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

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

Renal artery constriction in the unilaterally nephrectomized, trained dog, with maintained renal arterial hypotension, produces a prompt increase in systemic renin activity and blood pressure. The hypertension normally induced by renal artery stenosis is prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro (SQ 20, 881), which blocks conversion of angiotensin I to angiotensin II. Constant intravenous infusion of the inhibitor over several days of renal artery constriction prevents the development of chronic renovascular hypertension. Furthermore, a single injection of the nonapeptide restores blood pressure to normal in the early phase of renovascular hypertension, but becomes progressively less effective as salt and water retention occurs in the chronic stage when plasma renin activity returns to control levels. These data provide strong evidence that the renin-angiotensin system is responsible for the initiation of renovascular hypertension in the one-kidney Goldblatt dog, but that other factors become increasingly important in chronic renovascular hypertension.
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PMID:Inhibition of angiotensin conversion and prevention of renal hypertension. 23 18

In various kinds of hypertension clonidine induced a decrease in urinary catecholamines, plasma renin activity and urinary aldosterone, concommitant with a fall in blood pressure and pulse rate in both short term and chronic studies. Furthermore, clonidine lowered the plasma levels of noradrenaline and adrenaline but a postural increase in upright position still occurred. The capacity to increase renin during salt restriction seemed mainatined. When clonidine was withdrawn all parameters returned to pretreatment levels but in some cases a marked rebound increase in catecholamine production was seen. --During clonidine the increase in catecholamines and renin after insulin induced hypoglycemia was largely abolished. Under basal conditions oral penbutolol induced a decrease of pule rate and blood pressure but no change in plasma or urinary catecholamines. During treatment plasma renin was suppressed at rest and after exercise. A work load, which led to only minor changes in blood catecholamines before treatment, was associated with a marked increase during penbutolol. Medication with penbutolol reduced the response in plasma catecholamines after hypoglycemia and renin activity remained low. Clonidine seems to act mainly by central inhibtion of symapthetic tone. Penbutolol probably acts mainly peripherally but may also have a central effect.
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PMID:The effect of clonidine and penbutolol, respectively on catecholamines in blood and urine, plasma renin activity and urinary aldosterone in hypertensive patients. 23 81

An assay method has been developed to measure phospholipase A2 (PLA2) in ratserum and to study the possible role of this enzyme in experimental hypertension. Experiments with rat serum following 48 h of bilateral nephrectomy indicated a decrease inPLA2 activity, suggesting that kidneys might be playing an important role in regulating serum PLA2 activity and that kidneys might be a source of this enzyme. Experiments with renal hypertensive rats, spontaneously hypertensive rats, and rats receiving a low-salt diet demonstrated that a decrease in PLA2 activity was found only in those conditions in which elevated plasma renin activity was accompanied by elevated blood pressure. When elevated plasma renin activity was not accompanied by elevated blood pressure, serum PLA2 activity was unchanged. These observations represent the first biochemical separation between conditions of elevated plasma renin activity without an increase in blood pressure and conditions of elevated plasma renin activity with an increasein blood pressure.
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PMID:Phospholipase A2 in experimental hypertension. 23 1

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

A technique for continuous and quantitative collection of parotid saliva--including salivary flow rate determination--for in vivo experiments in rats is described. Excretion of kallikrein-like activity in parotid saliva of rats with various forms of arterial hypertension (genuine, renovascular and DOCTMA-salt hypertension) was studied. Kallikrein excretion was measured by its esterolytic activity. The levels of kallikrein-like activity in parotid saliva of normotensive control rats ranged between 2.5--4.0 mU/min during salivary flow stimulation with pilocarpine. In all forms of experimental hypertension salivary excretion of kallikrein-like activity was increased 2--4 fold. This increase was not related to the activity of the renin-angiotensin system.
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PMID:Kallikrein excretion in parotid saliva in rats with various forms of arterial hypertension. 26 42

beta-Aminopropionitrile, a specific inhibitor of lysyl oxidase prevented the rise in blood pressure induced by deoxycorticosterone-salt in rats. In addition, after the onset of hypertension, administration of beta-aminopropionitrile lowered the blood pressure. Concomitant with the lowering of blood pressure, there was a reduction in the more highly crosslinked form of vascular collagen. These findings would indicate that increases in vascular connective tissue are not only sequelae of hypertension, but may also contribute to the maintenance of elevated blood pressure.
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PMID:Reduction of blood pressure and vascular collagen in hypertensive rats by beta-aminopropionitrile. 26 88

Our way to prevention is to find a list of traits known to be predictors of elevated blood pressure. This list of predictors offers means for the early identification of susceptibile persons. Years of experience in preventive work indicate that such identification is always useful for developing preventive programmes, since it gives a focus for action (5). Most of the predictors show possible ways in which action could be directed towards prevention of hypertension and reduction of elevated blood pressure. We will focus on salt, control of obesity, physical exercise, and meditation. We would like to discuss preventive aspects of hypertension and the possibility of treating with other methods than drugs.
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PMID:The prevention of hypertension. 26 28

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

1. The concentration of catecholamines was measured in several brain areas of the Hewbrew University Sabra rat (SB rat), and in two substrains selected for their respective sensitivity (H) or immunity (N) to hypertension. 2. Hypertension was induced in SB rats by DOCA-salt, renal artery constriction and NaCl 1.7% drinking. The noradrenaline content was consistently elevated in the medulla oblongata of hypertension animals. In other brain areas the rise in noradrenaline varied in the different types of hypertension. 3. Administration of DOCA-salt to H and N rats, while causing marked hypertension in the former, had no effect on noradrenaline in either strain. 4. Untreated, normotensive N rats had in the medulla oblongata, significantly higher concentrations of noradrenaline than did H rats. 5. Differences in brain noradrenaline may explain the inherited susceptibility or resistance to hypertension in H and N rats.
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PMID:Hypertension and brain catecholamine distribution in the Hebrew University Sabra, H and N rats. 28 36


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