Higher Peripheral Resistance Research Articles

Development of Luminally Originating Vasa Vasorum in Arterially Implanted Autogenous Vein Graft and Related Anastomosis in Dogs

Using light and scanning electron microscopes, the authors examined the development of luminally originating vasa vasorum in the course of intimal hyperplasia of vein grafts implanted to the canine femoral artery under conditions of abnormal blood flow with a high peripheral resistance. Five days after the implantation, the luminally originating vasa vasorum in the autogenous vein grafts developed dominantly near the anastomosis and often at the site of the area of valvular sinus. This vasa vasorum took the form of numerous small holes on the luminal surface of the graft and along the suture materials at the site of the anastomosis. These holes were lined with endothelial-like cells two weeks after the implantation, and four weeks later these cells were distributed in the thickened neointima connecting the vasa vasorum in the media and adventitia. This vasa vasorum observed on the thickened neointima at the area of the valvular sinus of the vein graft at more than five days after the implantation was considered to have developed in the course of organization of the mural thrombi deposited on the suture line at and on the area of the valvular sinus. Thus, numerous interstices of the vessel wall, formed along the suture materials at the anastomosis, and some clefts, formed with shrinkage of the deposited mural thrombi at the area of the valvular sinus, are the source of the luminally originating vasa vasorum.

Microscopic and immunohistological studies on intimal hyperplasia of the arterially implanted autovein graft and its anastomosis in dogs.

The fate of intimal hyperplasia of arterially implanted autovein bypass grafts and their distal end-to-side anastomoses in dogs was studied microscopically and immunohistologically. The bypass grafting was done under conditions of abnormal blood flow and high peripheral resistance. Intimal hyperplasia of the graft first became evident 7 days after implantation and the thickness increased to about 500 microns 3 months or more after the implantation. The intimal hyperplasia was related to an active proliferation of smooth muscle cells which proved positive for alpha-smooth muscle actin staining. Moreover, it was more dominant at the toe and heel of the anastomosis and moderately apparent on the floor of the host artery. The constituent elements of the hyperplastic intima at the anastomosis were fibroblast-like cells and extracellular collagen fibers which were negative for alpha smooth muscle actin staining. This study revealed that the features of intimal hyperplasia at the distal anastomosis in autovein bypass grafting differed from those of the implanted autovein graft itself; the former being related to excessive proliferation of fibroblasts and collagen fibers while the latter displayed an active proliferation of smooth muscle cells.

Abnormal renal function and autoregulation in essential hypertension.

The goal of this presentation has been to emphasize two fundamental mechanisms in the development of essential hypertension. These are: 1) The basic cause of essential hypertension is the inability of the kidneys to excrete an adequate volume of urine at normal arterial pressure. Therefore, fluid accumulates in the body until the pressure rises high enough to balance fluid output with fluid intake. This fluid balancing act is an infinite gain feedback system for controlling arterial pressure to a very precise level determined by the kidneys. Furthermore, this infinite gain allows the kidney mechanism to dominate the other pressure control mechanisms for long-term pressure control. Because of this domination, as long as a person has normal intake of water and electrolytes, essential hypertension cannot develop without an elevated pressure setting of the kidneys. 2) An increase in total peripheral resistance will not cause hypertension as long as the kidneys can still excrete normal amounts of water and electrolytes at normal arterial pressure, because loss of excess fluid volume at high pressures will simply reduce the cardiac output until the pressure falls back to normal. Therefore, what is the cause of the very high total peripheral resistance found in almost all patients with essential hypertension? The answer is likely the long-term blood flow autoregulation mechanism that occurs in virtually all tissues of the body. That is, when the pressure rises too high for whatever reason, this in turn forces too much blood flow through the tissues. In response, the local blood flow control mechanisms all over the body increase the vascular resistances until the flows return to normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Rosetting of Plasmodium falciparum-infected red blood cells with uninfected red blood cells enhances microvascular obstruction under flow conditions

