UMLS:C0020538 - FACTA Search

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Query: UMLS:C0020538 (hypertension)
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The cause and mechanism of post-carotid endarterectomy hypertension remains unknown. To determine the influence of the sympathetic and renin-angiotensin system, we measured cranial and peripheral plasma levels of catecholamine and renin in patients undergoing carotid endarterectomy. Baseline samples were drawn just before carotid clamping (sample I) and compared with study samples drawn immediately after clamp release (sample II), 2 to 6 hours after surgery (sample III), and then 18 to 24 hours after surgery (sample IV). The patients with post-carotid endarterectomy hypertension had an associated increase of cranial and peripheral norepinephrine levels in the postoperative hypertensive period whereas the patients without post-carotid endarterectomy hypertension did not. This association was most pronounced and statistically significant in cranial samples II (p = 0.032) and III (p = 0.005). Epinephrine and dopamine values did not correlate with post-carotid endarterectomy hypertension. Renin values were higher in cranial than in peripheral samples at time period 2 (p = 0.011), suggestive of a central nervous system Goldblatt phenomenon. However, the renin values did not correlate with post-carotid endarterectomy hypertension. We conclude that post-carotid endarterectomy hypertension is associated with elevated cranial norepinephrine levels, suggestive of a central nervous system sympathomimetic mechanism. Optimal prevention and treatment of this brief but frequently occurring hypertension should include a central-acting sympatholytic agent.
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PMID:Post-carotid endarterectomy hypertension: association with elevated cranial norepinephrine. 264 44

Fifty-four untreated, mildly hypertensive men whose daily alcohol consumption was > or = 28 ml ethanol and who drank at least 4 times per week took part in a randomized, controlled crossover trial. The purpose of the trial was to test the effects of alcohol reduction on blood pressure. After a 2-week familiarization period, the participants were assigned to either a reduced alcohol drinking group or a usual drinking group for 3 weeks (experimental period 1). The situation was then reversed for the next 3 weeks (experimental period 2). The participants were requested to limit their daily alcohol consumption to zero or reduce it as much as possible for the reduced alcohol consumption period. The self-reported alcohol consumption was 56.1 +/- 3.6 (SEM) ml/day during the usual alcohol drinking period and 26.1 +/- 3.0 ml/day during the period of reduced alcohol consumption. Systolic and diastolic blood pressures in the intervention group were found by analysis of variance to be significantly lower (2.6-4.8 and 2.2-3.0 mm Hg, respectively) than those in the control group during experimental period 2 for systolic blood pressure and experimental period 1 for diastolic blood pressure. Significant (3.6 mm Hg) and nonsignificant (1.9 mm Hg) decreases in systolic and diastolic blood pressure, respectively, were observed. The method of Hills and Armitage was used, reducing ethanol in daily alcohol consumption by 28 ml. The lowering effect of reduced alcohol consumption on blood pressure was independent of changes in salt consumption, which were estimated by 24-hour urine collection and body weight.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1993 Feb
PMID:Effect of reduced alcohol consumption on blood pressure in untreated hypertensive men. 842 87

