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)

The levels and pathophysiological role of amino terminal C-type natriuretic peptide in heart failure are unknown. The potential of plasma amino-terminal C-type natriuretic peptide (N-CNP) as a marker of cardiac function was investigated in symptomatic patients. In 305 patients with recent-onset dyspnea and/or peripheral edema, presenting to primary care, assay of plasma amino-terminal C-type natriuretic peptide and other plasma vasoactive hormones was conducted together with echocardiography. Heart failure was diagnosed in 77 (of the 305) patients by rigorous application of predefined criteria. Plasma amino-terminal C-type natriuretic peptide concentrations were elevated in patients with heart failure, and by univariate analysis were related to age, renal function, and other hormones. On multivariate analysis, tertile of plasma N-CNP interacted with tertile of plasma amino-terminal B-type natriuretic peptide to predict heart failure independent of age, gender, renal function, or echocardiographic left ventricular fractional shortening. N-CNP showed significant relations to concurrent plasma CNP, atrial natriuretic peptide (ANP), N-ANP, B-type (or brain) natriuretic peptide (BNP), N-BNP, endothelin-1, and adrenomedullin but not to echocardiographic indicators of left ventricular systolic function. Plasma amino-terminal C-type natriuretic peptide is elevated in heart failure and is related to other plasma hormones in heart failure. These findings suggest a possible compensatory response from the peripheral vasculature to heart failure by an endothelium-based vasodilator peptide and mandate further exploration of the role of C-type natriuretic peptide in this condition.
Hypertension 2004 Jan
PMID:Amino-terminal pro-C-type natriuretic peptide in heart failure. 1465 55

Natriuretic Peptides like BNP or NT Pro BNP are diagnostic and prognostic makers largely used in clinical practice. Ageing may increase these peptides, especially in case of comorbidities like renal failure or hypertension and require adjustment for age. Diagnostic value of natriuretic peptides seems however preserved in elderly people.
 ...
PMID:[Brain natriuretic peptide, heart failure and elderly patients]. 1471 41

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

Recent recommendations for the management of hypertension have stressed the importance of assessing subclinical target organ damage for the evaluation of cardiovascular risk, the choice of antihypertensive treatment and the follow-up of hypertensive patients. In addition to classic hallmarks of target organ damage (left ventricular hypertrophy, renal dysfunction, microalbuminuria), new concepts emerging from basic research and technical progresses have allowed more accurate and earlier detection of target organ damage affecting the heart (plasma BNP, coronary calcifications), the brain (silent lacunar infarcts, advanced deep white matter lesions, microbleedings) and the vasculature. The latter include markers of diffuse atherosclerosis (carotid intima-media thickness), arterial stiffness (pulse wave velocity, augmentation index) and endothelial dysfunction (increased plasma levels of adhesion molecules). Current studies should help to better define the predictive power of these new phenotypes for the occurrence of overt cardio- and cerebrovascular diseases, their reversibility under antihypertensive treatment and the most adapted therapeutic strategy in at-risk patients. Furthermore, early identification of hypertensive patients more likely to develop target organ damage, will be facilitated by a more global evaluation of cardiovascular risk factors, a better use and wider acceptance of ambulatory BP measurement (including determination of nocturnal dip and blood pressure variability) and, maybe, an increased knowledge of the genetic factors underlying susceptibility to target organ damage. Lastly, randomized studies comparing different classes of antihypertensive drugs should help to test the well-known but frequently challenged concept of additional benefits of some antihypertensive drugs "beyond BP" on prevention and reversal of target organ damage.
 ...
PMID:Recent insights in the development of organ damage caused by hypertension. 1536 98

Diastolic dysfunction of the heart is characterized by normal left ventricular contractility and normal ejection fraction, however ventricular relaxation is impaired. In systolic dysfunction, ventricular contractility and ejection fraction are reduced, in addition to impaired relaxation. The prevalence of diastolic dysfunction is increased in the elderly, especially those who have had inadequately treated hypertension. Both diastolic and systolic dysfunction may result in similar clinical signs and symptoms. Therefore, echocardiography is needed to make the distinction. Left atrial (LA) enlargement, assessed by left atrial volume indexed to body surface area, appears to be the best measure to assess diastolic function. LA enlargement is likely when indexed LA volume is > or = 34-40 mL/m2. B-type natriuretic protein appears to be useful for the diagnosis, assessment and prognosis of heart failure, but it does not distinguish between the two types of dysfunctions. Several drug treatments that have effects on the mechanism of diastolic dysfunction are under investigation.
 ...
PMID:Diastolic dysfunction. 1568 7

