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

Recent studies have outlined both the importance and limitations of hemodynamic studies in hypertension. Characterization of any type of hypertension cannot be established in terms of cardiac output or total peripheral resistance alone. It depends more on the way in which various factors (hemodynamics, volume, humoral and neural) interrelate than on disturbances of one factor alone. More studies are needed, not so much of each variable alone as of correlations among those variables, e.g. correlations between humoral factors and hemodynamic characteristics. Further, hemodynamic analyses must be extended beyond calculations of TPR to evaluation of other variables such as magnitude and distribution of intravascular volume, indices of aortic distensibility, of velocity of ventricular ejection and of cardiac performance. Interpretation of the results must also take into account factors such as hemodynamic setting, age of patient, neurogenic stimulation and structural changes amongst others. Careful attention to these variables will allow more accurate conclusions regarding characteristics of different types of hypertension, and patterns of response to therapy. Accurate hemodynamic characterization may help orient diagnosis and a rational choice of treatment in initial stages but specially for evaluation of resistant cases.
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PMID:Hemodynamic characteristics in hypertension. 72 Oct 53

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

The presence of left ventricular hypertrophy (LVH) in either hypertensives -H- or in normotensives -N-, suggests that not only blood pressure is determining this anatomic change, but various factors, as neural or endocrine ones, could be involved in its genesis. In order to evaluate the role of sympathetic dys-reactivity on LVH, we studied three groups of subjects: a) 12 -H- (SBP 159+/-9; DBP 99.6+/-7; FC 80+/-7) with LVH, diagnosed by echocardiogram. b) 12 -N- (SBP 138.2+/-8; DBP 83+/-2; FC 75.6+/-4) with LVH. c) 12 -N- (SBP 136.6+/-11; DBP 81.8+/-5; FC 76.3+/-5) without LVH. Using computer interfaced equipment, we measured beat to beat, hemodynamic and extra-cardiovascular autonomic functions, during a session of stressors (Mental Arithmetic, Color Word Stroop, Cold Pressure and Handgrip Tests), preceded and followed by 10' of observation. Among the various considered indexes, we evaluated the Percentual Total Activity Index (PTAI), as percentual total activity change + percentual total recovery change. Our findings point out that the PTAI of N with LVH is significantly higher for SCL, PHT, HR, SV, CO, TPR than either in H with LVH or N without LVH. These data seem to demonstrate a prolonged reactivity in N without LVH and are according to the hypothesis that LVH could also be supported by a hyper-adrenergic state with sympathetic dys-reactivity, independently from high blood pressure values.
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PMID:[Left ventricular hypertrophy: physiopathological signs using a hemodynamic and cardio-autonomic approach]. 146 95

In order to evaluate the hemodynamic effects of INPV, eight patients with COPD (FEV1/FVC, 54 +/- 6 percent; mean +/- SD), respiratory failure (PaO2, 52 +/- 6 mm Hg; PaCO2, 56 +/- 4 mm Hg), and clinical signs of inspiratory muscle fatigue underwent right cardiac catheterization while performing 20 minutes of INPV by a cuirass ventilator at a pressure (-20 to -40 cm H2O) able to reduce the diaphragmatic electromyographic activity. Patients showed a mild basal pulmonary artery hypertension. During INPV, no changes in the mean values of HR (from 79 +/- 20 to 80 +/- 18 beats per minute), systolic BP (141 +/- 19 to 139 +/- 16 mm Hg), CO (5.2 +/- 0.8 to 5.1 +/- 1.3 L/min), mean PAP (23.8 +/- 3.8 to 23.9 +/- 4.4 mm Hg), RAP (4.3 +/- 2.6 to 5.5 +/- 2.5 mm Hg), PWP (10.3 +/- 4.5 to 9.4 +/- 2.9 mm Hg), TPR (369 +/- 76 to 392 +/- 124 dynes.s.cm-5), and PVR (199 +/- 51 to 233 +/- 94 dynes.s.cm-5) were observed. Direct systemic BP monitoring could be performed in six patients. During INPV, three patients showed "pulsus paradoxus," as assessed by an inspiratory fall in systolic BP of 11, 13, and 20 mm Hg, respectively. We conclude that INPV by cuirass ventilator does not induce adverse hemodynamic effects in patients with COPD who have pulmonary artery hypertension.
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PMID:Hemodynamic effects of negative-pressure ventilation in patients with COPD. 218 97

