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

A morphological restructuring of cardiac and arteriolar tissue is common in hypertension. The parallel evolution of these two processes as a compensatory response to pressure overload is a frequently assumed but unsubstantiated hypothesis. To evaluate this possibility, we have concomitantly measured left ventricular mass (LVM; two-dimensional echo) and minimal forearm vascular resistance (FVR; derived from the ratio of intra-arterial blood pressure: forearm blood flow by venous plethysmography) at maximal postischemic (13 min ischemia + 1 min hand exercise) reactive hyperemia. The study was performed on 29 essential hypertensive patients (15 males, 14 females, aged 50 +/- 10 years) who had not been undergoing treatment for hypertension for at least 15 days at the time of study. Minimum FVR was taken as a hemodynamic index of the integrated arteriolar lumen at the forearm level. LVM index and minimum FVR ranged from normal to clearly altered values. In spite of a wide spread of values, no correlation existed between the individual values of the two variables. Systemic mean blood pressure correlated with minimum FVR and tended to correlate with LVMI. Thus, morphological restructing of cardiac and arteriolar tissue does not seem to evolve in parallel in human hypertension. Pressure overload may contribute to cardiovascular hypertrophy, but other unrelated mechanisms may also underlie the development of cardiac and arteriolar abnormalities of human hypertension.
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PMID:Lack of correlation between cardiac mass and arteriolar structural changes in mild-to-moderate hypertension. 166 74

The effects of antiarrhythmic doses of lidocaine on efferent sympathetic outflow or sympathetic responses to autonomic stimuli in humans are unknown. In the present study, direct recordings of postganglionic muscle sympathetic nerve activity (MSNA), which modulates vascular tone, were obtained from the peroneal nerve of 22 healthy volunteers (aged 20 to 27 years). Baseline cardiac intervals (ECG), arterial pressure (radial artery), central venous pressure (CVP, jugular vein), forearm vascular resistance (FVR, Hg-in-Silastic plethysmography), and MSNA were identical in two randomized study groups (lidocaine [L], 1.5 mg/kg bolus, followed by 2 mg/min infusion, n = 12; and placebo [P] saline bolus and infusion, n = 10). Each underwent a cold pressor test (CPT, ice packs to foot for 90 seconds) and baroreceptor test (sequential boluses of 100 micrograms of sodium nitroprusside and 100 micrograms of phenylephrine). Five minutes after the bolus administration of L, plasma L levels were 3 micrograms/mL, which was associated with significant (P less than 0.05) increases in systolic and diastolic pressures (6.6 +/- 2.4 and 5.5 +/- 1.1 mm Hg). This elicited significant reflex decreases in MSNA (-3 +/- 1.1 bursts/100 cardiac cycles) and RR interval (-63 +/- 14 ms). The hypertension, tachycardia, forearm vasoconstriction, and MSNA increase in response to the CPT were significantly attenuated and the sympathoexcitatory response to baroreceptor unloading was blunted by L. These responses were not altered during the administration of P. In the steady-state L infusion period, plasma levels were subtherapeutic (1 microgram/mL) and were insufficient to consistently alter autonomic stress responses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lidocaine attenuates efferent sympathetic responses to stress in humans. 193 48