We know a great deal about the receptors and signaling pathways in cardiomyocytes that contribute to hypertrophic growth. Although drugs that target them have proven effective in substantially reducing left ventricular hypertrophy and associated mortality, cardiovascular disease remains the leading cause of death in the West. Another approach may rest with exploiting naturally occurring regulators of maladaptive cardiac hypertrophy that have been identified in the past few years. These endogenous negative regulators can be grouped, for the most part, into those constitutively active but whose activity is decreased by hypertrophic stimulation, and those with little or no baseline activity that are activated by hypertrophic stimulation. Spanning both groups are 4 systems that converge on cyclic guanosine 3', 5'-monophosphate (cGMP) generation, namely natriuretic peptides (ANP and BNP), kinins, nitric oxide (NO), and the angiotensin II type 2 receptor (AT2). Although holding promise as a means for restricting hypertrophy, each of these signaling molecules has certain limitations that need to be overcome. What follows is an overview of research over the past 2 years, much of it published in Hypertension, which has dealt with the antihypertrophic action of this particular group of endogenous signaling molecules. Understanding the function and regulation of the antihypertrophic NO-cGMP system offers the promise of novel therapeutic strategies for treating cardiac hypertrophy and heart failure.
Hypertension 2005 Mar
PMID:Putting the brakes on cardiac hypertrophy: exploiting the NO-cGMP counter-regulatory system. 1571 Jul 77

The diagnosis of heart failure in the elderly frequently represents a clinical challenge. Atypical symptoms and signs and confounding comorbid conditions are common situations in old patients with heart failure and may obscure the clinical picture, complicating the diagnostic evaluation. Furthermore in the elderly, especially in female gender with a long-lasting history of hypertension, heart failure commonly may ensue as a consequence of a predominating impairment of the diastolic function with normal or near-normal preserved systolic function. Echocardiography represents the gold standard for the confirmation of the clinical suspicion of heart failure and may provide detailed information about left and right ventricular dimensions and function, atrial dimensions, valvular function and pericardium. For this reason it is recommended as part of initial diagnostic evaluation in almost all cases of heart failure. However, the low diagnostic accuracy of the clinical picture in elderly patients with suspected heart failure, as suggested by the international guidelines, requires the corroboration of the clinical suspicion with the help of "first-line" traditional investigations like ECG and chest X-ray. Recently natriuretic peptides (B-type natriuretic peptide [BNP] and NT-proBNP) have emerged as an attracting "tool" to support the clinical signs in patients with suspected heart failure. In this review we discuss about the opportunity that BNP and NT-proBNP would be relevant in the diagnostic process of elderly patients with suspected heart failure.
 ...
PMID:[Clinical features and diagnostic evaluation of heart failure in the elderly]. 1571 9

30-50% of patients presenting with symptoms of congestive heart failure exhibit a near normal left ventricular systolic function at rest, and an impaired diastolic function of the heart may be causative. Despite a better prognosis than in systolic heart failure, frequency of hospitalizations due to diastolic heart failure is comparable with systolic heart failure. According to the criteria of Vasan and Levy diagnosis of diastolic heart failure is probable, if symptoms and signs of heart failure are accompanied in proximity (within 72 h) by objective evidence of normal left ventricular systolic function. Newer echocardiographic techniques (e. g., tissue Doppler) aid to confirm the diagnosis and to determine the severity of dysfunction and may substitute invasive demonstration of impaired left ventricular relaxation, filling, compliance or stiffness for standardized diagnosis. Incorporation of biochemical test (BNP [brain natriuretic peptide]) allows differential diagnosis and may increase the accuracy of diagnosis. Due to inconsistent diagnostic criteria, data from prospective randomized controlled trials for the treatment of diastolic heart failure are rare. Basic principles include treatment of the underlying disease, i. e., control of hypertension, diabetes, or obstructive airway disease. Angiotensin 1 antagonists (ARB) have proven effective in regression of left ventricular hypertrophy (LIFE) and may reduce morbidity, but not mortality (CHARM). Maintenance of sinus rhythm, heart rate control (beta-blockers, calcium channel blockers) and anti-ischemic therapy may be indicated in view of pathophysiological aspects. Diuretics should be administered with caution in patients with symptoms of congestion, digitalis is not useful in the treatment of isolated diastolic heart failure. The results of ongoing trials (e. g., I-Preserve) may offer new therapeutic options, and evidence-based guidelines for the so far often unsatisfactory treatment of diastolic dysfunction/heart failure are awaited.
 ...
PMID:[Dyspnea and normal systolic function]. 1591 35


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