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

Fifty hypertensive untreated outpatients (34 women, 16 men), with stage I and II essential hypertension, were studied in comparison to 50 age- and sex-matched controls with similar life-styles. Total cholesterol triglycerides, LDL-cholesterol, VLDL-cholesterol, and HDL-cholesterol were measured by enzymatic methods, and apolipoproteins AI, AII, B, CII, CIII and E by RID. The results showed significant differences between hypertensives and controls respectively in triglycerides (135.2 +/- 73.9 versus 90.2 +/- 33.8, P less than 0.01) and VLDL cholesterol (26.7 +/- 14.8 versus 17.7 +/- 6.6, P less than 0.01) while no significant differences were observed in total, LDL and HDL cholesterol. Significant differences between the two groups were also observed in apolipoproteins, particularly in apo AI (130.0 +/- 28.2 versus 144.9 +/- 27.9, P less than 0.05), apo AII (32.9 +/- 10.2 versus 39.6 +/- 11.4, P less than 0.01), apo CII (4.0 +/- 2.6 versus 5.4 +/- 2.9, P less than 0.05) and apo E (5.0 +/- 1.8 versus 4.3 +/- 1.8, P less than 0.05), while no significant differences were observed in apo B and CIII values. The results suggest that in untreated hypertensive patients alterations in the apolipoproteins profile are present which, in part, may be responsible for the elevated incidence of cardiovascular disease, independently from the blood pressure values.
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PMID:Serum lipids and apolipoproteins in patients with essential hypertension. 187 22

The study objective was to determine the effects of monotherapy with clonidine and atenolol versus placebo on serum lipids, apolipoproteins, and blood pressure in patients with mild primary hypertension. The protocol comprised a double blind, randomized, placebo-controlled 5-month prospective study carried out in an outpatient general internal medicine clinic in a university medical center. There were 92 patients ages 18 to 70, with mild primary hypertension (sitting diastolic blood pressure of greater than 90 mm Hg and less than 105 mm Hg) without significant cardiac, renal, cerebrovascular, hepatic, neoplastic, or hematologic disorders. Patients with severe hyperlipidemia or peripheral vascular disease were also excluded. All factors known to effect serum lipids were held constant throughout the study (i.e., diet, weight, exercise, caffeine, tobacco). Atenolol and clonidine significantly reduced blood pressure when compared with placebo. Atenolol caused significant increases in serum triglycerides and apolipoprotein B (p less than 0.05) and significant reductions in high-density lipoprotein-cholesterol, apolipoproteins A-I and A-II (p less than 0.05). Atenolol also induced a significant adverse effect on all lipid ratios, increasing total cholesterol/high density lipoprotein-cholesterol, low density lipoprotein-cholesterol/high density lipoprotein-cholesterol, apolipoprotein B/apolipoprotein A-I and apolipoprotein B/apolipoprotein A-II ratios and decreasing low density lipoprotein-cholesterol/apolipoprotein-B ratio (p less than 0.05). Clonidine caused significant reductions in high-density lipoprotein-cholesterol, apolipoproteins AI and AII (p less than 0.05 but was neutral on all other lipids, lipid subfractions, and apolipoproteins. Clonidine did not significantly alter any of the lipid ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of clonidine hydrochloride versus atenolol monotherapy on serum lipids, lipid subfractions, and apolipoproteins in mild hypertension. 219 93

In order to investigate the role of plasma angiotensin I (pAI) converting enzyme on the activity of the renin-angiotensin system, we measured plasma renin activity (PRA), plasma angiotensin II (pAII), and plasma angiotensin I converting enzyme (pACE) activity in fourteen patients with essential hypertension before and after two hours of ambulation combined with intravenous furosemide administration. Significant increases were observed in the values of PRA (p less than 0.005), pAII (p less than 0.005) and ACE activity (p less than 0.05) after ambulation. The ratios of log pAII/log PRA were increased significantly after ambulation (p less than 0.005), and a significantly positive correlation was observed between log pAII/log PRA and ACE activity (p less than 0.01). These results suggested that not only PRA but also ACE activity contributed to the activity of renin-angiotensin system through the generation of AII.
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PMID:The role of plasma angiotensin I converting enzyme in regulation of renin-angiotensin system activity in patients with essential hypertension. 283 30