Systemic inhibition of endothelium-derived relaxing factor (EDRF) synthesis leads to acute hypertension and increased peripheral vascular resistance. The changes in vascular resistance are not evenly distributed to all vascular beds. In this study, we compared the renal and femoral hemodynamic responses to EDRF synthesis inhibition. Renal blood flow (RBF) and femoral blood flow (FBF) were assessed in the presence and absence of DuP 753, an angiotensin II receptor antagonist. Inhibition of EDRF synthesis by a bolus dose of Lw-nitroarginine methyl ester (L-NAME) increased blood pressure (BP) by 21 +/- 1 mm Hg (p < 0.001) and decreased RBF by 32 +/- 5% (from 5.9 +/- 0.5 to 3.9 +/- 0.3 ml/min/g kidney weight; p < 0.005) while FBF remained unchanged (9.5 +/- 0.4 versus 9.4 +/- 0.4 ml/min). Renal vascular resistance (RVR) increased by 83 +/- 16% (p < 0.001), compared with only a 24 +/- 6% increase in femoral vascular resistance (FVR; p < 0.005). To eliminate the influence of systemic hypertension, we returned organ perfusion pressure to pre-L-NAME levels by partial aortic constriction. The kidney maintained RBF by decreasing RVR by 8 +/- 2% (p < 0.02), while FBF decreased by 15 +/- 5% (p < 0.01). When rats were pretreated with DuP 753, L-NAME still increased BP by 22 +/- 2 mm Hg, but RVR increased by only 26 +/- 5% (from 13.2 +/- 1.6 to 16.8 +/- 2.7; p < 0.01) and RBF did not change. DuP 753 had no effect on the femoral vascular response to L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal versus femoral hemodynamic response to endothelium-derived relaxing factor synthesis inhibition. 835 52

Hypercholesterolemia and hypertension are frequently associated with elevated sympathetic activity. Both are independent cardiovascular risk factors and both affect endothelium-mediated vasodilation. To identify the effects of cholesterol-lowering and antihypertensive treatments on vascular reactivity and vasodilative capacity, we studied 30 hypercholesterolemic hypertensive subjects. They received placebo for 4 weeks, either enalapril or simvastatin for 14 weeks, and, finally, both medications for an additional 14 weeks. Postischemic forearm blood flow (MFBF) and minimal vascular resistance (mFVR) were used as indices of vasodilative capacity and structural vascular damage, respectively. Total (resting-stress-recovery phases) cardiovascular (blood pressure [BP] and heart rate [HR]) and regional hemodynamic (FBF and FVR) reactivity to stressful stimuli were calculated as area-under-the-curve (auc) (valuextime). Compared with baseline levels, simvastatin reduced total (TOT-C) and LDL cholesterol (LDL-C) (1.27 mmol/L, P<0.001 and 1.33 mmol/L, P<0.001, respectively). Enalapril also reduced TOT-C and LDL-C (0.6 mmol/L, P<0.001 and 0.58 mmol/L, P<0.05, respectively). MFBF was increased substantially by both treatments (P<0.001). Enalapril had a greater effect (-1.7 arbitrary units (AU), P<0.001) than simvastatin (-0.6 AU, P<0.05) on mFVR. During stress, FBF increased more with enalapril (4.4 FBFxminutes, P<0.001) than with simvastatin (1.8 FBFxminutes, P<0.01). Conversely, FVR stress response was reduced more with enalapril (9.1 FVRxminutes, P<0.001) than with simvastatin (2.9 FVRxminutes, P<0.01). During combination treatment, a significant (0.001>P<0.05) additive effect on hypercholesterolemia, structural vascular damage, BP, and FVR was shown. The findings suggest that angiotensin-converting enzyme (ACE) inhibition induces a larger reduction than HMG-CoA reductase blockade in vascular reactivity and structural damage in hypercholesterolemic hypertensive subjects.
Hypertension 1999 Feb
PMID:Distinct and combined vascular effects of ACE blockade and HMG-CoA reductase inhibition in hypertensive subjects. 1002 35

We investigated the interplay of neural and hemodynamic mechanisms in postexercise hypotension (PEH) in hypertension. In 15 middle-aged patients with mild essential hypertension, we evaluated blood pressure (BP), cardiac output (CO), total peripheral resistance (TPR), forearm (FVR) and calf vascular resistance (CVR), and autonomic function [by spectral analysis of R-R interval and BP variabilities and spontaneous baroreflex sensitivity (BRS)] before and after maximal exercise. Systolic and diastolic BP, TPR, and CVR were significantly reduced from baseline 60-90 min after exercise. CO, FVR, and HR were unchanged. The low-frequency (LF) component of BP variability increased significantly after exercise, whereas the LF component of R-R interval variability was unchanged. The overall change in BRS was not significant after exercise vs. baseline, although a significant, albeit small, BRS increase occurred in response to hypotensive stimuli. These findings indicate that in hypertensive patients, PEH is mediated mainly by a peripheral vasodilation, which may involve metabolic factors linked to postexercise hyperemia in the active limbs. The vasodilator effect appears to override a concomitant, reflex sympathetic activation selectively directed to the vasculature, possibly aimed to counter excessive BP decreases. The cardiac component of arterial baroreflex is reset during PEH, although the baroreflex mechanisms controlling heart period appear to retain the potential for greater opposition to hypotensive stimuli.
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PMID:Hemodynamic and autonomic correlates of postexercise hypotension in patients with mild hypertension. 1189 7

