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

Cardiovascular responses to cold stress were investigated in hypertensive patients. There were few differences in the changes under cold stress of the serum catecholamine concentration between the juvenile group and middle-aged group. In the juvenile group, a remarkable increase in TPR was observed under cold stress, suggesting that the vascular reactivity is increased and at the same time the cardiac response to inotropic action was increased under cold stress. On the contrary, in the middle-aged group, there was less increase in TPR under cold stress and no increase in inotropic action was observed. From such results, hyperreactivity to stress in the cardiovascular system is thought to be an important factor in the pathogenesis of essential hypertension. Such cardiovascular responses are seen more easily in juvenile hypertension or initial stage of essential hypertension. In the hypertensive patients after middle-age, organic changes will develop by the repeated pressure load to the cardiovascular system caused by various stimulations and the reactivity of cardiovascular system to stress becomes less manifest.
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PMID:Stress as a causative factor of essential hypertension and its influence on the cardiovascular system. 115 88

These studies were undertaken to evaluate different manifestations of structural cardiovascular changes and the effects of antihypertensive therapy in essential hypertension. A meta-analysis of 109 studies that had examined the effect of different pharmacological blood pressure lowering regimens on left ventricular structure, examined by echocardiography, was undertaken to increase the statistical power, to resolve uncertainty and to improve the accuracy of estimation of the magnitude of effect. Strict preset criteria were applied. The effect of different drugs in monotherapy and in particular first line antihypertensive therapies were compared, using an analysis of covariance (ANCOVA). ACE-inhibitors, beta-blockers and calcium antagonists all reduced left ventricular mass (LVM) through a reduction in wall hypertrophy, the effect being most pronounced with ACE-inhibitors. Conversely, diuretics reduced LVM mainly through a reduction of left ventricular volume. Previously untreated males (n = 28, 86 kg, 46 years, 27 kg/m2) with non-malignant essential hypertension (supine diastolic blood pressure (DBP) > 95 mmHg 3-4 times (in triplicate) on placebo) were randomized to long-term double-blind treatment with enalapril (E) or hydrochlorothiazide (H). There were no significant differences between the groups at baseline. Vascular alterations in the retina (eyeground photo, refined grading), cardiac morphology (M-mode echocardiography, ASE), structural vascular changes of the hand (plethysmography, minimal resistance (Rmin)), total peripheral resistance ((TPR), calculated from dye-dilution) and blood pressure (intraarterial) were significantly interrelated at baseline except LVM and Rmin. After 6 months of therapy, E reduced the signs of vascular changes in the retina as well as Rmin in the hand circulation, while H did not change or increased these structural vascular changes. The blood pressure lowering effect of E (mainly through lowering of TPR) tended to be more pronounced, measured both intraarterially and indirectly, than that seen with H (mainly through lowering of cardiac output), however, there were no significant differences. LVM decreased progressively with E while the effect of H was non-significant. E reduced wall thickness but not left ventricular diameter and also improved left ventricular distensibility significantly. The effect on cardiac morphology was significantly different between therapies when taking change in blood pressure into account. After the longest follow-up on monotherapy (18 months) E had reduced LVM by 2.7 g/mmHg and H (14 months) by 1.3 g/mmHg (significant for E only). In univariate analysis the changes in cardiovascular structure were significantly related to the changes in the Renin-Angiotensin-Aldosterone System (RAAS).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Structural cardiovascular changes in essential hypertension. Studies on the effect of antihypertensive therapy. 134 61

In 35 patients with mild essential hypertension the influence of 9 week Viskaldix therapy on hemodynamics was evaluated. Twelve of them underwent repeated hemodynamic examinations after mean 13 months treatment. Viskaldix therapy lowered total peripheral resistance --TPR and there was no significant influence on the heart rate, stroke volume, and cardiac output. It was demonstrated that decrease of total peripheral resistance after treatment with Viskaldix was directly proportional to the initial values of TPR.
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PMID:[Evaluation of hemodynamic changes in patients with primary arterial hypertension after treatment with a combination of pindolol and clopamide (Viskaldix)]. 192 Nov 11

The responses to a supine rest, norepinephrine (NE) and angiotensin II (Ang II) were investigated in the absence and presence of calcium antagonist nifedipine or diltiazem in essential (genetic, arterial) hypertension and normotension in humans. A supine rest significantly decreased blood pressure (BP), heart rate (HR), stroke volume index (SI), and cardiac output index (CI). On the contrary, the rest increased total peripheral vascular resistance index (TPRI) in both normotensives and hypertensives. The decrease in BP was significantly greater in hypertensives than in normotensives. NE significantly increased BP and TPRI, whereas it decreased HR, SI, and CI. The increase in BP was greater in hypertensives than in normotensives. Nifedipine and diltiazem inhibited the NE-induced increases in BP and TPRI. Ang II increased BP and TPRI, but it decreased HR, SI, and CI. Diltiazem did not inhibit the Ang-II-induced increases in both BP and TPRI. The increased responses to a rest and NE were observed in the early stage of essential hypertension. The increased responses may contribute to both the increase in BP and the induction of high blood pressure in essential hypertension. The calcium antagonists inhibited the NE-induced increases in BP and TPR. The results suggest that the antagonists inhibit the NE-dependent calcium influx and calcium release in the arterial smooth muscle. The observed responses to Ang II suggest that the antagonists may not inhibit Ang-II-dependent calcium-channel activity in the smooth muscle.
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PMID:Increased cardiovascular responses to norepinephrine and calcium antagonists in essential hypertension compared with normotension in humans. 241 85

