Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the connection of diastolic activity of smooth muscles of blood vessels with development of hypertension, plasma cAMP, cGMP, TXB2, 6-K-PGF1 alpha, ANP, SP were determined with radioimmunoassay, of 173 hypertension patients with Liver Yang exuberance (LYE) 91 cases, and Yin deficiency and Yang exuberance (YDYE) 82 cases. In addition, 228 health subjects served as control. The results showed that the levels of cAMP, cGMP and TXB2 in both LYE and YDYE groups were higher than those in the control group, but the levels of ANP, SP and cAMP/cGMP ratio in LYE and YDYE groups were lower than those in the control. As to the level of 6-K-PGF1 alpha, no significant variance was found between these groups. After TCM-WM treatment, the levels of cAMP, cGMP and TXB2 in LYE and YDYE groups got down, as compared with those in the control, adversely the levels of ANP, SP and 6-K-PGF1 alpha in LYE and YDYE groups turned up significantly. However the cAMP/cGMP ratio had no remarkable change between these groups. The linear regression analyses between the diastolic pressure and ANP or SP both proved negative correlation (r = -0.36, P less than 0.05; r = -0.35, P less than 0.05). The findings indicated that the TCM-WM treatment was the most effective among the therapies employed in the study, and that this therapy affected the diastolic activity of smooth muscles by modulating the above factors existing in the nervous and endocrine systems of the patients with hypertension.
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PMID:[Experimental study on the treatment of hypertension with combined traditional Chinese and Western medicine]. 172 72

Atrial natriuretic peptide has been considered to be a major regulator in the body's water and salt homeostasis. Antagonizing those mechanisms leading to volume retention and overload (renin, angiotensin, aldosterone), ANP has been suggested to play a critical role in the pathology of certain diseases like renal failure, congestive heart failure or hypertension. In this regard, we measured ANP plasma concentration in normal healthy dogs and dogs with renal failure, congestive heart failure and Cushing syndrome. ANP levels were slightly decreased in dogs with Cushing disease (n = 9; 5.5 +/- 2 fmol/ml), increased in renal failure (n = 7; 16.2 +/- 5.8 fmol/ml, p less than 0.05) and markedly augmented in dogs with congestive heart failure (n = 14; 52.9 +/- 29.75 fmol/ml, p less than 0.01) as compared to healthy dogs (n = 6; 8.3 +/- 3.5 fmol/ml). Furthermore, characterization of the measured immunoreactivity (IR-ANP) revealed, that up to 50% of the IR-ANP in dogs with congestive heart failure corresponds to the ANP precursor molecule, not found in healthy subjects. This fact might present one possible explanation for the attenuated response to ANP in congestive heart failure. In addition, this finding may also serve a diagnostical purpose.
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PMID:[Diagnostic possibilities of ANP blood measurements in dogs]. 182 66

Atrial natriuretic factor (ANP) is present in neuronal cells of the locus coeruleus and its vicinity in the pontine tegmentum and moderate amount of ANP is detectable in this area by radioimmunoassay. The ANP (both peripheral and brain-born) is known as a neuropeptide which may influence the body salt and water homeostasis and blood pressure by targeting both central and peripheral regulatory mechanisms. Whether this pontine ANP cell group is involved in any of these regulatory mechanisms, the effect of various types of hypertension and experimental alterations in the salt and water balance on ANP levels was measured by radioimmunoassay in the locus coeruleus of rats. Adrenalectomy, as well as aldosterone and dexamethasone treatments failed to alter ANP levels in the locus coeruleus. Reduced ANP levels were measured in spontaneously hypertensive (both young and adult) rats, and in diabetes insipidus (Brattleboro) rats with vasopressin replacement. In contrast to these situations, elevated ANP levels were found in rats with DOCA-salt or 1-kidney-1-clip hypertension. These data suggest a link between ANP levels in the locus coeruleus and fluid volume homeostasis. Whether this link is causal and connected with the major activity of locus coeruleus neurons (noradrenergic influence on brain regulatory activities) needs further informations.
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PMID:Atrial natriuretic peptide in the locus coeruleus and its possible role in the regulation of arterial blood pressure, fluid and electrolyte homeostasis. 183 23