1. The adrenal cortical 'hybrid' steroids 18-oxocortisol (18-OF) and 18-hydroxycortisol (18-OHF) are elevated in patients with typical angiotensin-unresponsive aldosterone-producing adenoma (AII-unresponsive APA) and fall to normal following surgical removal of the adrenal containing the tumour. Since 18-OF was six times the upper limit of normal pre-operatively, the tumour was the site of overproduction of hybrid steroids. 2. The failure of angiotensin-responsive APA to overproduce the hybrid steroids may be linked to their more 'normal' production of cortisol, which falls significantly on removal of the tumours. 3. Hybrid steroid levels were also normal in patients with idiopathic hyperplasia of the adrenals (IHA) and in low renin essential hypertension. 4. In AII-responsive APA, glucocorticoid-suppressible hyperaldosteronism (GSH) and IHA, the hybrid steroids showed brisk responses to stimulation by ACTH and suppression by dexamethasone of endogenous ACTH. 5. Long-term suppression by dexamethasone of hybrid steroids in GSH is consistent with ACTH dependence, rather than angiotensin dependence. 6. Studies of the regulation of hybrid steroid secretion in various categories of hypertension will further define the biosynthetic distinctiveness which is already useful diagnostically.
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PMID:Adrenal transitional zone steroids, 18-oxo and 18-hydroxycortisol, useful in the diagnosis of primary aldosteronism, are ACTH-dependent. 285 57

Plasma angiotensin I and II (AI and AII) were measured in 13 patients with essential hypertension before and during chronic treatment with enalapril (MK 421) and in seven subjects during an acute study. Two techniques were used for simultaneous extraction of AI and AII. Despite appropriate correction for cross-reaction of AI with the AII antibody, one of the techniques gave consistently higher AII and lower AI levels in plasma of subjects treated with enalapril. The possibility of in vitro conversion of AI into AII-immunoreactive material during the purification or the radioimmunoassay steps should be considered. The use of the alternative technique is proposed for simultaneous processing of blood samples for AI and AII.
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PMID:Apparently high plasma angiotensin II levels in patients with essential hypertension treated by converting enzyme inhibition. 298 12

Alert spontaneously hypertensive (SH) rats, prepared with indwelling carotid artery catheters, demonstrated heightened and prolonged blood pressure (BP) responses to intracerebroventricular (i.c.v.) injections of 10 and 100 pmol angiotensin II and III (AII and AIII) as compared with Wistar-Kyoto (WKY) and Sprague-Dawley normotensive animals. Pretreatment with the aminopeptidase B inhibitor bestatin (10 nmol, i.c.v.) potentiated and prolonged the heightened pressor response to AIII (100 pmol, i.c.v.) in SH rats. These results suggest that dysfunction of angiotensin peptidase activity may be contributing to the progressive and sustained elevations in blood pressure noted to occur in the SH rat model of human essential hypertension.
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PMID:Dysfunction of central angiotensinergic aminopeptidase activity in spontaneously hypertensive rats. 300 99

Multiple lines of evidence suggest that intrarenal angiotensin AII formation participates in the control of renal perfusion and function. Inappropriate activation of this intrarenal system may participate in the pathogenesis of hypertension in about 45 percent of patients with essential hypertension, a group that we call "non-modulators" (NM). In NM the renal vascular response to AII is blunted when the subjects are on a high-salt diet, but appropriate when they are on a low-salt diet. Converting enzyme inhibition in NM induces a larger increase in renal blood flow, than occurs in normal subjects or other patients with essential hypertension, most evident when they are on a high-salt diet. The renal vasodilatation is not due to prostaglandin or bradykinin accumulation in the kidney, since the increase in renal blood flow induced by converting enzyme inhibition is associated with an enhanced renal vascular response to AII. When NM are shifted from a low to a high sodium intake, they show more positive sodium balance, gain more weight and increase their blood pressure more--the characteristics of sodium sensitive hypertension. Converting enzyme inhibition corrects their inability to handle a sodium load as it improves renal blood flow, and induces a depressor response that does not correlate with plasma renin activity. Many of these characteristics are shown in a normotensive offspring of essential hypertensives: since sodium handling is genetically determined, this abnormality may represent the inherited renal abnormality. An abnormality in the control of the renal circulation by AII, reversed by converting enzyme inhibition, may represent a fundamental abnormality in the pathogenesis.
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PMID:The renal response to converting enzyme inhibition and the treatment of sodium-sensitive hypertension. 303 17