In six hospitalized subjects with mild or moderate and untreated essential hypertension, we measured mean blood pressure (MBP, brachial artery catheter), heart rate (HR, electrocardiogram), cardiac output (CO, thermodilution), and total peripheral resistance (TPR, MBP divided by CO) at rest and during a cold pressor test (CPT, 60 s), a hand-grip exercise (HG, 40% maximum strength for 90 s), and a cyclette exercise (CE, 50 W for 5 min). The study was performed in a no-drug condition, 1 h after 20 mg oral nitrendipine (aN) and 1 week after daily administration of 20 mg oral nitrendipine (pN). Compared with the no-drug condition, aN reduced resting MBP from 137.3 +/- 7.3 (mean +/- SEM) to 112.3 +/- 9 mm Hg (p less than 0.05), increased resting HR from 72.3 +/- 6.9 to 85.3 +/- 8.8 beats/min) (p less than 0.05), increased resting CO from 6,191 +/- 508, to 8,700 +/- 1,050 ml/min (p less than 0.05), and reduced resting TPR from 1,807 +/- 119 to 1,140 +/- 228 dynes/s/cm5 (p less than 0.05). The reduction in resting MBP and TPR were unchanged by pN, whereas the increase in HR and CO were attenuated by 47 and 42%, respectively (p less than 0.05). Neither aN nor pN altered the hemodynamic responses to CPT, HG, and CE. As a result, the peak MBP and TPR values that were measured during these maneuvers were always lower (p less than 0.05) during aN and pN than in the no-drug condition. Thus, nitrendipine exerts marked antihypertensive and vasodilatatory effects that are evident at rest and during conditions elevating BP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of acute and prolonged administration of nitrendipine in essential hypertension. 245 12

The acute and chronic hemodynamic effects of nisoldipine were studied in 19 patients (17 men, 2 women; mean age 43 years) with essential hypertension at rest supine and sitting and during steady state 100 W bicycle exercise. At rest supine, the first dose response (1 h) was reduction of intraarterial (IA) pressure (9%) and total peripheral vascular resistance (TPR; 19%) and rise in heart rate (HR; 9%) and cardiac output (CO; 12%). Thereafter, the effect leveled off: at 3 h, IA pressure, CO, and TPR were reduced 6%, 1%, and 4%, respectively. Similar results were seen at rest and during exercise. After 1 year treatment, the changes were more marked: at rest, IA pressure and TPR fell (16% and 20%, respectively) while stroke volume and CO rose slightly (4% and 6%, respectively). There was no reflex tachycardia. During 100 W exercise, IA pressure fell (14%) due to reduction both in TPR (7%) and CO (6%). Thus, at rest, nisoldipine lowers blood pressure by reduction of TPR both acutely and chronically. The initial rise in CO is lost after long-term therapy. During exercise, falls in both TPR and CO contribute to the hypotensive effect.
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PMID:Central hemodynamic effects at rest and during exercise of acute and chronic treatment with nisoldipine in essential hypertension. 245 28

To examine the influence of dietary sodium, prostaglandin, and captopril on vascular reactivity, 12 patients with essential hypertension (EH) and seven normotensive subjects (NT) were given a high sodium diet and thereafter a low sodium diet, each for ten days. Indomethacin (IND) (150 mg/d) was administered during the last three days of each dietary period. Blood pressure and cardiac output (CO) (by impedance cardiography) were measured during the angiotensin II (Ang II) infusion before and after the IND treatment of each dietary period. In eight patients with EH, captopril 100 mg was given before Ang II infusion. EH patients were classified as either salt sensitive (SS) or nonsalt sensitive (NSS). The mean blood pressure (MBP) response to Ang II was significantly higher on high sodium intake than on low sodium intake in NSS and NT, but not in SS. IND significantly increased the MBP response to Ang II on low sodium intake in NSS and NT, but not in SS. IND significantly increased the TPR response to Ang II on low sodium intake, remarkably in NSS and NT compared with SS. Salt sensitivity (% decrease in MBP from high to low sodium intake) highly correlated with the increase in the TPR response to Ang II by IND on low sodium intake (r = -0.90). After captopril administration, IND still increased the MBP and TPR response to Ang II on low sodium intake. These results suggest that the modulation of the vascular responsiveness to Ang II by prostaglandins is altered by sodium balance and salt sensitivity in EH.
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PMID:Effects of salt, prostaglandin, and captopril on vascular responsiveness in essential hypertension. 267 1

