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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the relative importance of hormonal factors in mediating the hypotensive response to converting enzyme inhibition (CEI), plasma renin activity (PRA), angiotensin II, and bradykinin responses to SQ20,881 were measured in 20 supine patients with essential hypertension in balance on a 10 mEq sodium diet. Patients were divided into two groups according to their diastolic blood pressure response: responders had a decrement in diastolic pressure which exceeded 9 mm Hg, the upper value of the 95% confidence limits for normotensive patients studied under similar conditions; nonresponders did not. Compared to the nonresponders, responders not only had a higher control PRA (8.7 +/- 1.7 ng/ml/hr vs 4.8 +/- 2.1, p < 0.05) and larger decrement in plasma angiotensin II (18.7 +/- 4.9 pg/ml vs 3.2 +/- 1.7, p < 0.01), but also had a higher control bradykinin (3.2 +/- 0.7 ng/ml vs 1.1 +/- 0.2, p < 0.05) and larger increment in bradykinin (4.5 +/- 1.3 ng/ml vs 1.0 +/- 0.4, p < 0.05) following SQ20,881. Because SQ20,881 altered both angiotensin II and bradykinin concentrations, we assessed the contribution of blockade of angiotensin II formation by administering angiotensin II infusions to seven responders during coverting enzyme blockade, with the angiotensin II dose adjusted to restore diastolic pressure to control levels. The plasma angiotensin II level required to return blood pressure to control was 45 +/- 15 pg/ml higher than the control plasma angiotensin II level (p < 0.01), suggesting that some other factor(s), perhaps bradykinin, are also responsible for the hypotensive response to converting enzyme inhibition.
Hypertension
PMID:Converting enzyme inhibition in essential hypertension: the hypotensive response does not reflect only reduced angiotensin II formation. 23 66

One hundred fourteen hypertensives and 20 normal controls were examined using a new clinical technique of measuring 24-h urinary free 18-hydroxy-11-desoxycorticosterone (18-OH-DOC) excretion in response to dietary salt manipulations and ACTH injections. The object was to avoid potential errors of random plasma sampling. Mean urinary free 18-OH-DOC in normals on 110 milliequivalent sodium diet was 1.84 +/- 0.69 microgram (mean +/- SD) and represented about 2% of the daily secretion rate of this steroid. Both in normals and hypertensives, urinary free 18-OH-DOC approximately doubled on low salt (P less than 0.01 for each) and rose about 10 times in response to ACTH injection (P less than 0.05 and P less than 0.01, respectively). Plasma and urinary free 18-OH-DOC showed good correlation in patients with essential hypertension on a low salt diet (r = 0.45, P less than 0.01). Suppressed renin patients showed no propensity toward excess 18-OH-DOC excretion and hypertensives with elevated 18-OH-DOC could not be distinguished by their aldosterone levels, cortisol levels, nor their responses to various stimuli. These data suggest 18-OH-DOC is predominantly secreted under ACTH control and, to a smaller extent, in response to salt changes. Hypertension characterized by chronic overproduction of 18-OH-DOC forms only a small percentage of the hypertensive population. It is proposed that measuring 24-h urinary free 18-OH-DOC excretion may be the best method of assessing its rate of secretion without resorting to injection of radiolabeled material.
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PMID:Urinary free 18-hydroxy-11-desoxycorticosterone excretion in normal and hypertensive patients. 23 84