The aims of this retrospective study were to assess renal function and blood pressure after subtotal parathyroidectomy (PTx) performed in renal transplant (RT) patients presenting with persistent hypercalcemic hyperparathyroidism. We identified 34 patients (group A) from our records who had undergone PTx between 1981 and 1994. Group A included 18 women and 16 men with a mean age of 45 +/- 12 years and a mean time on dialysis therapy of 102 +/- 59 months. Thirty of the patients received cyclosporine A (CsA) with or without steroids and/or azathioprine (AZA) and the remaining 4 patients received conventional therapy i.e. AZA and steroids. Twenty-three patients were treated for hypertension and 11 were normotensive. PTx was performed in 21 patients within the first year following renal transplantation and in 13 patients after this period. The study was divided into 3 periods: period 1-pre-PTx; period 2-the month following PTx; period 3-six months after PTx. Parameters were assessed for every patient in each of these periods. Results of group A were compared to those observed in 34 matched (control) RT patients (group B) who did not experience secondary hyperparathyroidism. PTx was associated with a significant decrease in parathyroid hormone (PTH) levels (45 +/- 8 pg/ml vs 338 +/- 54 pg/ml; p = 0.0002) and in calcemia (2.32 +/- 0.18 mmol/l vs 2.75 +/- 0.15 mmol/l; p = 0.0003) during period 3. However, we observed a significant increase in serum creatinine (124 +/- 30 mumol/l vs 110 +/- 25 mumol/l, p = 0.0016) in this group during period 3. Nevertheless, an increase in serum creatinine greater than 30% from baseline which still persisted six months after PTx was only observed in 8 patients (23.5%). There were more hypertensive patients in this latter subgroup (7 out of 8 i.e. 87.5%) than in the rest of the group (16 out of 26 i.e. 64.5%). Renal function impairment in group A was not related to pre-PTx SBP, DBP, MBP, calcemia, creatinine, CsA whole blood trough levels or PTH levels. Conversely, we did not observe significant changes in serum creatinine in the control group during the same periods. During period 2 there was a significant decrease in SBP (134 +/- 16 vs 140 +/- 16 mmHg; p = 0.046), DBP (81 +/- 9 vs 85 +/- 9 mmHg; p = 0.03) and MBP (99.5 +/- 10.5 vs 103.5 +/- 11 mmHg; p = 0.03) of group A. These differences persisted in period 3, with the exception of SBP, although they were no longer statistically significant. Following PTx we were able to discontinue (n = 4) or decrease (n = 4) antihypertensive drugs. In the control group baseline SBP, DBP and MBP were lower than in the PTx group, although the difference was statistically significant only for SBP (132.5 +/- 17 vs 140.5 +/- 16 mmHg; p = 0.05). During the study periods there was no significant changes in SBP, DBP or MBP in the control group. This study shows that RT patients with hypercalcemic hyperparathyroidism are often hypertensive (68%). Subtotal PTx is associated with a significant but transient decrease in SBP, DBP and MBP. Surprisingly we observe a significant and persistent increase in serum creatinine levels in 8 patients (23.5%), particularly in those presenting with hypertension before PTx. These results could reflect a dual effect of parathyroid hormone i.e. a balance between a vasodilating and hypertensive effect.
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PMID:Changes in blood pressure and renal function following subtotal parathyroidectomy in renal transplant patients presenting with persistent hypercalcemic hyperparathyroidism. 912 92

In seven healthy, young subjects on a 240 mmol sodium diet, mean arterial pressure (MAP), renal hemodynamics, and renal handling of Na and exogenous Li were measured at baseline and during short-term nitric oxide (NO) blockade with a 90-minute infusion of 3.0 microg x kg(-1) x min(-1) of N(G)-L-arginine methyl ester (L-NAME). The infusion was performed twice: after a 3-day pretreatment with either placebo or 50 mg losartan to block Ang II receptors. With placebo, L-NAME produced no change in MAP from 0 to 45 minutes (period 1) and only a 5% increase at 45 to 90 minutes (period 2) of infusion. Effective renal plasma flow (ERPF, PAH clearance) and glomerular filtration rate (GFR, inulin clearance) declined by 11.7% and 8.0%, respectively in period 1 and by 14.6% and 11.6%, respectively, in period 2. Calculated renal vascular resistance (RVR) increased by 13.0% to 20.6%. Fractional excretion of Na (FE(Na)) and Li (FE(Li)) fell by 30.0% and 21.0%, respectively, in period 1 and by 44.2% and 31.1% in period 2. All these variations were significant versus baseline. With losartan, the rise in MAP at 45 to 90 minutes was completely abolished, whereas all changes in ERPF, GFR, RVR, FE(Na), and FE(Li) in response to L-NAME were the same as those observed with placebo. The present data show that NO blockade with low-dose systemic infusion of L-NAME produces renal vasoconstriction, reduced GFR, and increased tubular Na reabsorption independent of changes in MAP. Reduced FE(Li) indicates an effect of NO on the proximal tubule. Since these changes are not prevented by losartan, we conclude that in Na-repleted humans, renal vasoconstriction and Na-retaining effects of inhibition of basal NO production are not due to the unopposed action of endogenous Ang II.
Hypertension 1997 Sep
PMID:Angiotensin II blockade does not prevent renal effects of L-NAME in sodium-repleted humans. 932 81