Carvedilol (BM14190) is a new compound with combined properties of nonselective beta-adrenoceptor blockade, devoid of ISA, and precapillary vasodilatation. Its acute hemodynamic effects were studied with invasive technique (dye-dilution using Cardio-Green) in 10 patients taking 25 mg orally and noninvasive (fore-arm plethysmography) in 10 patients taking 25 mg and in 10 patients taking 50 mg orally, all with essential hypertension. Significant reductions of systolic and diastolic blood pressures (p less than 0.05 - 0.001) were observed in all groups. TPR did not change acutely whereas resistance in the fore-arm was reduced by 16% (p less than 0.05). When a comparison with propranolol (80 mgx2) was made in a randomized, double-blind placebo controlled trial comprising 30 patients with essential hypertension, carvedilol acutely reduced blood pressure significantly 13/6 mm Hg (25 mg) and 17/10 mm Hg (50 mg) in contrast to propranolol. Resistance in the fore-arm (plethysmography) fell significantly with carvedilol 50 mg whereas propranolol caused a significant rise. After 4 weeks both compounds had reduced blood pressure significantly and to the same extent. Blood flow was still reduced with propranolol in contrast to the findings with carvedilol. We conclude that carvedilol given orally has a useful antihypertensive effect both acutely and during prolonged treatment. It has an attractive hemodynamic profile.
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PMID:Hemodynamic effects of combined beta-adrenoceptor blockade and precapillary vasodilatation in hypertension. 285 39

The relationship of continuous ambulatory intra-arterial blood pressure over a 24-hour period and awake resting hemodynamic parameters measured by echocardiography was studied in 21 patients with essential hypertension (WHO stage I & II): Left ventricular wall thickness at end-diastole correlated strongly with average SBP and weakly with average DBP during both waking and sleeping periods. Variability of blood pressure taken during waking and sleeping periods was not significantly correlated with any hemodynamic parameters measured by echocardiography. Variability of SBP during sleep had a significant correlation with age; however the fall of blood pressure during sleep had no significant correlation with age. Fall of blood pressure during sleep was significantly correlated to resting awake TPR. In patients with essential hypertension, the above results demonstrate that subjects with thicker left ventricular wall have higher average continuous blood pressure over 24-hours and suggest that there is a tendency for greater falls in blood pressure during sleep to occur in subjects with higher TPR and that older subjects have greater variabilities of SBP during sleep.
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PMID:Variability of direct arterial blood pressure in essential hypertension--relationships between the fall of blood pressure during sleep and awake resting hemodynamic parameters. 294 40

The purpose of this study was to evaluate the acute and long-term effects on blood pressure and hemodynamics both at rest and during acute exposure to loud noise of drugs with beta-adrenoceptor blocking and vasodilating properties. Prizidilol and carvedilol both act as nonselective beta-blocking and precapillary vasodilating compounds. Prizidilol (200 mg X 2) was compared to propranolol (80 mg X 2) plus hydralazine (25 mg X 2) and showed similar antihypertensive effect in a long-term double-blind randomized trial. Carvedilol was evaluated acutely with invasive (dye-dilution) and noninvasive (plethysmography) technique and showed an acute antihypertensive effect without causing a rise in TPR and with a decrease in regional resistance in the fore-arm. Acutely, carvedilol (25 mg and 50 mg) decreased blood pressure and regional resistance (50 mg) in contrast to propranolol (80 mg) which did not lower blood pressure acutely and caused an increase in regional resistance. In a long-term double-blind, randomized comparison, both propranolol (80 mg X 2) and carvedilol (25 mg X 2 and 50 mg X 2) showed a useful antihypertensive effect. After 29 days, however, it was still possible to demonstrate an acute decrease in resistance with carvedilol (50 mg) after tablet intake, indicating the vasodilating activity of this compound. When patients with essential hypertension were exposed to an even broad band noise (100 dBA), there was a rise in blood pressure due to an increase in TPR. Alpha 1-adrenoceptor blockade (prazosin 2 mg) prevented the rise in TPR but blood pressure increased in spite of this due to a rise in CO. Moreover, nonselective beta-adrenoceptor blockade and alpha 1-adrenoceptor blockade in combination (labetalol 200 mg) were unable to prevent the rise in blood pressure induced by noise. Finally, precapillary vasodilatation and beta-adrenoceptor blockade (prizidilol 400 mg) given as long-term treatment were also inefficient in preventing the noise-induced (105 dBA) rise in blood pressure. The absolute level of blood pressure obtained, however, was significantly lower than during placebo administration.
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PMID:Beta-adrenoceptor blockade and vasodilatation in essential hypertension. Hemodynamic studies at rest and during exposure to stress. 615 43


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