Information defining the renin-angiotension-aldosterone axis as a control system concurrently regulating salt balance and blood pressure has been applied to reexamine the role of renin in experimental and clinical forms of renovascular and renal hypertension, and thence to develop criteria for differentiating these entities. Experimentally, there are two models of renovascular hypertension; one is characterized by excess renin with reduced sodium (vasoconstrictor form) and the other by excess sodium with reduced renin (volume form). But with sodium depletion, the volume form converts to a vasoconstrictor form illustrating how the two factors coordinate to maintain blood pressure. In man, renovascular and renal hypertensions appear to be sustained by the same two mechanisms. Studies in man show that, in the absence of unilateral disease, the supine renal venous renin level in each kidney is consistently 24 percent higher than the peripheral level. Because of this constant relationship, the peripheral renin level is a measure of the renal secretion rate. Our studies indicate the curable unilateral renovascular hypertension is, in fact, renin-dependent vasoconstrictor hypertension. Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when indexed against sodium excretion. (2) Lateralization of renin secretion with contralateral suppression rules out occult bilateral disease. It is indicated by V-A equal 0 from the uninvolved kidney. (3) (V-A)/A greater than 48 per cent from the ipsilateral kidney supports unilateralization. With data derived from patients with essential hypertension as a reference, the degree to which (V-A)/A is greater than 0.48 can be used to estimate the degree of renal ischemia, using Fick's principle. Corroborative evidence to support these three criteria can be developed from the blood pressure response to angiotensin blocking drugs or to antirenin therapy with propranolol. Clinical analysis validates these criteria to identify curable hypertension from unilateral renovascular or parenchymal disease. In patients with either occult or overt bilateral renal disease, the volume factor often predominates and is expressed by some suppression of plasma renin levels. Continued
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PMID:The renin axis and vasoconstriction volume analysis for understanding and treating renovascular and renal hypertension. 23 77

Neurohumoral mechanisms operating via the catecholamines are discussed in their relationship to such hypertensive diseases as pheochromocytoma and labile and established essential hypertension. 2. In pheochromocytoma, diagnosis depends almost entirely on identification of increased amounts of catecholamine metabolites in the urine. Because of the danger, manipulative or invasive procedures both for diagnosis and during surgery should be kept at a minimum. 3. In established essential hypertension, reactivity to norepinephrine and plasma norepinephrine are increased, whereas norepinephrine uptake and apparent secretion rate are decreased. 4. In labile essential hypertension, reactivity to epinephrine and probably plasma epinephrine are increased and uptake of epinephrine decreased. 5. Labile hypertension with all its characteristics may or may not coexist with established essential hypertension with all its features. 6. The sympathetic nervous system is also involved in other types of hypertensive disease. Many patients with renovascular hypertension as well as with primary and secondary hyperaldosteronism also have essential hypertension. Angiotensin II affects the sympathetic nervous system and the juxtaglomerular apparatus appears to be beta adrenergic receptor activated, at least in part.
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PMID:Neurohumoral mechanisms in hypertension. 23 64

The antihypertensive effect of atenolol, a new beta-1-receptor blocking agent, was studied in a double-blind trial in which 45 patients with essential hypertension were randomly assigned to placebo or atenolol treatment. Atenolol caused a statistically significant and clinically relevant reduction of blood pressure. The optimum daily dose for moderately severe hypertension was considered to be 200 mg. Several irrelevant side effects were collected by the use of a check list, but there was no difference in the number of complaints during placebo and active treatment. Atenolol has a useful antihypertensive effect and, at least theoretically, has advantages over other beta-adrenergic blocking agents.
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PMID:Controlled study of atenolol in treatment of hypertension. 23 10

Three hundred fifteen patients with essential hypertension were classified according to low (18 percent), normal (59 percent) or high (23 percent) renin-sodium index. The proportion of patients with low renin hypertension progressively increased with increasing age and blood pressure, there being no difference between the sexes. Two high renin groups emerged: a younger group with early moderate hypertension, and an older group with severe hypertension consequent to possibly ischemic renal disease. Long-term beta blocking monotherapy in 137 patients resulted in a reduction of idastolic pressure to 95 mm Hg or less in 65 percent: 85 percent in those with high and 73 percent in those with normal renin activity; pressure was reduced to this level in only 1 of 24 patients (4 percent) with a low renin index. Antihypertensive efficacy was also related to age, since diastolic pressure was normalized in 80 percent of patients under age 40 years, in 50 percent of those aged 40 to 60 years, but in only 20 percent of those over age 60 years. Age may heolp in patient selection but is no substitute for the more reliable renin index, especially in patients over age 40 years, or with high pressure. Using studiew with propranolol as a standard, similar renin responses were obtained with two cardioselective beta1 type blocking drugs, atenolol and metoprolol, as well as with two nonselective beta2+1 receptor antagonists, LL21945 exhibiting prolonged receptor affinity and oxprenolol in slow release form. These long-acting drugs, which proved effective in single daily doses, could be of value in improving patient compliance...
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PMID:Antihypertensive beta blocking action as related to renin and age: a pharmacologic tool to identify pathogenetic mechanisms in essential hypertension. 24 9

