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

Several studies (including ours) in patients with moderate hypertension indicate that beta-adrenergic blockers exert their antihypertensive action in part by increasing ANP secretion. There is also strong evidence that (beta 1- adrenergic receptors are mainly involved in this action. In this article we provide an overview on some of these studies.
 ...
PMID:Beta-blockers and atrial natriuretic peptide (ANP) in hypertension. 1265 98

Regular physical activity can have a favourable impact on other risk factors of ischaemic heart disease (IHD) and associated diabetes (DM), such as obesity, hypertension, dyslipidaemia, insulin resistance and others. This important part of treatment of diabetes is frequently difficult to implement because of the lack of willingness ("adherence") of type 2 diabetics to practice regular exercise, and unequivocal data are lacking on the intensity of exercise which will influence effectively these risk factors and be at the same time safe, readily available and psychologically acceptable. The objective of the work was to find out whether walking, i.e. locomotor activity with a low to medium intensity can effectively influence parameters of aerobic capacity and blood lipids. The authors submit the results of two groups of type 2 diabetics. The experimental group B (n = 10, age 57 +/- 7 years, BMI 31 +/- 3, duration of DM 8 +/- 5 years) participated in a 12-week training programme of walking; at the beginning and at the end of this period indicators of aerobic capacity at the level of the anaerobic threshold (VO2ANP) were evaluated as well as at the level of the symptom limited maximum (VO2SL, TepO2SL), and the blood lipid levels. In the control group A (n = 6, age 58 +/- 7 years, BMI 32 +/- 4) indicators of aerobic capacity and blood lipids were assessed after a 12-week period of the usual habitual physical activity. In group B the 12-week walking training led to significant improvement of parameters of aerobic capacity at the level of the anaerobic threshold (ANP), oxygen pulse at the level of the symptom limits maximum (SL) and a significant reduction of total and LDL cholesterol. In the control group no significant changes occurred in aerobic capacity nor blood lipid values. The training programme where walking was selected as physical activity with a low to medium intensity can be considered suitable for everyday life of motivated patients with type 2 diabetics, preferably in the form of a domestic training programme. The prerequisite of success is its regular and frequent evaluation by health professionals.
 ...
PMID:[The effect of walking exercise on aerobic capacity and serum lipids in type 2 diabetics]. 1272 89

The heart produces two related hormones, atrial (ANP) and B-type natriuretic peptides (BNP). Both are synthesized in the atria and ventricles as polypeptides, which upon release are split into ANP and BNP and the N-terminal fragments N-ANP and N-BNP (together named natriuretic peptides, NPs). The most important function of ANP and BNP is protection against volume-overload, by increasing natriuresis and diuresis amongst other things. Both peptides can be considered the natural antagonist of the renin-angiotensin system. Clearance occurs through a specific receptor and through enzymatic break-down by neutral endopeptidase (NEP). All 4 NPs circulate in plasma. Elevated concentrations of NPs are found when the filling pressures of the heart are elevated, as in acute coronary syndromes and congestive heart failure. Measurement of NPs is a useful tool in the differential diagnosis of cardiac versus non-cardiac dyspnoe (high negative predictive value), in the identification of heart failure patients most at risk and in optimising therapy in heart failure. In right ventricular overload caused by (corrected) congenital heart diseases and acute lung embolism, NP concentrations are also elevated, as they are in renal failure and in hypertension associated with left ventricular hypertrophy. Infusions of ANP and BNP lead to increased natriuresis and diuresis. Pharmacologically, increases in ANP and BNP can be accomplished with NEP-inhibitors or beta-blockers. Measurement of NP(s) will become as important for estimation of heart function as creatinine is for estimation of renal function.
 ...
PMID:[Atrial and B-type natriuretic peptides: from the research lab to clinical practice]. 1273 63

