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

The role of vasopressin in human hypertension was examined in a series of studies. In patients with primary hyperaldosteronism and benign essential hypertension, circulating vasopressin was generally lower than in normotensive subjects. In contrast, plasma vasopressin was increased (p less than 0.001) in patients with malignant-phase hypertension. However, compared to infused vasopressin in normal subjects, when plasma levels of up to 120 pg/ml did not affect blood pressure, the increased levels found in malignant hypertension could not account for the hypertension. The possibility that there may be an increased pressor sensitivity to vasopressin in hypertension was examined by infusing the peptide into nine patients with essential hypertension. This showed a slight increase in sensitivity compared to normotensive subjects, but again this was insufficient to account for the discrepancy between the circulating level of vasopressin and the extent of the raised blood pressure in the hypertensive patients. The effect of chronically elevated levels of vasopressin was studied in a group of patients with the syndrome of inappropriate ADH excess as a consequence of bronchogenic carcinoma. In spite of having chronically elevated levels of vasopressin, these patients had normal blood pressures for their age and sex. Our results suggest that, although vasopressin is elevated in malignant hypertension, it does not contribute significantly to the raised blood pressure, and its increase is probably a consequence of volume shrinkage through renal salt and water loss.
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PMID:Vasopressin and hypertension in man. 243 62

We studied two groups of hypertensive patients in order to ascertain whether the acute natriuretic effect of nifedipine is mediated by humoral factors such as renal kallikrein or atrial natriuretic factor (ANF). First, 17 patients with mild to moderate essential hypertension maintained on a 130-mmol/day diet, received either nifedipine (10 mg orally) or placebo during a 6-h infusion of the kallikrein inhibitor aprotinin (2 x 10(6) KIU) or saline as control. Aprotinin, while significantly reducing urinary kallikrein activity, did not interfere with the acute effects of nifedipine on blood pressure, heart rate, urinary volume, urinary Na+ and creatinine clearance. In another group of eight patients on a constant daily Na+ intake of 130 mmol and in the supine position, placebo or nifedipine (10 mg sublingually) were administered, and blood pressure, heart rate, plasma renin activity, plasma aldosterone and plasma ANF, urinary Na+, urine volume and creatinine clearance, were monitored for 2 h. While placebo did not induce changes in any of the above parameters, nifedipine administration induced a significant decrease in blood pressure and increase in urinary Na+, urine volume and creatinine clearance, and a significant rise in ANF levels, from 19.4 +/- 2.8 pg/ml to a maximum of 23.9 +/- 2.5 and 24.1 +/- 2.2 pg/ml (P less than 0.05) at 60 and 90 min, respectively. In conclusion, our data do not support a role for renal kallikrein as a humoral mediator of the natriuretic effect of calcium antagonists, but do not exclude the possibility that ANF might participate in the nifedipine-induced increase in sodium and water excretion.
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PMID:Studies on the natriuretic effect of nifedipine in hypertensive patients: increase in levels of plasma atrial natriuretic factor without participation of the renal kallikrein-kinin system. 245 Jan 87

To elucidate the renal effects and especially the natriuretic properties of calcium entry blockers, we studied the effect of sublingual nifedipine 20 mg in 16 patients with mild to moderate essential hypertension. The lithium clearance technique was utilized and constant infusion technique was employed to measure glomerular filtration rate (GFR) and renal plasma flow (RPF). Nifedipine induced a significant reduction of systolic and diastolic blood pressure and an increase in heart rate. RPF increased and renal vascular resistance fell significantly, whereas GFR was unchanged. A significant increase in diuresis and in clearance of sodium and lithium was seen. The absolute and fractional proximal reabsorption of sodium and water was reduced. The absolute distal reabsorption increased significantly. The results indicate that the natriuretic action of nifedipine in hypertensives is a proximal tubular event.
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PMID:Acute natriuresis induced by inhibition of proximal tubular reabsorption of sodium and water in hypertensives following acute calcium entry blockade with nifedipine. 245 22