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

Regional blood flow distribution (microspheres) and cardiac output (CO, thermal dilution) were measured during the Cushing response in unblocked (UB), beta-receptor-blocked (BB, 2 mg/kg propranolol iv), or alpha-receptor blocked (AB, 0.5 mg/kg + 0.5 mg X kg-1 X min-1 phentolamine iv) chloralose-anesthetized dogs. Intracranial pressure was increased to 150 mmHg by infusion of temperature-controlled artificial cerebrospinal fluid into the cisterna magna. Similar increases in mean arterial pressure were seen in UB and BB, but in AB a Cushing response could not be sustained. In UB, cerebral blood flow (CBF) decreased 50%, coronary blood flow (CoBF) increased 120%, and peripheral tissue blood flow was reduced only in the kidneys (18%) and the intestines (small 22%, large 35%). Blood flow to the other viscera, skin, and skeletal muscle was unchanged. CO (16%) and heart rate (HR, 38%) decreased, and total peripheral resistance (TPR, 68%) and stroke volume (SV, 38%) increased. In BB, CBF decreased 50%, CoBF decreased 20%, and blood flow was reduced 40-80% in all peripheral tissues. CO (69%) and HR (62%) decreased, TPR increased 366%, and SV was unchanged. We conclude that the Cushing response in UB animals combines an alpha-receptor-mediated vasoconstriction with a beta-receptor cardiac stimulation. The beta-mechanism is neither necessary nor sufficient for the hypertension. However, the combination of alpha- and beta-adrenergic mechanisms maintains cardiac output and peripheral tissue blood flow relatively constant while producing a systemic hypertension.
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PMID:Regional blood flow distribution during the Cushing response: alterations with adrenergic blockade. 285 27

The contribution of chloride to the haemodynamic changes of salt-dependent deoxycorticosterone (DOC) hypertension was studied in young Wistar rats subjected to dietary loading with sodium chloride (NaCl) or sodium bicarbonate (NaHCO3). Mean arterial pressure (MAP), cardiac output, systemic resistance (TPR) and arterial rigidity (estimated from pulse pressure/stroke volume ratio, PP/SV) were determined in conscious chronically cannulated rats. DOC-induced increase of MAP and TPR appeared earlier in NaCl-loaded than in NaHCO3-loaded rats. After 4-6 weeks of hypertensive treatment MAP, TPR and PP/SV ratio were higher in DOC-treated rats fed NaCl diet than in those fed NaHCO3 diet. In contrast, after a long-term hypertensive regimen (lasting for 7-9 weeks) there was no significant difference in either MAP or TPR between rats loaded with NaCl or NaHCO3. On the other hand, DOC hypertension induced by a long-term feeding of NaHCO3 diet was not associated with an increase of arterial rigidity which was characteristic for DOC-NaCl hypertensive rats. Thus, a sufficiently long selective dietary sodium loading is capable to increase the systemic resistance but not to alter the arterial rigidity. This was also confirmed by a comparison of blood pressure-matched DOC hypertensive rats fed NaCl or NaHCO3 diets. These animals did not differ in the degree of systemic resistance elevation but the arterial rigidity was increased only in NaCl-loaded rats.
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PMID:Haemodynamic changes induced by short- and long-term sodium chloride or sodium bicarbonate intake in deoxycorticosterone-treated rats. 794 57

Hypertension is one of the risk factors of cardiovascular diseases, which are widely prevalent maladies that result in burdensome medical expenditures. Therefore, it is important to explore primary preventive measures for hypertension. Until recently, it was thought that exercise was a risk factor for hypertension, but recent reports have suggested that low-intensity physical training actually lowers blood pressure. However, habitual physical exercise has still not been clearly proven to prevent the development of hypertension. To clarify this point, one must first establish a method for predicting hypertension and second examine the possibility of preventing the development of hypertension by changing the subject's environment. In this study we have investigated a method for predicting hypertension by classifying blood pressure responses to increasing exercise intensity and the effect of habitual exercise on blood pressure response. This study was composed of three experiments. Experiment one involved female students (n = 42) and experiment two, male students (n = 38), in whom blood pressure response rates during exercise were recorded. In experiment three, the same group of female students (n = 23) was subjected to training in order to chart its effects on blood pressure response, both while exercising and while at rest. The exercises were performed with a bicycle ergometer in an upright position. There were four different degrees of work intensity. Blood pressure was measured using the auscultation method, with Riva-Rocci mercury measured by the same investigator. High blood pressure responses at rest were noted among some normotensive female and male students. The systolic blood pressure responses during the peddling exercise showed significant individual differences at the lowest work load; the distribution of the increment of the systolic blood pressure ratio at the lowest work load against the increment while resting showed two peaks. This result suggests that this increment ratio is an important variable related to the prediction of hypertension. The increment ratio showed no significant change in female students after three months of aerobic exercise. The high-response group showed high readings of the TPR indicator (MBP/VO2). Aerobic training was shown to be effective in significantly lowering the TPR indicator both at rest and during exercise. This result suggests that habitual exercise may contribute to preventing the development of hypertension.
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PMID:[A study on the primary prevention of essential hypertension (1). Evaluation of blood pressure response during exercise and effect of habitual exercise]. 833 89