1. Homozygous deletion of the pro-atrial natriuretic peptide (Nppa) gene (ANP-/-) has been associated with both cardiac hypertrophy and salt-sensitive hypertension in mice, suggesting that cardiac hypertrophy in ANP-/- mice may be related, at least in part, to increased afterload. 2. To test the hypothesis that cardiac hypertrophy in ANP-/- mice is independent of blood pressure, male ANP-/- and wild-type ANP+/+ mice were fed a low (0.05%) or basal (0.55%) NaCl diet. Five weeks later, mean arterial pressure (MAP) was measured in conscious mice; the whole heart, atria, left and right ventricles (LV and RV, respectively), brain, lung, kidney, liver and spleen were weighed and fixed for histological analysis. Separate groups of mice were subjected to echocardiographic examination under tribromoethanol anaesthesia. 3. Mean arterial pressure and atrial, LV and RV mass were greater in ANP-/- mice than in ANP+/+ mice fed the basal salt diet. Salt depletion equalized MAP in the two genotypes, but did not alter the relative cardiac hypertrophy in ANP-/- mice. The ANP-/- mice had significant LV cardiomyocyte hypertrophy when fed either basal or low-salt diets. 4. Left ventricle chamber dimensions did not differ between genotypes, but were significantly reduced in mice fed the low-salt diet; LV posterior wall and septal thickness were greater in ANP-/- than ANP+/+ mice and were not altered by diet, indicating a concentric pattern of LV hypertrophy in ANP-/- mice. Left ventricle function (cardiac output, stroke volume, ejection fraction, circumferential wall stress and velocity of circumferential wall shortening) did not differ between strains on either diet; circumferential wall stress was reduced in the low-salt groups; other functional parameters were not altered by diet. 5. These findings indicate that ANP deletion results in cardiomyocyte hypertrophy and biventricular hypertrophy independent of blood pressure, supporting the concept that ANP has direct antihypertrophic effects in the heart.
 ...
PMID:Pressure-independent enhancement of cardiac hypertrophy in atrial natriuretic peptide-deficient mice. 1285 24

Left ventricular hypertrophy, in particular concentric, accompanying hypertension is an independent risk factor of sudden death and other serious cardiovascular complications. It is still not clear how ANP and BNP are related to various types of left ventricular geometry and whether BNP is a better predictor of left ventricular hypertrophy and dysfunction than ANP. The aim of the study was estimation of plasma ANP and BNP levels in patients with hypertension in relation to the changes of left ventricular geometry. Investigations were carried out in 80 patients aged 52.5 +/- 12.6. In every patient plasma levels of ANP and BNP were estimated, blood pressure was measured and echocardiographic study was performed. Based on echocardiographic measurements every patient was classified into one of four left ventricular geometric patterns. It was found that in patients with left ventricular concentric hypertrophy plasma level of ANP and BNP was increased whereas in patients with concentric remodeling and eccentric hypertrophy only plasma level of ANP was elevated. In patients with concentric hypertrophy higher levels of ANP and BNP were found compared to patients with concentric remodeling and eccentric hypertrophy.
 ...
PMID:[Plasma levels of atrial and brain natriuretic peptide and left ventricular geometry in patients with essential hypertension]. 1291 98

The decrease in plasma protein and colloid osmotic pressure (COP) in the nephrotic syndrome is accompanied by a decrease in tissue-fluid protein and COP. The latter protects against a fall in blood volume. However, the range and speed of this protective mechanism are limited, and a decrease in blood volume can be expected if plasma COP is below approximately 10 mmHg, or (temporarily) if the protein loss starts very fast. In addition, due to this protective mechanism volume retained by the kidneys cannot effectively expand blood volume, explaining that hypertension is rarely grave and pulmonary congestion unusual, whereas peripheral oedema can be gross. The renal derangement leading to volume retention involves a decreased filtration per nephron, increased tubular reabsorption, and decreased sensitivity to ANP but the relation between these changes is incompletely resolved.
 ...
PMID:Pathophysiology of oedema in idiopathic nephrotic syndrome. 1295 39

Heart failure is known to be a complication of insulin-dependent (IDDM) and noninsulin-dependent diabetes mellitus (NIDDM) even in the absence of coronary heart disease or hypertension. The mechanisms leading to diabetic cardiomyopathy are unknown. The aim of the study was to characterize structural and functional alterations in hyperinsulinemic Zucker diabetic fatty (ZDF) rats treated with or without insulin. Diabetic animals showed a twofold increase in cardiomyocyte volume with increased left ventricular ANP but not BNP mRNA levels in spite of a reduced plasma renin activity (PRA) 2 months after onset of diabetes compared to nondiabetic littermates. These changes were associated with an increase in left ventricular performance as assessed by echocardiography. Insulin treatment led to a significant increase in body weight (BW), total heart weight, myocardial protein content, and left ventricular mass (LVM). Perivascular fibrosis and laminin thickness were significantly augmented in diabetic rat myocardium irrespective of insulin treatment, whereas interstitial collagen I and fibronectin were similarly found in diabetic and control myocardium. Initial stages of diabetic cardiomyopathy in hyperinsulinemic rats are characterized by cardiomyocyte hypertrophy and enhanced cardiac contractility. It is suggested that hyperinsulinemia may be involved in cardiac hypertrophy.
 ...
PMID:Myocardial hypertrophy and enhanced left ventricular contractility in Zucker diabetic fatty rats. 1476 80