The occurrence of rosetting of Plasmodium falciparum-infected human red blood cells (IRBC) with uninfected red blood cells (RBC) and its potential pathophysiologic consequences were investigated under flow conditions using the perfused rat mesocecum vasculature. Perfusion experiments were performed using two knobby (K+) lines of P falciparum, ie, rosetting positive (K+R+) and rosetting negative (K+R-). The infusion of K+R+ IRBC resulted in higher peripheral resistance (PRU) than K+R- IRBC (P less than .0012). Video microscopy showed that under conditions of flow, in addition to cytoadherence of K+R+ IRBC to the venular endothelium, rosette formation was also restricted to venules, especially in the areas of slow flow. Rosettes were absent in arterioles and were presumably dissociated by higher wall shear rates. The presence of rosettes in the venules must therefore reflect their rapid reformation after disruption. Cytoadherence of K+R+ IRBC was characterized by formation of focal clusters along the venular wall. In addition, large aggregates of RBC were frequently observed at venular junctions, probably as a result of interaction between flowing rosettes, free IRBC, and uninfected RBC. In contrast, the infusion of K+R+ IRBC resulted in diffuse cytoadherence of these cells exclusively to the venular endothelium but not in rosetting or large aggregate formation. The cytoadherence of K+R+ IRBC showed strong inverse correlation with the venular diameter (r = -.856, P less than .00001). Incubation of K+R+ IRBC with heparin and with monoclonal antibodies to glycoprotein IV/CD36 abolished the rosette formation and resulted in decreased PRU and microvascular blockage. These findings demonstrate that rosetting of K+R+ IRBC with uninfected RBC enhances vasocclusion, suggesting an important in vivo role for rosetting in the microvascular sequestration of P falciparum-infected RBC.

Rosetting of Plasmodium falciparum-Infected Red Blood Cells With Uninfected Red Blood Cells Enhances Microvascular Obstruction Under Flow Conditions

The occurrence of rosetting of Plasmodium falciparum-infected human red blood cells (IRBC) with uninfected red blood cells (RBC) and its potential pathophysiologic consequences were investigated under flow conditions using the perfused rat mesocecum vasculature. Perfusion experiments were performed using two knobby (K+) lines of P falciparum, ie, rosetting positive (K+R+) and rosetting negative (K+R-). The infusion of K+R+ IRBC resulted in higher peripheral resistance (PRU) than K+R- IRBC (P less than .0012). Video microscopy showed that under conditions of flow, in addition to cytoadherence of K+R+ IRBC to the venular endothelium, rosette formation was also restricted to venules, especially in the areas of slow flow. Rosettes were absent in arterioles and were presumably dissociated by higher wall shear rates. The presence of rosettes in the venules must therefore reflect their rapid reformation after disruption. Cytoadherence of K+R+ IRBC was characterized by formation of focal clusters along the venular wall. In addition, large aggregates of RBC were frequently observed at venular junctions, probably as a result of interaction between flowing rosettes, free IRBC, and uninfected RBC. In contrast, the infusion of K+R+ IRBC resulted in diffuse cytoadherence of these cells exclusively to the venular endothelium but not in rosetting or large aggregate formation. The cytoadherence of K+R+ IRBC showed strong inverse correlation with the venular diameter (r = -.856, P less than .00001). Incubation of K+R+ IRBC with heparin and with monoclonal antibodies to glycoprotein IV/CD36 abolished the rosette formation and resulted in decreased PRU and microvascular blockage. These findings demonstrate that rosetting of K+R+ IRBC with uninfected RBC enhances vasocclusion, suggesting an important in vivo role for rosetting in the microvascular sequestration of P falciparum-infected RBC.