Essential hypertension is increasingly recognized as a nonhomogenous disorder by various methods of study. The hemodynamic approach, coupled with clinical determination of the range and lability of blood pressure, has resulted in the description of several subgroups: labile hypertension with normal or elevated cardiac output, fixed or established hypertension with varying cardiac output and advanced hypertension with normal or low cardiac output. There is a tendency to postulate that these categories are stages of one disorder, but this remains to be proved. Still other patients have been described who may be further set off by exceptionally labile or hyperkinetic features. In some hypertensive patients, the peripheral resistance is normal; however, regardless of its numerical value, it is now considered to be increased if it fails to decrease normally in the presence of elevated cardiac output. Because an elevated cardiac output is the hemodynamic function that differentiates these groups, and renovascular hypertension as well, it is the focus of much current work. New interest in the central blood volume, the peripheral veins, and the portal veins and splanchnic circulation is focused on their connection with cardiac out-put. Newly appreciated, too, is the existence of parasympathetic inhibition in hypertension, which not only contributes to elevations of heart rate, cardiac output and possibly renin secretion, but also depresses baroreflex responses. Thus far, hemodynamic and endocrine mechanisms of hypertension have not been studied together, except possibly through the blood volume, which remains a highly controversial topic. In this paper, some recent work in the above areas is reviewed and emphasis is given to studies in man.
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PMID:Hemodynamic lesions in hypertension. 24 10

1. Urinary kallikrein was measured in 67 patients with essential hypertension and 25 normotensive subjects variously on unrestricted and low sodium diet. Also, the effect of orally applied hog pancreatic kallikrein on elevated blood pressure and kallikrein excretion was evaluated. 2. Urinary kallikrein was reduced in a large subgroup of patients with sustained essential hypertension. 3. With salt restriction, urinary kallikrein rose markedly in normotensive subjects and patients with borderline hypertension but not in those with sustained hypertension. 4. Oral kallikrein normalized reduced kallikrein excretion and lowered elevated blood pressure. 5. The rise in urinary kallikrein with oral kallikrein was due to an increased formation of endogenous enzyme. 6. A defective kallikrein-kinin system may be involved in both the low urinary kallikrein excretion and the hypertension.
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PMID:Low urinary kallikrein excretion and elevated blood pressure normalized by orally kallikrein in essential hypertension. 26 17

Noncompliance with follow-up is a serious problem in the management of hypertension. A retrospective cohort study examined dropout rates and their determinants among 249 randomly selected outpatients with essential hypertension from the medical clinic of an urban teaching hospital. Data were abstracted from hospital records and a subset of dropouts was interviewed. A lifetable analysis revealed that patients who were initiating therapy or who had been under therapy for less than six months had a 50% chance of remaining in care two years later, while 70% of patients who had been under therapy for more than six months at entry were still in care after this period. Patients who were less severely ill by several indicators were the most likely to drop out. It is hypothesized that the low perceived severity of illness, coupled with the costs and inconvenience of care and the lack of physician enthusiasm for the treatment of mild hypertension leads to non-compliance with follow-up.
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PMID:Determinants of dropout rate among hypertensive patients in an urban clinic. 26 42

The use of plasma renin assays in clinical practice is reviewed and experience with an assay for plasma renin activity (PRA) is reported. In normal subjects, 10am ambulant PRA was significantly related to plasma angiotensin II levels but not related to daily urine sodium exretion in these subjects consuming normal diets. PRA was suppressed in patients with mineralocorticoid hypertension and in a small proportion of patients with essential hypertension. Very high values were observed in patients with untreated primary adrenal insufficiency, treatment of which resulted in a prompt fall of PRA to normal. PRA was usually normal in adrenalectomised patients and those with chronic adrenal insufficiency receiving satisfactory steroid replacement therapy. It is concluded that provided standardised conditions are used for the collection and assay, PRA is helpful in the assessment of hypokalaemic hypertension as well as in the early detection and management of patients with primary adrenal insufficiency or related conditions of salt wasting.
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PMID:Clinical use of plasma renin assays. 27 2


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