The results of recent studies have demonstrated that angiotensin (Ang)-(1-7) contributes to the antihypertensive actions of either combined ACE/Ang II type 1 receptor blockade or ACE inhibition alone. The vasculature is a key site of action for either drug regimen, and evidence favors a local Ang system within these tissues. Because ACE may degrade Ang-(1-7), we determined whether ACE inhibition alters Ang-(1-7) release from the rat hindlimb perfused with Krebs-Ringer buffer containing Ficoll. Ang-(1-7) release averaged 36+/-13 fmol (period 1, 15-minute collection) and 44+/-11 fmol (period 2) in the control buffer. The addition of the ACE inhibitor lisinopril to the perfusion buffer augmented levels of Ang-(1-7) in periods 3 (144+/-39 fmol) and 4 (163+/-35 fmol; P<0.05 versus 1 or 2, n=8). HPLC and radioimmunoassay of effluent from control or lisinopril treatment demonstrated a single immunoreactive peak with a retention time identical to that of Ang-(1-7). The addition of the neprilysin inhibitor SCH 39370 reduced Ang-(1-7) release in the lisinopril buffer from 177+/-32 (period 1) and 173+/-39 (period 2) fmol to 112+/-24 (period 3) and 87+/-23 fmol (period 4; P<0.05 versus 1 or 2, n=6). Ang I metabolism in the collected perfusate revealed the formation of Ang-(1-7) that was sensitive only to thimet oligopeptidase inhibition; Ang II generation was not detected. The present study demonstrates the recovery of endogenous Ang-(1-7) from the perfused hindlimb. The release of Ang-(1-7) is significantly influenced by inhibition of ACE, which may reflect both increased substrate (Ang I) levels and reduced metabolism of the peptide. Neprilysin inhibition reduced but did not abolish Ang-(1-7) release, which suggests that other endopeptidases may contribute to the release of the peptide.
Hypertension 2000 Jan
PMID:Release of angiotensin-(1-7) from the rat hindlimb: influence of angiotensin-converting enzyme inhibition. 1064 23

Eight Na-repleted volunteers underwent 3 separate 90-minute infusions of either N(G)-nitro-L-arginine methyl ester (L-NAME) 3.0 mg. kg(-1). min(-1) or endothelin-A receptor (ET-A) blocker BQ-123 (BQ) 0.125 nmol. kg(-1). min(-1) or both. Mean arterial pressure (MAP), glomerular filtration rate (GFR), renal blood flow (RBF), renal vascular resistances (RVR), and sodium excretion rate (UNaV) were measured at baseline (b) and from 0 to 45 minutes (period 1) and 45 to 90 minutes (period 2) of infusion. BQ alone had no effect. GFR declined by 4.9% (P<0.001 versus b) in period 1, to 9.9% (P<0. 001) in period 2 with L-NAME, and by 3.3% (P<0.01) to 6.6% (P<0.001) with L-NAME plus BQ (P=NS between L-NAME and L-NAME plus BQ). UNaV fell equally with L-NAME or L-NAME plus BQ. MAP rose significantly in period 2 with L-NAME (6.9%; P<0.001) but not with coinfused BQ (2. 1%; P=NA versus b, P=0.005 versus L-NAME alone). RBF declined by 12. 2% (P<0.001) to 18.3% (P<0.001) with L-NAME and by 4.6% (P<0.005) to 8.2% (P<0.001) with L-NAME plus BQ. These changes were smaller with L-NAME plus BQ (P<0.05 in period 1 and P<0.02 in period 2). Blunted changes were also seen for RVR (P<0.005 in period 1 and P<0.001 in period 2 between L-NAME alone and L-NAME plus BQ). These findings show that systemic and renal vasoconstriction due to L-NAME are attenuated by BQ, which suggests that an interaction between endogenous nitric oxide production and ET-A activity participates in the maintenance of baseline systemic and renal vascular tone in humans.
Hypertension 2000 Jan
PMID:Endothelin-A blockade attenuates systemic and renal hemodynamic effects of L-NAME in humans. 1064 52

The whole blood and plasma viscosity changes in course of acute myocardial infarction were examined. The examination were performed at the beginning of acute phase of myocardial infarction (period 1), at second to third day (period 2) and after about 10 days of infarction episode (period 3). 77 patients (mean age 56.8 +/- 9.8 years) suffered from myocardial infarction were examined. The whole blood viscosity at following shear rates [s-1]: 0.116; 1.0; 4.59; 150 and plasma viscosity were performed. Besides the viscometric examinations the total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, glucose and fibrinogen as well as blood morphology and ESR were determined. All rheological measurements were carried out at the temperature of 37 degrees C immediately after blood drawing. The control group consisted of 110 healthy persons (aged 56.6 +/- 10 years). Some persons of control group have got risk factors of atherosclerosis as: obesity, artery hypertension and cigarette smoking. The following additional parameters were investigated: hematocrit, the artery pressure, the body mass index, total cholesterol concentration, serum LDL-cholesterol, HDL-cholesterol, fibrinogen and blood morphology. The corrected whole blood viscosity was adjusted to 45% of hematocrit. It was stated that the native whole blood viscosity was disturbed at all periods of disease. The corrected whole-blood viscosity in all periods of acute myocardial infarction comparing with controls increased. The greatest rise of corrected whole blood viscosity was especially observed in second period of acute myocardial infarction. Plasma viscosity in patients with acute myocardial infarction is increased in all periods. The greatest rise of plasma viscosity was in second period of disease. The rheological blood and plasma disturbances were connected with increase of total cholesterol, LDL-cholesterol, triglycerides and fibrinogen. These disturbances of blood and plasma viscosity may play a role in promoting myocardial infarction factors.
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PMID:[The whole blood and plasma viscosity changes in course of acute myocardial infarction]. 1264 42