To determine whether prostaglandins contribute to the depressor response to the converting enzyme inhibitor, captopril, we measured the plasma prostaglandin levels by radioimmunoassy before and after captopril administration, and then examined the effect of prostaglandin synthetase inhibition on captopril's antihypertensive effect. When a single oral captopril dose (25-100 mg) was given to 31 sodium-restricted patients with essential hypertension, the levels of the stable transformation product of prostacyclin remained unmeasurable and that of thromboxane A2 did not change, while the metabolite of PGE2 (PGE-M) increased by 53% (34 +/- 4pg/ml pre-captopril, 52 +/- 5 pg/ml after; p less than 0.001). As expected, blood pressure (BP) and angiotension II (AII levels fell, and kinin levels rose (all changes p less than 0.001). We then blocked prostaglandin synthesis in 18 of these subjects for 24 hours with either indomethacin (n = 10) or aspirin (n = 8) before repeating the captopril dose, to assess the importance of these PGE-M increments. The PGE-M responses to captopril were effectively blocked in nine of 10 subjects receiving indomethacin and four of eight receiving aspirin. In these 13 patients, the depressor response to captopril was significantly blunted (-20 +/- 3mm Hg pre-synthetase inhibition vs - 13 +/- 2 mm Hg post; p less than 0.05). When these agents did not block the PGE-M response to captopril, the BP response was also unchanged (-15 +/- 4mm Hg pre, -18 +/- 5mm Hg post). Neither indomethacin nor aspirin changed the AII or kinin responses to captopril. We conclude that the prostaglandins may be important mediators of captopril's antihypertensive effect in the sodium-restricted state.
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PMID:Contribution of prostaglandins to the antihypertensive action of captopril in essential hypertension. 626 Jun 45

The renal hemodynamic response to subpressor doses of angiotensin II (AII; 0.1 and 0.5 ng/min/kg) was investigated in untreated 49-year-old men (n = 50) representing a wide blood pressure range. Renal blood flow, renal vascular resistance (RVR), glomerular filtration rate (GFR), filtration fraction (FF), plasma renin activity (PRA), plasma AII, plasma aldosterone, and the urinary excretion of sodium and norepinephrine were studied. The higher the initial blood pressure the greater was the increase in RVR in response to AII infusion (p less than 0.002), indicating an increased renal vascular reactivity with increase in initial blood pressure. The AII infusion gave a significant rise in RVR in both the borderline and hypertensive group, but gave no increase in RVR in the normotensive group, implying an enhanced sensitivity of the renal vasculature in the borderline and hypertensive group. The increase in RVR was greater in the hypertensive than in the borderline group, i.e., the hypertensives had a steeper dose-response curve than the borderline group, which points to the presence of structural vascular changes in the renal vessels in the hypertensives. The increase in RVR in response to AII was positively correlated to sodium intake and plasma aldosterone concentration, indicating that these two factors might modulate the renal vascular reactivity. These factors could, however, only partly explain that RVR increased more the higher the initial blood pressure. Thus, the results indicate that there is an increased reactivity of the renal vascular bed to AII in essential hypertension. The increased reactivity seems to be mediated through an increased sensitivity of the renal vasculature to AII in mild essential hypertension and also through the presence of structural vascular changes in established hypertension. These factors may lead to a reduced excretion of sodium and water and may therefore be of importance in the development and progression of essential hypertension.
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PMID:Effects of subpressor doses of angiotensin II on renal hemodynamics in relation to blood pressure. 634 Dec 20

The biological actions of angiotensin III (AIII) in animals have been reported to be stimulation of aldosterone secretion and vasoconstriction. However, the biological actions of AIII in human essential hypertension (EH) have not been evaluated. Twenty ng/Kg/min of AIII was infused intravenously for 30 min into 6 normal subjects and 24 patients with EH. The systolic blood pressure was elevated significantly, from 116 +/- 5 (mean +/- SD)/68 +/- 4 to 137 +/- 9/74 +/- 5 mmHg in normal subjects and from 155 +/- 29/95 +/- 17 to 176 +/- 26/106 +/- 20 mmHg in EH patients. The elevation in systolic BP of low-renin EH patients was significantly larger than that of normal-renin EH patients. Plasma renin activity (PRA) decreased significantly from 1.64 +/- 1.07 to 1.21 +/- 1.05 ng/ml/hr in normal subjects and from 0.88 +/- 0.66 to 0.76 +/- 0.63 ng/ml/hr in EH. Plasma aldosterone concentration (PAC) increased significantly from 57 +/- 34 to 116 +/- 34 pg/ml in normal subjects and from 66 +/- 56 to 91 +/- 24 pg/ml/ in EH. There was no significant difference between the increase of PAC in low-renin EH and in normal-renin EH. Plasma cortisol concentration (PCC) did not change in these subjects. There were no significant relationships between the changes of PRA and PAC or PRA and blood pressure. These results suggest that the pressor action of AIII appeared in relation to the basal PRA in EH. In EH, PRA is suppressed by the direct action of AIII in the kidney and neither by increased PAC nor by increased blood pressure. The small changes in blood pressure caused by AII infusion suggest that a test using an AIII infusion for aldosterone stimulation would be preferable to an angiotensin II infusion.
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PMID:Effect of angiotensin III on blood pressure, renin-angiotensin-aldosterone system in normal and hypertensive subjects. 637 63


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