A Forced Perturbation Method of Assessing Pulmonary Mechanical Function in Intubated Infants

Short pulses in airway pressure were used to assess the pulmonary mechanical function of nine infants suffering acute respiratory distress syndrome or bronchopulmonary dysplasia. All patients were intubated, spontaneously breathing, and mechanically ventilated at the time they were examined. The endotracheal tube was disconnected from the ventilator and connected to a mechanical oscillator that produced brief pulses in airway pressure at a rate of two pulses/s. These pulses were applied to the infants airway for 20-30 s, at which time the infant was replaced on the ventilator. The mean airway pressure during the procedure was maintained at the level of the positive and expiratory pressure that was set on the ventilator. Two classes of patients were identified from the pulse response primarily by the presence or absence of a local resonance in the impedance spectra. Similar results were obtained in five other patients who were examined with zero mean airway pressure, suggesting that the pulse response is little influenced by changes in mean lung volume or total lung compliance. Patient classification appeared related to the duration of ventilation therapy and the transition from one class to another was consistent with the development of high peripheral airway resistance and significant volume shunting in the central airways. These results suggest that brief pulses in airway pressure can be used to detect changes in the pulmonary mechanical function of preterm infants that result from long-term ventilation therapy.

Characteristics of systolic time intervals in patients with pheochromocytoma.

The effect of chronic catecholamine excess on cardiac function was assessed in 8 patients with surgically proven pheochromocytoma and the results compared with data obtained from normal controls and essential hypertensives. Major findings in systolic time intervals (STI) in patients with pheochromocytoma were a marked shortening of electromechanical systole and left ventricular ejection time (ET), but pre-ejection period (PEP) remained within normal limits. These findings were not altered by correction for heart rate. The ET/PEP ratio was very low (1.87 +/- 0.31) due to the remarkable shortening of ET. The ET/PEP ratio in essential hypertensives was also low (1.77 +/- 0.38), but this was mainly due to a remarkable prolongation of PEP. Low cardiac index, low stroke index and high total peripheral resistance index were preoperative characteristics in patients with pheochromocytoma, but returned to normal after operation. These results suggest that chronic excessive production of catecholamines from pheochromocytoma has deleterious effects on the heart, and that wide differences in STI exist between patients with pheochromocytoma and those with essential hypertension.

The central hemodynamics of severe preeclampsia

Swan-Ganz hemodynamic monitoring in 49 antepartum patients with severe preeclampsia revealed a variable hemodynamic profile. The majority of patients had normal left ventricular filling pressure (8.4 +/- 0.2 mm Hg), normal to high cardiac index (4.4 +/- 0.1 L.min-1.m2), and upper normal to moderately elevated systemic vascular resistance (1226 +/- 37 dynes.sec.cm-5). Eight patients had pulmonary edema and their findings included high wedge pressure (18 +/- 1 mm Hg), upper normal to high cardiac index (4.9 +/- 0.5 L.min-1.m2), and normal systemic vascular resistance (964 +/- 50 dynes.sec.cm-5). Left ventricular function was hyperdynamic in 73% of the 49 patients. Patients with chronic hypertension and superimposed preeclampsia were hemodynamically indistinguishable from patients with preeclampsia alone. We conclude that, in general, preeclampsia is a high cardiac output state associated with an inappropriately high peripheral resistance. The normal wedge and central venous pressures suggest central redistribution of intravascular volume if the generally accepted reports of decreased plasma volume in preeclampsia are correct.

Controlled Pressure-Volume Factors in the Enlargement of Intracranial Aneurysms

Pressure-volume relations were investigated on a model aneurysm wall made of elastic tissue and collagen. The model wall had a Young's Modulus of 2 x 10(7) dynes/cm2, approximating the elastance of fresh aneurysm walls obtained at autopsy. The model wall was fixed over the top of a glass T-tube, 6 mm in diameter. Pressure pulse waves of water or outdated human blood entered at the bottom of the T-tube and exited by way of a controlled resistance, while pressure was monitored by a strain gauge and recorded on an ink writer from the other arm. Incremental increases in systolic pressure produced a nonlinear N-shaped pressure-volume curve. There was an initial linear enlargement in volume with increased pressure until a pressure threshold was reached at a point of high nonlinear compliance. At this point there was an abrupt jump in volume (mean increase = 70 +/- 14%) to a new stable equilibrium volume. A further increase in pressure (24 +/- 7 mm Hg) could eventually cause aneurysm rupture. This always occurred in the thinner, more compliant part of the wall. With higher pulse rates, the jump in volume occurred at a smaller volume, whereas with thinner aneurysm walls of higher compliance the pressure threshold for a jump in volume was significantly lower. At a higher peripheral resistance there was a higher pressure threshold. The authors suggest that there is one possible mechanism that may occur in the neck of some developing human aneurysms and could explain early and rapid initial growth in size.