The aim of the present study was to examine the effects of felodipine, a dihydropyridinic calcium ions channels blocker, on mean arterial blood pressure (MAP), cardiac output (CO), peripheral resistances (TPR) and blood flow distribution in spontaneously mildly hypertensive female Wistar 30-34 months old rats. Under pentobarbital anesthesia, CO and regional organ blood flow were measured by the radioactive microspheres method, before and 30 min after administration of felodipine 0.5 mumol/kg b. w. by gastric gavage. They were compared to the corresponding values in normotensive rats of the same strain and age. Fifteen (from twenty five) rats were hypertensive with a MAP averaging 139 +/- 2 mm Hg. CO and TPR were slightly higher in these hypertensive rats. Cerebral blood flow (CBF) was lower, though the difference did not reach significant values. MAP significantly decreased after felodipine with no significant changes in CO and TPR in hypertensive as well as in normotensive animals. Renal blood flow (RBF) was similar before and after felodipine which significantly decreased renal vascular resistance in both groups. Felodipine administration did not induce significant changes in CBF but a significant increase in portal venous inflow (PVI) in hypertensive rats only. In conclusion, in old female rats with mild spontaneously hypertension, acute felodipine oral administration reduced arterial blood pressure without diminishing CBF.
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PMID:Effect of felodipine on systemic hemodynamics of spontaneous mild-hypertensive aged rats. 857 83

1. Hypertension secondary to renal disease was studied in non-pregnant and pregnant ewes to determine whether there were any changes in arterial pressure and the distribution of cardiac output and, in particular, whether uteroplacental blood flow was affected. 2. In six non-pregnant, chronically catheterized, uninephrectomized ewes, a reduction in renal blood flow (RBF) to 40-50% of control caused hypertension within 3 h. This was maintained for as long as RBF was reduced (72 h) and returned to control 24 h after the occluder around the renal artery was released. When this experiment was repeated in 16 uninephrectomized pregnant ewes (118-134 days gestation) hypertension occurred within 3 h and was sustained for as long as RBF was reduced (between 24 and 72 h). Arterial pressure returned to control within 24-72 h of restoring RBF. 3. Compared with non-pregnant ewes, pregnant ewes had similar arterial pressures, higher cardiac outputs (CO; P < 0.001) and heart rates (HR; P < 0.001), lower total peripheral resistances (TPR; P < 0.001) and similar blood flows to brain, ovary, pancreas, kidney and spleen. Splenic vascular resistance (VR) was greater (P = 0.006), gut blood flow was greater (P < 0.05) and gut VR was less (P < 0.05). Myoendometrial blood flow/g was greater (P < 0.005) and myoendometrial VR was less (P = 0.006). 4. In pregnant sheep with renal clip hypertension, there was no change in CO and HR, but TPR increased (P < 0.01), as did plasma renin activity. Gut, brain, pancreatic and myoendometrial VR were increased as long as RBF was reduced; in addition, myoendometrial VR remained high for the rest of the experiment. Placental blood flow was unchanged at 3 h; 24-72 h later it was reduced (P < 0.05) and remained low. Placental VR was increased 24-72 h after RBF was restored when ewes were again normotensive. 5. Thus, one-clip, one-kidney renal hypertension in the pregnant ewe was due to increased TPR associated with a fall in uteroplacental blood flow that persisted even when RBF was restored and ewes were normotensive. This reduction in uteroplacental blood flow could account for the high foetal morbidity and mortality that occurs in pregnant women with renovascular hypertension.
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PMID:Effects of one-clip, one-kidney hypertension in chronically catheterized pregnant ewes. 914 84


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