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

Interpretation of results obtained with angiotensin-converting enzyme inhibition in hypertensive patients has been obscured by the possibility of nonangiotensin-mediated mechanisms, particularly rats, we have compared the effects of converting enzyme inhibition (CEI) by oral captopril administration to those of dextrose. In this setting of constant angiotensin II levels, any apparent effects of CEI must be mediated by a nonangiotensin-related mechanism. Angiotensin II infusion at 30 ng/min increased mean blood pressure by an average of 22 mm Hg. Following 7 days of CEI, effective blockade of converting enzyme was established both by a 10-fold elevation of vasodepressor sensitivity to exogenous bradykinin and a markedly decreased plasma converting enzyme activity. On the ninth day of angiotensin II infusion, mean arterial pressure, heart rate, and plasma renin activity were not different between CEI and dextrose-treated groups. Similarly, blockade of angiotensin II by saralasin induced a comparable fall in blood pressure in both groups. Metabolic studies also revealed no long-term differences in water and food intake, weight change, or sodium and potassium metabolisms. These findings suggest that, in the continued presence of angiotensin II, there is no detectable hemodynamic or metabolic effect of chronic converting enzyme inhibition, and therefore that bradykinin plays little or no role in its long-term antihypertensive action.
Hypertension
PMID:Converting enzyme inhibition during chronic angiotensin II infusion in rats. Evidence against a nonangiotensin mechanism. 626 Jun 47

It has been suggested that an inappropriate relationship between renin and exchangeable sodium is responsible for the hypertension of patients with chronic renal failure. Long-term blockade of the renin system by captopril made it possible to test this hypothesis in 8 patients on maintenance hemodialysis. Captopril was administered orally in 2 daily doses of 25 to 200 mg. Previously, blood pressure averaged 179/105 +/- 6/3 (mean +/- SEM) pre- and 182/103 +/- 7/3 mm HG post-dialysis, despite intensive ultrafiltration and conventional antihypertensive therapy. The 4 patients with the highest plasma renin activity normalized their blood pressure with captopril alone, whereas in the 4 remaining patients, captopril therapy was complemented by salt subtraction which consisted in replacement of 1-2 liters of ultrafiltrate by an equal volume of 5% dextrose until blood pressure was controlled. After an average treatment period of 5 months, blood pressure of all 8 patients was reduced to 134/76 +/- 7/5 mm Hg (P less than 0.001) pre- and 144/81 +/- 9/5 mm Hg (P less than 0.001) post-dialysis without a significant change in body weight. The present data suggest that captopril alone or combined with salt subtraction normalizes blood pressure of patients on chronic hemodialysis with so called uncontrollable hypertension.
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PMID:Uncontrollable hypertension in patients on hemodialysis: long-term treatment with captopril and salt subtraction. 626 27

Reports on spontaneously hypertensive rats suggested that naloxone blocked the antihypertensive effects of clonidine. We compared the effects of an 8-hr intravenous naloxone infusion (6 micrograms/kg/hr) or 5% dextrose in water (D5/W) begun 2 hr before single oral doses of clonidine (0.3 mg) in six men with mild to moderate essential hypertension (EHT). Supine and standing (after 5 min) blood pressure (BP) and heart rate (HR) were measured every 20 min. Initial treatment with naloxone or placebo (D5/W) infusion was randomly allocated, with the alternate treatment given 1 wk later. Naloxone did not modify either supine or standing BP or HR. Clonidine induced a gradual, sustained reduction in both supine and standing systolic and diastolic BP and in supine HR, and there was an increase in standing HR. Naloxone did not modify the onset, maximal effect, or recovery of the hypotensive and HR effects of clonidine in both the supine and standing positions. Our data indicate that hypotensive and bradycardiac effects of clonidine in EHT are not mediated by naloxone-sensitive opioid receptors. They also suggest that opioid receptors play no role in the maintenance of hypertension nor in the BP and HR adjustments induced by postural changes in EHT.
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PMID:Naloxone does not antagonize the antihypertensive effect of clonidine in essential hypertension. 630 46