In the past several years great progress has been made in the understanding of the (patho) physiology of ANP. Because an inhibitor of ANP is not available for human use, there is still discussion about the physiological role of ANP. Nevertheless, from the studies described above the evidence is accumulating that ANP has a role in protecting against fluid overload and hypertension by means of inducing natriuresis, inhibition of the renin-angiotensin-aldosterone system and vasopressin and by vasodilation. The therapeutic potential of modulation of the ANP system seems promising, but must await further research.
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PMID:Atrial natriuretic peptide. 183 64

Since pulmonary artery hypertension (PH) complicates advanced stages of cystic fibrosis (CF), we wondered whether plasma concentrations of h-ANP would be increased in adult patients with CF. Furthermore, if only the right ventricle is faced with an increased afterload in these patients, the increased h-ANP plasma levels should stem primarily from the right atrium. To test this hypothesis we studied 12 adult patients with CF in a clinically stable condition using right heart catheterization. Mean pressures were measured in the right atrium (Pra) and pulmonary artery (Ppa), pulmonary capillary wedge (PCWP) position, and blood were drawn from the pulmonary artery and from a peripheral vein to determine h-ANP. Plasma levels in the pulmonary artery were significantly higher than in a peripheral vein (54.3 +/- 6.0 pg/ml vs. 32.2 +/- 4.4 pg/ml; p less than 0.001). Four of the 12 patients had PH (Ppa, 25.8 +/- 2.9 mmHg) whereas 8 patients exhibited normal pulmonary artery pressures (Ppa, 15.9 +/- 0.7 mmHg). Patients with PH had higher Pra (4.2 +/- 0.4 mmHg) than patients with CF without PH (1.9 +/- 0.7 mmHg; p less than 0.05). Plasma h-ANP concentrations were significantly higher in patients with CF with PH (70 +/- 10.4 pg/ml in the pulmonary artery; 42.6 +/- 4 pg/ml in a peripheral vein) than in patients with normal pulmonary artery pressure (43 +/- 3.3 pg/ml in the pulmonary artery; p less than 0.01; 24.7 +/- 5.6 pg/ml in a peripheral vein; p less than 0.05). Although our results are derived from a small group of patients with CF, we conclude from our results that in patients with CF PH may cause increased h-ANP secretion. The right atrium seems to be a major source.
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PMID:Raised circulating plasma levels of atrial natriuretic peptide in adolescent and adult patients with cystic fibrosis and pulmonary artery hypertension. 183 29

Chronic (12 weeks) peroral administration of cadmium chloride to albino rats in a dose of 2.5 mg/100 g body weight results in arterial hypertension characterized by the increase in systolic blood pressure up to 148 +/- 1.8 mm Hg (vs. 115.4 +/- 1.5 mm Hg in the control animals); the increase in vascular resistance, left ventricular cardiomyocyte hypertrophy, as well as by hypertrophy of arterial walls, the decrease in the ventricular index, the activation of synthesizing function of atrial endocrine cardiomyocytes; enhanced secretion of ANP; a more than two-fold increase in plasma myoglobin concentration, as well as by the development of cadmium-induced nephropathy. In the rehabilitation period (9 weeks) a relatively quick fall in the blood pressure is observed, as well as morphological features of myocardial and renal function recovery, suggesting the nonpersistent nature of cadmium-induced hypertension.
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PMID:[Morphofunctional characteristics of cadmium-induced arterial hypertension]. 189 57