The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) published its main findings in December, 2002. It recommended thiazide diuretics as a first-line treatment of hypertension. The current study describes the prescribing patterns of thiazide diuretics in four regions of Kaiser Permanente, a large national United States Health Maintenance Organization--two regions that had an ALLHAT clinical center and two that did not. We tested the hypothesis that participation in a clinical trial leads to quicker and greater adoption of study recommendations than non-participation in a trial. The relative percentage of filled outpatient prescriptions for the period 2 or 3 years before the ALLHAT main publication through December 31, 2004 was calculated by region for thiazide-type diuretics and for calcium channel blockers (CCBs), beta-blockers, central alpha-blockers, angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and other antihypertensive diuretics. In the 2 years after publication of the ALLHAT trial findings, the percentage of all prescriptions for thiazide diuretics increased from 11.2% to 12.4% in the two regions with an ALLHAT clinical site and from 8.9% to 10.1% in the two regions without an ALLHAT clinical site (p > 0.05). The percentage of new prescriptions for thiazide diuretics increased from 13.7% to 16.6% in the two regions with an ALLHAT clinical site and from 10.8% to 13.0% in the two regions without an ALLHAT clinical site (p > 0.05). Participation in a clinical hypertension study does not appear to accelerate adoption of study recommendations.
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PMID:Prescribing patterns for thiazide diuretics in a large health maintenance organization: relationship to participation as an ALLHAT clinical center. 1676 53

Whether intensive pharmacologic cardiovascular risk factor management reduces metabolic syndrome (MetS) prevalence is unknown. The authors compared the number of secondary prevention medications and National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III)-defined MetS prevalence in coronary artery disease patients entering cardiac rehabilitation from 1996 to 2001 (period 1, n=516) with those entering from 2002 to 2006 (period 2, n=609). Age, sex, and ethnicity were similar in both periods. From period 1 to period 2, participants took more secondary prevention medications (2.8+/-1.3 vs 3.5+/-1.0, P<.001). Prevalence of low high-density lipoprotein cholesterol (66% vs 66%), diabetes (37% vs 38%), and hypertension (81% vs 81%) were unchanged. The prevalence of hypertriglyceridemia decreased (48% vs 36%, P<.001), but the proportion meeting criteria for elevated waist circumference increased (51% vs 58%, P<.05), resulting in no change in overall MetS prevalence (60% vs 59%, P=NS). More emphasis on therapeutic lifestyle change in addition to intensive pharmacologic therapy is needed to reduce MetS prevalence in patients with coronary artery disease.
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PMID:Drugs are not enough: the metabolic syndrome--a call for intensive therapeutic lifestyle change. 1924 12

Sesamin, one of the lignans contained in sesame, has been considered to have medicinal effects. It has been reported that sesamin suppressed the development of hypertension in rats. In this study, using a double-blind, cross-over, placebo-controlled trial, we investigated the effect of 4-wk administration of sesamin on blood pressure (BP) in mildly hypertensive humans. Twenty-five middle-aged subjects with mild hypertension were divided into two groups, matched by age and body mass index. Twelve subjects were allocated to 4-wk intake of capsules with 60 mg sesamin per day and 13 subjects to 4-wk intake of a placebo (period 1). After a 4-wk washout period, the subjects received the alternative administration for 4 wk (period 2). BP decreased with statistical significance with the administration of sesamin (systolic: 137.6+/-2.2 to 134.1+/-1.7 mmHg, p=0.044, diastolic: 87.7+/-1.3 to 85.8+/-1.0 mmHg, p=0.045), but little changed with the placebo (systolic: 135.0+/-1.8 to 135.1+/-1.7 mmHg, diastolic: 85.9+/-1.2 to 86.6+/-1.2 mmHg). In conclusion, 4-wk administration of 60 mg sesamin significantly decreased BP by an average of 3.5 mmHg systolic BP and 1.9 mmHg diastolic BP. These results suggest that sesamin has an antihypertensive effect in humans. Epidemiological studies suggested that a 2-3 mmHg decrease in BP reduces the rate of cardiovascular diseases; therefore, it is considered that BP reduction achieved by sesamin may be meaningful to prevent cardiovascular diseases.
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PMID:Antihypertensive effects of sesamin in humans. 1935 68

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