume expansion and acute salt loading on the plasma levels of immunoreactive atrial natriuretic peptides (ir-ANP's) were investigated in conscious adult (16 weeks) Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Basal plasma concentrations of ir-ANP's were similar (108 +/- 9 pg/ml and 105 +/- 8 pg/ml, respectively) in hypertensive and normotensive rats. In both strains mean arterial pressure, heart rate and plasma catecholamines were unaltered by acute volume expansion but significantly elevated by acute salt loading. However, both acute volume expansion and acute salt loading increased plasma concentrations of ir-ANP's similarily in SHR and WKY rats, independent of blood pressure or plasma catecholamine levels. Our findings show that chronic hypertension in SHR does not result in changes in basal or VOL- and SAL-stimulated levels of circulating ir-ANP's.
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PMID:Plasma levels of atrial natriuretic peptides in conscious adult spontaneously hypertensive rats. 294 Nov 86

The hypothesis of a natriuretic factor-originally an intriguing possibility and now an experimentally documented reality-has occupied the minds of scientists for more than 30 years. It has attracted not only experts in salt and water metabolism but also those interested in hypertension, because of the well known link between sodium homeostasis and blood pressure regulation. There are at least two distinct types of natriuretic substances: one is an inhibitor of the Na+K+ATPase and has been proposed to contribute to a rise in blood pressure; the other, now isolated from atrial tissue, is vasodilatory, natriuretic, diuretic, and has been demonstrated to decrease blood pressure. Our knowledge of regulation and function of this ANP has increased rapidly since its detection. Its role in blood pressure regulation is now fairly well understood. As depicted in Fig. 1, both synthesis and release of ANP are induced by atrial and ventricular wall stretch. In hypertension, distension of the left atrium and ventricle may be of particular importance for ANP release. The endocrine function of myocardial cells is stimulated in response to wall stretch in the ventricle. ANP is synthesized and stored as a 126 amino acid prohormone. Enzymatic processing of this prohormone to the circulating forms ANP 1-98 and ANP 99-126 takes place within the myoendocrine cells. The biological effects of ANP 1-98 are as yet unknown. ANP 99-126 acts at multiple sites to reduce blood pressure. One may distinguish between acute and more chronic effects. The acute effects include shift of fluid to the extravascular compartment and vasorelaxation. This shift is indicated by the rapidly developing rise in haematocrit, which is observed in intact as well as in nephrectomized rats and therefore not due to diuresis alone. The reduction of blood volume in addition to an increase in venous capacitance may be responsible for the reduced cardiac output. The latter may cause a reflex activation of the sympathetic nervous system and an increase in peripheral resistance, thereby overriding the vasodilator effects of the peptide. ANP appears to have a 'de-pressor' effect rather than a direct vasodilator effect. A lowering of peripheral resistance in response to ANP is not observed in normotensives, but is readily seen in at least certain forms of hypertension associated with an increased vascular tone. This most likely explains the discrepancy in the haemodynamic responses to ANP in normotensives and hypertensives.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Atrial natriuretic peptide: a new factor in blood pressure control. 295 21


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