Male Sprague-Dawley rats were uninephrectomized and given either deoxycorticosterone (DOC) pivalate (12.5 mg three times weekly) and 1% NaCl/0.2% KCl to drink for 4 weeks (DOC-treated), after which DOC was stopped and tap water substituted (post-DOC), or tap water to drink throughout (controls), DOC treatment increased blood pressure, serum sodium, plasma atrial natriuretic peptide (P-ANP) and plasma deoxycorticosterone (P-DOC) (P less than 0.05), while serum potassium, plasma renin and plasma angiotensin II were lower (P less than 0.05) than in control animals. Plasma vasopressin (P-AVP) was also raised but not significantly. These changes persisted for up to 4 weeks post-DOC and, in the case of plasma renin, plasma angiotensin II, P-AVP and P-ANP, for up to 12 weeks. Total body sodium was also increased at 2 weeks post-DOC (P less than 0.05). Rats which were adrenalectomized after 4 weeks of DOC treatment in which DOC injections were stopped, then drank either NaCl/KCl or tap water; blood pressure and P-DOC remained elevated while plasma renin remained suppressed. There were more deaths in rats given NaCl/KCl (five of six) than in the group given water (one of six). Rats treated with a subcutaneous DOC silastic implant had a comparable rise in blood pressure to rats given DOC injections. However, after removal of the implant, while blood pressure remained elevated, P-DOC levels were not raised and plasma renin rose to control levels after 4 weeks. These findings indicate that, in rats given DOC injections, post-DOC hypertension results from sodium and fluid retention as a consequence of chronic hangover of exogenously administered DOC.
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PMID:Hormone and electrolyte changes in post-deoxycorticosterone salt hypertension in rats. 196 84

In order to investigate the possible involvement of ANP in the salt dependent hypertension of the DS rats the concentrations of immunoreactive atrial natriuretic peptides (ANP-IR) in atria, plasma and brain of salt loaded and control fed DS and DR rats were determined. On a low salt diet the ANP-IR concentrations in atria, hypothalamus and basal ganglia of DS rats were higher versus DR rats. Salt loading results in a decrease of ANP-IR in left DS atria and an increase in plasma and brain stem of DS rat versus control and DR rat. The data are compared with other studies about ANP performed in Dahl rats, SHR and WKY rats. The possible reasons for the found distribution of ANP-IR are discussed.
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PMID:ANP concentrations of atria, plasma and brain in Dahl S (DS) and Dahl R (DR) rats. 214 Jul 37

The heart atrium, as well as under certain pathophysiological conditions the ventricle, synthesize and release ANP. Exerting natriuretic, diuretic and vasorelaxant effects, this peptide plays an important role in the body's blood volume and blood pressure homeostasis. Whereas the pharmacological actions of ANP have been quite convincingly demonstrated, its physiological and pathophysiological role is less well defined. ANP plasma levels tend to be increased in diseases with salt and water retention, such as essential hypertension, congestive heart failure, renal failure or liver cirrhosis. With regard to its hemodynamic effects, ANP seems to be beneficial in patients with hypertension. ANP appears to have little therapeutic potential as a diuretic in patients with congestive heart failure and liver cirrhosis, possibly due to the decreased renal responsiveness to ANP in these diseases. However, ANP might to be a valuable therapeutic agent in acute renal failure.
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PMID:[Atrial natriuretic peptide. II. Pathophysiology and possible clinical significance. Review]. 214 57

We determined plasma and cardiac immunoreactive atrial natriuretic polypeptide (ir-ANP) levels in rats treated with deoxycorticosterone acetate (DOCA) and sodium chloride for 1, 7, and 28 days. Systolic blood pressure of DOCA-salt rats began to increase from the 7th day and reached 191 +/- 7 mmHg at the 28th day. One day after treatment with DOCA-salt, plasma levels of ir-ANP were increased compared to that of control rats. This was accompanied by decreased cardiac ir-ANP content. However, at the 7th day of DOCA-salt treatment, both plasma and cardiac ir-ANP levels of DOCA-salt rats were not different from those of control animals. At the 28th day, DOCA-salt rats had high plasma ir-ANP levels and no significantly different cardiac ir-ANP content compared to the controls. These data suggest that there are time-related changes in plasma ANP concentration during the development of DOCA-salt hypertension and higher plasma ANP levels might not necessarily be associated with a decreased cardiac ANP content.
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PMID:Phasic plasma atrial natriuretic polypeptide changes in DOCA-salt hypertensive rats. 214 77


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