Echocardiographic functions and blood pressure levels in children and young adults from a biracial population: The bogalusa heart study

M-mode echocardiograms were obtained on 651 healthy subjects, 7-22 years of age, whose diastolic blood pressure levels remained in the same height-, race-, and sex-specific decile during two biannual examinations. Echocardiographic measures of heart size and dynamics were compared across the total blood pressure distribution. Left ventricular stroke volume, cardiac output and ejection fraction, minor axis shortening, velocity of circumferential fiber shortening, and peripheral vascular resistance were correlated with blood pressure levels. There were positive correlations (p less than .001) of cardiac output and stroke volume with both systolic and diastolic blood pressure levels. Left ventricular output and stroke volume were associated with measures of body size, especially height, weight, ponderal index, and body surface area (p less than .001). The left ventricular output and stroke volume increased with age and with systolic blood pressure quintiles in the four race-sex groups. With adjustment for systolic blood pressure and measures of body size, white males had greater cardiac output (1.25 l/minute for ages 18-22 years, p = .01) and stroke volume than black males. Black males had higher peripheral resistance (4.5 mm Hg/(l/minute), p = .01) than whites. These results suggest that different hemodynamic mechanisms operate in the early phase of hypertension in blacks vs. whites in this population.

The importance of hemodynamic considerations in essential hypertension

Hypertension is a major risk factor for cardiovascular morbidity and mortality. Antihypertensive therapy consistently reduces complications from stroke and congestive heart failure, whereas benefits from the treatment of ischemic heart disease events are variable. Several plausible explanations, including hemodynamic hypotheses, have been put forth to account for the failure of treatment to more favorably influence mortality from ischemic heart disease. The effect of hypertension on coronary heart disease is probably much more complex than a simple elevation of arterial pressure. Some of these complexities include the potential separate risks of high total peripheral resistance, high cardiac output, increased myocardial power that reflects pressure times flow, and several structural and functional vascular changes. These factors may act in concert to unfavorably alter the balance between myocardial oxygen supply and demand. Several of these factors will be highlighted in an attempt to offer alternative or adjunctive pathophysiologic examinations for the high-risk subgroups of obesity and the failure of antihypertensive therapy to normalize the rate of coronary heart disease events.

Transition from high cardiac output to elevated vascular resistance in hypertension

The early phase of hypertension (borderline hypertension) is characterized by a hyperkinetic circulation caused by excessive sympathetic drive and decreased parasympathetic inhibition to the heart. In later phases the cardiac output becomes normal, but the hypertension is still neurogenic, as demonstrated by the fact that continued pharmacologic parasympathetic, β- and α-adrenergic inhibition normalizes the blood pressure. In both of these phases of the process, plasma norepinephrine values are elevated. These patients also show characteristic behavioral patterns; they are outward oriented, submissive, but experience unexpressed anger and frequently harbor hostile feelings. In late phases of hypertension the cardiac output is normal and the total peripheral resistance is elevated. This hemodynamic transition can be explained by a secondary response to elevated blood pressure. The heart becomes less responsive as a result of altered receptor responsiveness and decreased cardiac compliance, whereas the responsiveness of arterioles increases because of vascular hypertrophy, which leads to changes in the wall-to-lumen ratio. However, one observation eludes explanation: the absence of plasma norepinephrine elevation in later phases of hypertension. We propose a new conceptual framework to explain the disappearance of elevated plasma norepinephrine in the course of hypertension. The concept is based on a wide range of observations with the use of various receptor-blocking agents during neurogenic pressor responses. Invariably, the blood pressure response is preserved, but the hemodynamic pattern can be altered from a high cardiac output to high total peripheral resistance or vice versa. The “blood pressure-seeking behavior” of the central nervous system suggests that the negative feedback to the central nervous system is pressure and not flow related. If the central nervous system indeed seeks to obtain a certain pressure and maintains the high blood pressure in early phases by an elevation in cardiac output, later as structural arteriolar changes evolve and the arterioles become hyperresponsive, the same blood pressure elevation could be achieved with less sympathetic drive, and the plasma norepinephrine values return to the normal range.