The dihydropyridine calcium antagonist nitrendipine offers a pathophysiologically based antihypertensive treatment with a potent dilation of resistance vessels, increased arterial compliance, and an acute natriuretic/diuretic response. Prolonged nitrendipine treatment in essential hypertension is not associated with stimulation of the sympathetic nervous and the renin-angiotensin systems or accumulation of sodium and water. The antihypertensive effectiveness is similar to that of diuretics and beta-blockers, and the responsiveness appears to be greater in elderly and black patients. During long-term (approximately 1 year) nitrendipine treatment in mild to moderate hypertension, the blood pressure reduction is well sustained in "short-term" nitrendipine responders. In patients with severe hypertension, nitrendipine has a potent antihypertensive effect in combination with beta-blockers and/or diuretics. In mild-moderate hypertension, a single daily dose (10-40 mg) may be sufficient, whereas two daily doses (20-80 mg/day) seem necessary in severe hypertension. Common side effects are headache, flush, and palpitations (approximately 20-30%), but these are generally mild and transient. Dizziness and malaise occur in approximately 5%, often later during treatment. Peripheral edema in 5-20% of the patients is generally mild but persistent. Nitrendipine has no adverse effects on glucose and lipid metabolism or on plasma levels of electrolytes and urate. The ultimate aim of antihypertensive treatment is to prevent cardiovascular complications. As for other calcium antagonists, no study on primary prevention of cardiovascular complications in hypertension has been published. With regard to regression of left ventricular hypertrophy accompanying essential hypertension, conflicting results have been found with nitrendipine.
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PMID:Review of long-term trials with nitrendipine. 246 50

A study of metabolism of sodium, water and body components in male patients suffering from essential hypertension, with normal body mass and alimentary obesity, has shown an increase in the space of sodium distribution both in absolute and relative values, a decrease in sodium excretion from the body and blood, change in sodium distribution between the vascular and interstitial parts of the space, "dry retention" of sodium in the body. The detected disturbances have been shown to play an important role in the pathogenesis of essential hypertension.
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PMID:[Whole-body radiometry in assessing metabolism in hypertension]. 249 63

Understanding the sequence of events responsible for pressure-related natriuresis and their pathophysiologic alterations may be useful in distinguishing various types of essential hypertension of renal origin. The perturbation of a distal step in the sequence is likely to be reflected in a simple physiologic defect. For instance, pathophysiologic alterations in the medullary production of prostaglandin E2 might directly influence natriuresis and diuresis because of its modulatory effect on tubular reabsorption of sodium and water. Perturbation of more proximal steps in the sequence could influence all the distal events as well. For instance, prostaglandin I2 and endothelium-derived relaxing factor may be produced by the preglomerular vasculature in response to alterations in renal perfusion pressure and may modulate the release of renin from the juxtaglomerular cells. Thus, variations in the production of prostaglandin I2 or endothelium-derived relaxing factor may be reflected by various renal vascular, tubular, and systemic homeostatic events related to the renin-angiotensin system.
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PMID:Alterations in blood pressure by derangement of the mechanisms that regulate sodium excretion. 251 60

Efferent renal sympathetic nerve activity (ERSNA) is elevated in human essential hypertension as well as several forms of experimental hypertension in animals. In addition, bilateral complete renal denervation delays the development and/or attenuates the magnitude of the hypertension in several different forms of experimental hypertension in animals. Efferent renal sympathetic nerve activity is known to have dose-dependent effects on renal blood flow and glomerular filtration rate, renal tubular sodium and water reabsorption, and renin secretion rate that are capable of contributing, singly or in combination, to the development, maintenance, and exacerbation of the hypertensive state. Of the many factors known to influence the central nervous system integrative regulation of ERSNA, two environmental factors, dietary sodium intake and environmental stress, are capable of significant interaction. This resultant increase in ERSNA and subsequent renal functional alterations can participate in the hypertensive process. This is especially evident in the presence of an underlying genetic predisposition to the development of hypertension. Thus, interactions between environmental and genetic influences can produce alterations in the sympathetic neural control of renal function that play an important role in hypertension.
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PMID:Sympathetic nervous system influences on the kidney. Role in hypertension. 264 2