This is a report of the effects of sugars on salt metabolism and on blood pressure. Twenty young men, none of whom had a personal or family history of hypertension, were orally hydrated after an overnight fast and required to lie recumbent for 6 h except for urinary voiding and blood pressure measurements which were performed at 1/2 h intervals. Venous blood samples were drawn at hourly intervals. The volunteers were kept constantly hydrated by giving them water to drink equivalent to the volumes of urine voided. Two hours from the start of the experiment each subject was given one of the following sugars: glucose, fructose, sucrose, galactose, lactose, or water alone. After oral hydration the subjects appeared to develop natriuresis and kaliuresis. This was quickly abolished by ingestion of either glucose, fructose, sucrose, or lactose, but not by galactose or water alone. Fructose was the most potent antinatriuretic agent. Both glucose and sucrose significantly elevated systolic blood pressure. This lasted for 2 h after glucose ingestion and 1 h after sucrose ingestion.
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PMID:Short-term effects of various sugars on antinatriuresis and blood pressure changes in normotensive young men. 634 11

Reversal of early Goldblatt two-kidney, one-clip hypertension is associated with a fall in plasma renin. To define the role of this in blood pressure normalization we maintained preoperative hypertension for 12 h after unclipping or removal of the ischemic kidney, by angiotensin II or norepinephrine infusions during continuous blood pressure monitoring. High infusion rates of angiotensin II (1 microgram X kg-1 X min-1) were needed to reproduce hypertensive pressures. On stopping angiotensin II there was a rapid initial fall in blood pressure but not to normal (176 +/- 3.1 to 138 +/- 4.3 mmHg at 1 h), and a later slower fall to normal by 24 h (114 +/- 3.9). This response was identical to that of dextrose-infused animals (180 +/- 8.2 to 146 +/- 7.0 at 1 h and 113 +/- 5.6 at 24 h), apart from a transient rise in blood pressure associated with hyperreninemia in unclipped animals 12 h postinfusion. In contrast, after norepinephrine blood pressure fell immediately to normal. Similar responses were seen in normal rats after 12-h pressor infusions of angiotensin II or norepinephrine. These results show that the fast and slow components of the blood pressure fall following reversal of Goldblatt hypertension are delayed but otherwise unaltered specifically by angiotensin II. The need for pharmacologic doses, however, suggests that mechanisms in addition to the direct vasopressor action of angiotensin II are involved.
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PMID:Delayed reversal of Goldblatt hypertension by angiotensin II infusion in the rat. 637 14

In contrast to healthy persons, microvillous antigens of the proximal tubule were excreted at an increased rate in patients with kidney diseases as could be shown using specific antisera against brush border (BB) fragments (tissue-proteinuria, histuria). These urinary membrane components were immunologically completely identical with those antigens prepared from isolated kidney cell membranes. A glycoprotein of 240 000 dalton, containing mannose and N-acetylglucosamine was identified as a major immunoreactive constituent of the brush border surface and found to be part of a multienzyme complex. BB-antigens were excreted in urine of patients with glomerulonephritis, hypertension, pyelonephritis, multiple myeloma, after operations, after kidney transplantation, under cytostatic treatment, and after administration of radiopaque agents. Histuria of BB-antigens was significantly higher in patients with multiple myeloma and Bence-Jones-proteinuria compared to those patients where no Bence-Jones L-chains in urine became apparent. Selective kidney angiography and intravenous urography caused a significantly higher output of BB-antigens as compared to the control period (2 p less than 0,005). In a volunteer model, on the basis of BB-histuria, a different nephrotoxic potency of cephalosporins and aminoglycosides arose. In addition, beside soluble BB-antigens, also high molecular weight membrane vesicles were discovered in urine of patients after cytostatic treatment (cis-platinum), after x-ray contrast media, and after kidney transplantation. Both, soluble as well as supramolecular membrane vesicles were isolated from urine applying immunospecific affinity chromatography (anti-BS-agarose beads). Labeled antisera directed against the vesicle material of urine revealed a specific immunofluorescence of cortical tubule only.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunodiagnosis of kidney tubular cell injuries using specific anti-membrane antibodies]. 638 21