Pharmacologic management of systemic hypertension in blacks

This article contrasts the characteristics of essential hypertension found in the black population with that seen in the nonblack population. Socioeconomic and pathophysiologic factors are discussed. Different pharmacologic classes of drugs are compared for their effectiveness in treating the black hypertensive patient. Because black hypertensives tend to have salt-sensitive, low-renin hypertension coupled with decreased cardiac output and high peripheral vascular resistance, an ideal antihypertensive should have natriuretic effects but also the physiologic capability of reducing vascular resistance. Such an ideal hypertensive drug would be able to lower systemic blood pressure while improving organ perfusion and function.

Plasma Membrane and its Abnormalities in Hypertension

The plasma membrane is composed of proteins embedded in a discontinuous fashion in a lipid bilayer. These proteins maintain the integrity of the membrane and play fundamental roles as ion transport channels and as receptors for agents that regulate cell function. The membrane is therefore an important regulator of vascular smooth muscle contraction. The plasma membrane in the hypertensive animal exhibits abnormal permeability for monovalent ions and defective calcium handling. This is reflected in fewer calcium-binding sites and, as a result, in deficient membrane stabilization. These defects have been identified in several cell types, including lymphocytes, red blood cells, adipocytes, and vascular smooth muscle cells. Evidence presented in the current review suggests that hypertension is associated with a generalized membrane defect. Abnormalities in ion transport in vascular smooth muscle cells are the most relevant to the pathogenesis of hypertension since they could be directly responsible for the rise in blood pressure. We hypothesize that the impaired stabilizing effect of calcium in vascular smooth muscle cells of hypertensive subjects renders the membrane more excitable and that this in turn leads to increased vascular reactivity and higher peripheral resistance. Peripheral vascular reactivity usually is increased in hypertension, suggesting increased responsiveness of the smooth muscle cells. Possible abnormalities of the several components of the contractile process of these cells have been investigated for the role they might play in this altered response. Abnormalities in the plasma membrane have been most clearly defined and are emphasized in this review.

Computer Models for Designing Hypertension Experiments and Studying Concepts

This paper demonstrates how computer models along with animal experiments have been used to work out the conceptual bases of hypertensive mechanisms, especially the following: (1) The renal-fluid volume pressure control mechanism has a feed-back gain for pressure control of infinity. Therefore, the chronic level to which the arterial pressure is controlled can be changed only by altering this pressure control mechanism. (2) An increase in total peripheral resistance is not sufficient by itself to cause hypertension. The only resistances in the circulatory system that, when increased, will cause hypertension are those along a restricted axis from the root of the aorta to Bowman's capsule in the kidneys. (3) Autoregulation in the peripheral vascular beds does not increase the arterial pressure in hypertension. However, autoregulation can convert high cardiac output hypertension into high peripheral resistance hypertension. (4) In a computer simulation that cannot yet be performed in animals, a simulated hypertension caused by a combination of increased renal afferent and efferent arteriolar resistances has characteristics that match almost exactly those of essential hypertension.

Regional blood flows and resistances in conscious one-kidney, one-clip renovascular hypertensive rats.

Three regional blood flows were measured in one-kidney, one-clip renovascular hypertensive (one-kidney hypertensive) rats with chronically implanted electromagnetic flow probe. One-kidney hypertensive rats showed about 30% greater superior mesenteric flow, about 20% greater hindquarter flow at the terminal aorta, and an almost unchanged renal flow at the clipped renal artery when compared with control rats, but the sum of the mean values of these three regional blood flows in one-kidney hypertensive rats was almost the same as that of control rats. One-kidney hypertensive rats had a higher peripheral resistance in all the investigated vascular areas. The increase in peripheral resistance of the renal area including the clipped and removed arteries was greater than that in peripheral resistance of the superior mesenteric area or hindquarter area. These findings suggest that the remaining renal area which failed to compensate for the flow deprived by uni-nephrectomy plays a role in the etiology of this kind of hypertension.