Hypertension is a common problem encountered after renal transplantation. Many different mechanisms may be responsible for hypertension in this setting, and therapy will depend upon the mechanism(s) affecting the individual patient. Factors that may cause or aggravate post-transplantation hypertension include renal dysfunction secondary to rejection or other diseases of the transplanted kidney, renin production from the diseased native kidneys if these kidneys have not been surgically removed, extracellular fluid volume expansion, toxic effects of medications used after transplantation, especially cyclosporine and intravenous prednisolone, or primary hypertension in the donor or recipient. Renal artery stenosis may predispose to acute renal failure in the presence of treatment with angiotensin-converting enzyme inhibitors. Severe renal artery stenosis may also lead to refractory salt and water retention and fluid overload with congestive heart failure and hypertension, mediated primarily due to extracellular fluid volume excess. Therapy with percutaneous transluminal renal angioplasty or, as a last resort, surgery, can be successful in controlling these problems.
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PMID:Refractory hypertension after renal transplantation. 266 26

Plasma from black male patients with essential hypertension was bioassayed for vascular Na+-K+ pump inhibitory activity. Halves of the same rat tail artery were incubated for two hours in boiled plasma supernates from a hypertensive patient and a paired age-, sex-, and race-matched normotensive subject and then ouabain-sensitive 86Rb uptake was measured. Ouabain-sensitive 86Rb uptake by their leukocytes was also measured. Eighteen pairs of subjects were studied. The uptakes were not significantly different in the hypertensive patients and control subjects. However, when we selected from the eighteen hypertensive patients, nine with low plasma renin activity on the day of the study, uptakes were reduced in the hypertensive patients relative to the paired control subjects. We also assayed plasma supernates from normotensive black and white male subjects before and after acute volume expansion (2.5 L saline IV + 1.5 L distilled water orally over a three-hour period) and from paired normotensive subjects before and after sham volume expansion and obtained a positive bioassay in the expanded subjects both on intraindividual and interindividual comparisons. These studies demonstrate increased vascular Na+-K+ pump inhibitory activity in the plasma of black male patients with low renin essential hypertension and in the plasma of normotensive subjects after acute volume expansion. The findings suggest that the inhibitory activity in the hypertensive subjects' plasma is related to volume expansion, relative or absolute.
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PMID:Humoral Na+-K+ pump inhibitory activity in essential hypertension and in normotensive subjects after acute volume expansion. 266 73

Short term angiotensin converting enzyme inhibition may induce a transient salt and water retention in patients with hypertension or heart failure. To verify the glomerular and tubular effects of short term converting enzyme inhibition, thirteen patients with mild to moderate essential hypertension (WHO I-II) were treated orally either with perindopril (4 mg o.d.) or captopril (25 mg b.i.d.) for one week. Both drugs reduced supine mean blood pressure significantly (p less than 0.01) (perindopril from 126 +/- 11 to 108 +/- 7 mmHg, mean +/- SD, and captopril from 132 +/- 12 to 121 +/- 16). Plasma volume (radio-iodinated albumin space) was unchanged while mean extracellular fluid volume (inulin space) increased although not significantly (from 5.05 +/- 1.32 l/sqm to 5.71 +/- 2.21 with perindopril and from 4.96 +/- 2.6 to 5.6 +/- 1.7 with captopril). Sodium clearance decreased (from 1.4 +/- 0.6 to 1.1 +/- 0.5 ml/min 1.73 sqm with perindopril, p less than 0.05, and from 0.97 +/- 0.44 to 0.88 +/- 0.51 with captopril, n.s.). In 9 patients (6 on captopril and 3 on perindopril) extra-cellular fluid volume increased simultaneously with reduction in glomerular filtration rate and in proximal tubule sodium re-absorption as well as an increase in distal tubule sodium reabsorption. In these patients the changes in proximal and distal tubule sodium reabsorption were significantly (p = 0.05) different from those of the patients with no extra-cellular fluid expansion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Volume of the extracellular liquid and renal function during short-term administration of angiotensin converting enzyme inhibitors in essential hypertension]. 267 Jun 57


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