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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium antagonists may increase glomerular filtration rate and renal plasma flow by antagonizing the intrarenal effects of angiotensin II and/or norepinephrine. We prospectively studied the effects of amlodipine, a once-a-day dihydropyridine calcium channel antagonist, in 19 patients with essential hypertension. Studies were performed after 4 weeks of placebo and 6 weeks of amlodipine therapy, and included the assessment of systolic and diastolic BP, renal clearances of inulin and p-aminohippurate, and determination of body fluid composition. Systolic and diastolic BPs were reduced following 6 weeks of amlodipine monotherapy. In spite of significant decreases in mean arterial pressure, there were increases in inulin clearance (+ 13%), and p-aminohippurate clearance (+ 19%). Filtration fraction was not changed. Renal vascular resistance was decreased (-25%). Total blood volume, extracellular fluid volume, and total body water and body weight were not changed. We conclude that amlodipine therapy has the potential to reverse renal abnormalities encountered in the hypertensive state.
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PMID:Amlodipine therapy corrects renal abnormalities encountered in the hypertensive state. 296 Dec 56

In man, atrial natriuretic peptide (ANP) is released in pulsatile fashion into the right as well as left atrium in relation to atrial pressure and volume, i.e. wall tension. These responses are documented by a new radioenzymatic assay to measure ANP in human plasma relative to hemodynamic measurements during diagnostic cardiac catheterization, atrial pressure changes during various types of pacemaker stimulation, and changes in cardiopulmonary volumes during head-out water immersion or upper leg cuff occlusion. During the infusion of synthetic 1-28 alpha-human-ANP and attendant high normal plasma ANP concentrations, natriuresis and peripheral vasodilatation (using venous occlusion plethysmography) can be shown. The antipressor action of ANP, especially against angiotensin II (but less against noradrenaline), together with the antirenin and anti-aldosterone effects, suggest that the ANP system acts as a functional counterpart to the renin-angiotensin-aldosterone system. Accordingly, plasma ANP is elevated whenever renin is low (e.g. low-renin essential hypertension) and/or cardiopulmonary volume is elevated (e.g. cardiac or renal failure). In man, ANP probably plays a (patho-) physiological role, though its antipressor and natriuretic effects do not appear to be very potent.
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PMID:[Does atrial antipressor natriuretic peptide play a pathophysiological role?]. 296 81

Clinico-biochemical investigation of 76 persons with borderline arterial hypertension (BAH) aged 15 to 64 and 60 controls with assessment of some parameters of lipid, carbohydrate and water-salt metabolism was carried out. Gustatory sensitivity to sodium chloride was studied. Differences in the levels of these indices were revealed in patients with BAH with relation to the presence or absence of basal changes on ECG and fundus of the eye; there were also some differences in risk factors in BAH and essential hypertension.
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PMID:[Clinico-biochemical characteristics of persons with borderline arterial hypertension]. 296 28

ANF is a newly discovered peptide hormone that has significant implications for critical care physicians. This hormone, released from the heart, is especially responsive to fluid challenges as well as to many of the drugs commonly used in the ICU, including pressor and anesthetic agents. It has potent arterial vasodilating effects in pharmacologic doses and may be an important natural vasodilating agent, especially in the renal vascular bed. In patients on dopamine, it may potentiate the renal vasodilating effect and may provide an effective therapy for developing acute renal failure. Children with congenital heart disease and patients with CHF have elevated levels that clearly alter the aldosterone-angiotensin II system and may help us to understand and treat these conditions more effectively. Additionally, ANF may be a marker for adequacy of treatment in these disease states. The potential uses for ANF include diuresis in patients with fluid overload and diuretic resistance, treatment of CHF, and as a short-acting vasodilator. In the ICU, many therapies affect cardiac pressures and volume regulation. Positive-pressure ventilation may decrease the release of ANF by decreasing venous return and thus contribute to water retention. Drugs used in the ICU may directly affect ANF levels and markedly affect the homeostasis of fluid and electrolyte balance. This hormone system interacts intimately with renin, angiotensin II, and aldosterone. These interactions may play a significant role in the development of essential hypertension. Although not addressed in this article, the treatment and understanding of essential hypertension may be significantly advanced by understanding these relationships. It is clear that ANF acts as a hormone with complex interactions between the heart, volume status, electrolyte balance, renin-angiotensin II-aldosterone, vasopressin, and vascular tone. Although currently no definitive picture exists for these complex interactions, this is an exciting new hormone with significant implications for patient management in the ICU. As research continues, the picture will become clearer and our understanding of this new hormone more precise.
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PMID:Atrial natriuretic factor in the pediatric intensive care unit. 297 48

Enalapril is a new, oral, long-acting nonsulfhydral angiotensin converting enzyme inhibitor. Thirty-nine patients with primary hypertension were entered into a randomized, double-blind protocol to assess the efficacy of enalapril (10 to 20 mg bid), hydrochlorothiazide (25 to 50 mg bid), or combined drug therapy. Enalapril, either alone or in combination with hydrochlorothiazide, effectively controlled blood pressure. Enalapril monotherapy was associated with an increase in plasma renin activity and a decrease in angiotensin II concentration; in patients with an initial inulin clearance less than or equal to 80 mL/min/1.73 m2, inulin and para-aminohippurate clearances were markedly improved, without producing adverse effects on salt and water excretion or body fluid composition. Combination therapy was associated with a marked increase in plasma renin activity; however, only those patients with an initial inulin clearance less than or equal to 80 mL/min/1.73 m2 demonstrated suppression of angiotensin II concentration and marked improvement in inulin and para-aminohippurate clearances. These observations suggest that enalapril, either alone or in combination with a diuretic, has the potential to reverse renal function abnormalities encountered in the hypertensive state.
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PMID:Effects of enalapril alone, and in combination with hydrochlorothiazide, on renin-angiotensin-aldosterone, renal function, salt and water excretion, and body fluid composition. 299 32