Moxonidine, an imidazoline receptor agonist that acts centrally to inhibit sympathetic activity, has been shown to reduce effectively blood pressure, fasting insulin levels, and free fatty acids. In this study, we investigated the long-term effects of moxonidine treatment on cardiac natriuretic peptides (ANP and BNP) in Spontaneously Hypertensive Obese Rats (SHROBs), a rat model that resembles human Syndrome X. SHROBs expressing spontaneous hypertension, insulin resistance, and genetic obesity (weight 590 +/- 20 g, at 30 weeks) received moxonidine in chow at 4 mg/kg/day for 15 days. Moxonidine significantly reduced not only systolic blood pressure (187 +/- 6 versus 156 +/- 5 mm Hg, P < 0.05) but also plasma ANP (1595 +/- 371 versus 793 +/- 131 pg/mL, P < 0.05) and BNP (22 +/- 3 versus 14 +/- 1 pg/mL, P < 0.04), without influencing cardiac content of either peptide. Semi-quantitative PCR revealed that atrial ANPmRNA/GAPDHmRNA decreased to 39% 6 10% of pair-fed controls, P < 0.03. In left ventricles, moxonidine also decreased ANP mRNA to 69% +/- 7% and BNP mRNA to 74% +/- 6% of control, P < 0.02, but right ventricular ANP and BNP mRNA were not affected. These findings indicate that chronic inhibition of sympathetic activity with moxonidine in SHROB is associated with decreased ventricular natriuretic peptide transcription, consistent with the cardioprotective effects of moxonidine given the role of ANP and BNP as markers of cadiac disease. Moxonidine also improves the metabolic profile in these rats, thus it may be considered the drug of choice in treatment of metabolic syndrome X.
 ...
PMID:Cardiac effects of moxonidine in spontaneously hypertensive obese rats. 1502 94

This study aimed to characterize the vasorelaxing effects of ANP, BNP and CNP in isolated renal resistance arteries (RRA) from wild-type mice and mice with either systemic (GC-A -/-) or smooth muscle-restricted deletion of GC-A (SMC GC-A KO). In RRA from wild-type (GC-A +/+) mice natriuretic peptides (NP) induced concentration-dependent vasorelaxations with the rank order of potency ANP>BNP>CNP. In RAA obtained from mice with systemic or smooth muscle-restricted deletion of GC-A, the effects of ANP and BNP were abolished. In contrast, CNP induced concentration-dependent vasorelaxations of GC-A -/- and SMC GC-A KO RRA. However, the efficacy of CNP for vasorelaxation was markedly diminished compared with wild-type RRA. Such changes in CNP responsiveness did not affect large arteries as the aorta and they were not due to vascular changes secondary to chronic arterial hypertension in GC-A -/- mice. Unaltered vasorelaxing effects of acetylcholine and sodium nitroprusside demonstrated unaltered function of downstream targets regulated by cGMP in vascular smooth muscle. An increased expression of the clearance receptor (NPR-C) or diminished expression of GC-B were not found to account for the differences in CNP responsiveness. In conclusion, observations in isolated aortic rings do not necessarily allow conclusions concerning the physiology of natriuretic peptides in the smaller resistance size arteries. Changes at the GC-B receptor level are likely to explain the diminished responsiveness of GC-A-deficient RRA to CNP.
 ...
PMID:Diverging vasorelaxing effects of C-type natriuretic peptide in renal resistance arteries and aortas of GC-A-deficient mice. 1509 94

Although important advances have been made over past decades in studying the mechanisms of hypertension, the nature of cellular signaling patterns involved and their relationship remain unclear. High cGMP production rates in isolated renal glomeruli have been presented as a characteristic of spontaneously hypertensive rat (SHR) even before the development of hypertension, which suggests that this event might be a cause of the increase in blood pressure. Using cross-breeding between SHR and WKY parental strains to obtain F1 and F2 hybrids, we have investigated the patterning of high blood pressure and cGMP production rates. We have found that, in the F2 population, the mean blood pressure and both basal and ANP(1-28)-stimulated cGMP production are similar to the parental SHR. In addition, we have found a positive correlation between blood pressure and high cGMP production rates in the F2 population. The higher cGMP production was not a consequence of hypertension, since in DOCA-salt hypertensive rats cGMP production was similar to that observed in normotensive WKY rats. These observations suggest that high cGMP production is a characteristic linked to hypertension. Finally, reciprocal crosses between the SHR and WKY parental strains showed that in the F1 population blood pressure but not cGMP production are associated with the Y chromosome.
 ...
PMID:Patterning of renal cGMP production by the natriuretic peptide receptor type A and blood pressure in spontaneously hypertensive rats. 1509 96


<< Previous 1 2 3 4 5 6 7 8 9 10