1. Much attention has been given to the effects of various classes of antihypertensive drugs on blood pressure and haemodynamics. The effects of a single bout of exercise on post-exercise blood pressure have also been studied by several investigators. However, the combined effects of prior exercise and antihypertensive medication has drawn less attention. 2. We examined the separate and combined effects of a single bout of exercise and of angiotensin converting enzyme (ACE) inhibition with a new ACE inhibitor (fosinopril, 20 mg day(-1)) on post-exercise blood pressure and systemic and regional haemodynamics. Ten patients with mild-to-moderate hypertension were studied with a double-blind, randomized crossover, placebo- and rest period-controlled study design. 3. At rest, mean arterial pressure (MAP, -10 +/- 2 mm Hg), total peripheral resistance (TPR, -11 +/- 5%) and forearm vascular resistance (FVR, -17 +/- 8%) were significantly (P < 0.05) reduced during ACE inhibition as compared with the placebo phase. 4. During the placebo phase, MAP (-3 +/- 1 mm Hg), TPR (-10 +/- 4%) and FVR (-9 +/- 4%) were lower after exercise as compared with the control rest period. 5. During ACE inhibition, MAP (-3 +/- 1 mm Hg) and TPR (-8 +/- 4%) were lower, but FVR (+32 +/- 15%) was increased after exercise as compared with the control rest period. 6. Thus, blood pressure and TPR decreased similarly after exercise during the placebo phase and during ACE inhibition. However, differences in post-exercise forearm haemodynamics during the placebo phase and during ACE inhibition indicate that underlying regional haemodynamics are modified.
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PMID:Post-exercise reduction in blood pressure in hypertensive subjects: effects of angiotensin converting enzyme inhibition. 1295 11

The authors have utilized capillaroscopy and forearm blood flow techniques to investigate the role of microvascular dysfunction in pathogenesis of cardiovascular disease. Capillaroscopy is a non-invasive, relatively inexpensive methodology for directly visualizing the microcirculation. Percent capillary recruitment is assessed by dividing the increase in capillary density induced by postocclusive reactive hyperemia (postocclusive reactive hyperemia capillary density minus baseline capillary density), by the maximal capillary density (observed during passive venous occlusion). Percent perfused capillaries represents the proportion of all capillaries present that are perfused (functionally active), and is calculated by dividing postocclusive reactive hyperemia capillary density by the maximal capillary density. Both percent capillary recruitment and percent perfused capillaries reflect the number of functional capillaries. The forearm blood flow (FBF) technique provides accepted non-invasive measures of endothelial function: The ratio FBF(max)/FBF(base) is computed as an estimate of vasodilation, by dividing the mean of the four FBF(max) values by the mean of the four FBFbase values. Forearm vascular resistance at maximal vasodilation (FVR(max)) is calculated as the mean arterial pressure (MAP) divided by FBF(max). Both the capillaroscopy and forearm techniques are readily acceptable to patients and can be learned quickly. The microvascular and endothelial function measures obtained using the methodologies described in this paper may have future utility in clinical patient cardiovascular risk-reduction strategies. As we have published reports demonstrating that microvascular and endothelial dysfunction are found in initial stages of hypertension including prehypertension, microvascular and endothelial function measures may eventually aid in early identification, risk-stratification and prevention of end-stage vascular pathology, with its potentially fatal consequences.
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PMID:Non-invasive assessment of microvascular and endothelial function. 2340 62