The effect of the chronic administration of captopril on plasma levels of vasopressin (PVP) were studied in 14 patients with moderate essential hypertension and 10 normal volunteers. All patients were studied after 10 days without drugs and under a constant diet (120 mmol sodium and 80 mmol potassium/day). Plasma levels of renin activity (PRA), aldosterone (PA) and PVP were assayed before and after captopril treatment (50-100 mg/day for 1 month). In addition to the well-known effect of captopril treatment on PRA and PA, a statistically significant reduction of PVP was observed. This finding suggests that the renin-angiotensin-aldosterone system influences vasopressin release, and its inhibitors may contribute to the absence of water retention during captopril treatment compared with the effect of other vasodilatory drugs.
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PMID:Relationship between vasopressin and the renin-angiotensin-aldosterone system in essential hypertension: effect of converting enzyme inhibitor on plasma vasopressin. 300 2

This review focuses on the renal effects of the angiotensin converting enzyme inhibitors, captopril and enalapril. Emphasis is placed on the renal response to these drugs in patients with primary essential hypertension, and in hypertension accompanying renal parenchymal disease. Specifically reviewed are the renal function and hemodynamic, salt and water, body fluid composition, and urinary protein excretion responses. The interruption of the renin-angiotensin-aldosterone axis has the potential to produce a variety of favorable renal responses, including reduction of renal vascular resistance, enhancement of renal blood flow, enhancement of glomerular filtration rate, acute natriuresis, sustained diuresis, and a decrease in urinary protein excretion. Data in support of these potential renal perturbations are presented and discussed. The results suggest that the angiotensin converting enzyme inhibitors are important therapeutic agents in the treatment of hypertensive disease, in that they may modify pathophysiologic renal abnormalities encountered in this disease state.
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PMID:Renal effects of angiotensin converting enzyme inhibitors in hypertension. 302 81

More than half of the United States population over 65 years of age has essential hypertension. In 1984, there were 10 million elderly hypertensive persons and this number will reach 25 million in the near future. These patients are at high risk for congestive heart failure, stroke, heart attack, and dissecting aneurysm. Successful reduction of blood pressure can lower these risks considerably, but rational treatment depends on understanding the complex pathophysiology of hypertension in older patients. In fact, treatment that does not take into account the combined effects of aging and hypertension on the cardiovascular system and the kidneys may do more harm than the hypertension itself. Among the prominent age-related cardiovascular changes are stiffening of the arterial tree, with or without a contribution from atherosclerosis. This reduces arterial compliance and increases afterload, resulting in the left-ventricular hypertrophy seen in old age and leading to a progressive rise in systolic pressure. There is considerable shrinkage of the kidneys, due primarily to loss of glomerular and tubular tissue in the cortex, along with sclerosis of the glomeruli and formation of tubular diverticula. Arteriolar changes lead to reduced renal blood flow, the shunting of blood around the glomeruli, and thus a reduction in glomerular filtration rate. Renal water and electrolyte excretion are changed, making homeostasis more difficult to maintain, and the renin-angiotensin system is altered, helping to blunt the kidneys' response to pressure changes. Essential hypertension superimposed on all the foregoing effects exacerbates them. Peripheral resistance is usually markedly elevated in older hypertensive persons, which increases afterload directly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiology of hypertension in older patients. 304 95

Prostaglandins PGE2, PGD2, PGI2, and PGF2 alpha, as well as thromboxanes and leukotrienes, are synthesized by the fetal and neonatal kidney. The major prostaglandin, PGE2, PGD2, and PGI2, increase RBF, free water clearance, urine flow, and natriuresis. Alterations in the synthetic and catabolic activity of renal prostaglandins with advancing gestational and postnatal age occur along with concomitant alterations in RBF, GFR, and water and electrolyte excretion, suggesting that the prostaglandins play an important role in renal functional development. Indomethacin treatment may affect both fetal and neonatal renal function. Long-term maternal indomethacin treatment may decrease fetal urine output enough to alter amniotic fluid volume. Neonatal indomethacin therapy may cause transient dose-related renal dysfunction characterized by a decrease in urine output, but this renal dysfunction also depends in part on dosage, timing of therapy, and the cardiovascular and renal status of the infant prior to treatment. New areas of research interest include urinary prostaglandins as a marker for development of essential hypertension, and the possible interaction between antenatal steroids and renal function in the newborn.
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PMID:Prostaglandins and the developing kidney. 310 70

Sodium consumed in excess may make a significant contribution to the causes of many diseases, especially for those who suffer from hypertension. More than 90% of hypertension is essential hypertension. Drinking water may contribute 10% to one's total sodium intake; for patients on sodium restricted regimens, drinking water may account for 64% of total intake. At present, insufficient evidence is available to conclude whether sodium in drinking water causes elevation of blood pressure. It is possible that reducing sodium intake early in life may minimize the risk of hypertension in the later years. Dietitians play a key role in the control of hypertension. Many communities in the U.S. exceed the recommended 20 mg/L or less sodium in drinking water; this may present a hazard to some members of our population.
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PMID:Does the sodium level in drinking water affect blood pressure levels? 318 65


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