In a patient with severe hypertension in association with insulin-induced hypoglycemia and prior therapy with propranolol hydrochloride, intravenous 50% dextrose significantly reduced arterial pressure on two occasions. Subsequent reduction of arterial pressure was observed with prazosin hydrochloride, an alpha-receptor antagonist. The hypertensive episode may have been caused by hypoglycemia stimulating excessive release of epinephrine. In the presence of vascular beta 2-receptor blockade by propranolol, the hypertensive action of epinephrine was mediated by vascular alpha-receptors. When beta-antagonists must be used in insulin-dependent diabetic patients, beta 1-selective antagonists appear to be a better choice.
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PMID:Hypertensive crisis caused by hypoglycemia and propranolol. 639 8

To counter the paucity of documention on thromboembolic disorders caused by oral contraceptives (OC), a case study is presented describing the incidence of occlusion of arteria centralis retinae in a 24-year old woman after prolonged use of an OC, Bisecurin. She had taken Bisecurin for 4.5 years and had gained 20 kg during that time, but stopped usage 1 month before admission. She was hospitalized with severe deterioration of vision in the left eye. An eye examination indicated an edematous condition of the retina and reddening of the macula. Acuity of vision value for the left eye was .01 vs. 1.0 for the right, which was confirmed by fluorescein fundus angiography. Moderately decreased antithrombin III (AT III) activity was also ascertained. Treatment consisted of immediate retrobulbar injection with Tolazolin followed by Rheomacrodex, Cavinton infusions, B1 and B12 injections, Oradexon subconjunctival injection as well as vitamin B complex, Cavinton, and Colfarit tablets and a fat-free diet. Significant improvement of the left eye condition appeared 4 weeks later. Periodic follow-ups showed the healing of the condition around the macula; however, the patient suffered permanent damage to the retina due to the arterial occlusion above and below the macula. The disturbed lipid values of metabolism were also returned to normal, as borne out by normal dextrose loading results 8 months later (glucose tolerance was abnormal during examination at admission). The estrogen and progesterone components of OCs have been shown to reduce AT III levels, shorten heparin-thrombin coagulation time, increase fibrinogen levels, decrease HDL cholesterol levels, and produce excess TXA2 (thromboxan) resulting in vasoconstriction and thrombocyte aggregation. The risk of thrombosis is 6 times higher in OC users than in nonusers, although other susceptibility factors (obesity, diabetes, hypertension) also contribute to thrombosis.
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PMID:[Arterial occlusion in the ocular fundus induced by oral contraceptives]. 651 54

The effect of alterations in extracellular fluid volume (ECV) and solute concentration on excretion of urinary kallikrein was examined in conscious Sprague-Dawley rats. Animals were given infusions of either dextrose and water, saline, or albumin according to a variety of protocols. These were designed to evaluate possible relationships between excretion of kallikrein, volume, sodium, and potassium. A reproducible pattern of kallikrein excretion was noted in all volume expanded groups. This consisted of a short lived increase during the initial hour of expansion with a subsequent fall to lower levels than baseline and a gradual recovery. To define the role of aldosterone in these studies, an adrenalectomized group and a group of appropriately prepared sham controls were expanded with saline. Adrenalectomy did not effect this pattern. We postulate a tubular "washout" phenomenon as the etiology of these observations. Results of these studies fail to demonstrate a consistent relationship between urinary volume, sodium, or potassium and the simultaneous amount of kallikrein found in the urine.
Hypertension
PMID:Effect of alterations in extracellular fluid volume on urinary kallikrein in the conscious rat. 692 Nov 55

Labetalol administered intra-gastrically in a dose of 30 mg/kg twice a day for 3 weeks significantly lowered systolic tail blood pressure (STBP) in chronic two-kidney Goldblatt hypertension in rats. Hypotensive response of labetalol in normotensive rats has also been demonstrated. Plasma renin activity (PRA) measured at the end of the treatment was similar in labetalol-treated and in dextrose-treated rats. The bradycardial response was evident in both hypertensive as well as in normotensive animals; however,, this change was statistically significant for the hypertensive rats only. Hypertension was associated with increase in the heart weight, which was not affected by labetalol treatment. Antihypertensive effect of labetalol is neither related to renin suppression nor to beta blockade.
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PMID:Effects of labetalol in chronic two-kidney Goldblatt hypertension (2-KGH) in rats. 699 Aug 87


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