Three-element model for total systemic circulation: Emphasis on the accuracy of parameter estimates

In this study, the accuracy achievable in the parameter estimates of a three-element linear model for the systemic vascular bed is considered. The model neglects inertial effects and includes only three elements representing arterial compliance, peripheral resistance and venous compliance, in agreement with recent sensitivity investigations. Parameter estimation starts from arterial and right atrial pressure signals generated by a closed-loop simulator of the cardiovascular circulation and corrupted with normal noise to account for measurement errors. In this way, the influences of a wide variety of circulatory conditions were investigated. The results achieved give evidence that arterial compliance is generally well estimated, while venous compliance is more variable, particularly at high peripheral resistance where measured signals appear to be less sensitive to this parameter. However, presence of cardiac disease, such as heart failure and valvular stenosis has minimal influence on compliance estimates. These results suggest that this simple model can be conveniently applied even under noisy conditions.

Use of diuretic agents in obese or black patients with systemic hypertension

Any increase in arterial pressure is the result of either an increase in cardiac output, an increase in total peripheral resistance or a combination of the two. Hypertension is not a homogeneous disease, however, and different mechanisms may be operative during the life span of the patient. Hypertension in the young, nonobese patient is usually hemodynamically characterized by high cardiac output, normal to slightly contracted intravascular volume and numerically normal total peripheral resistance. In contrast, hypertension in the middle-aged or elderly patient is usually hemodynamically characterized by normal to low cardiac output, contracted intravascular volume and high total peripheral resistance. Two further subgroups of hypertensive patients can be identified: obese patients, whose hypertension is characterized by high cardiac output, expanded intravascular volume and normal or low total peripheral resistance, and black patients, whose hemodynamic and fluid volume findings are similar to those of their white counterparts, but who tend to have lower heart rates and greater responsiveness to intravascular volume depletion than white hypertensive subjects. A rational therapeutic approach to essential hypertension should take into account these variable pathophysiologic features. Thiazide diuretics continue to be appropriate and generally well-tolerated choices for initial antihypertensive therapy in obese or in black patients. Many obese patients or black patients, however, are likely to develop early left ventricular (LV) hypertrophy. Patients with electrocardiographic or echocardiographic evidence of LV hypertrophy have been shown to have a higher prevalence of ventricular ectopic activity and to be at higher risk of sudden death than patients without evidence of LV hypertrophy. Some studies have shown that obese patients and black patients are at higher risk of developing LV hypertrophy. Thiazide diuretic-induced hypokalemia may exacerbate ventricular ectopic activity and cause more serious arrhythmias. Potassium depletion should, therefore, be prevented in patients with evidence of the LV hypertrophy. If thiazide diuretics are used in this context, the addition of a potassium sparing agent, such as amiloride, is recommended.

Does gravitational pressure of blood hinder flow to the brain of the giraffe?

1. 1. Vascular pressure consists of the sum of two pressures: (a) pressure developed by the pumping of the ventricles against the resistance of vessels, designated as viscous flow pressure, and (b) pressure caused by gravity, traditionally called hydrostatic, better described as gravitational pressure. 2. 2. In a conduit, both of these pressures must be overcome when a liquid is discharged to a higher level of gravitational potential energy. If a liquid is returned to its original level, gravity neither helps nor hinders flow because of the siphon effect. This circumstance prevails in the circulatory system. Hence, P 1− P 2 in the Poiseuille equation excludes gravitational pressure between those points. The long neck of the giraffe, therefore, poses no impediment to blood flow in the erect posture. 3. 3. The giraffe has a high aortic pressure. This is not for driving the blood to its head but is for minimizing the gravitational drop of intravascular pressure and collapse of the vessels. The cerebral circulation is protected by the cerebrospinal fluid which undergoes parallel changes in pressure with posture. Other vessels in the head are less protected by connective tissue, surrounding muscles and other structures. 4. 4. The high aortic pressure in the giraffe is probably caused by the high total peripheral resistance of the systemic circuit due to vascular adaptations related to the overall height of the animal.

Left ventricular function in early primary hypertension. Functional consequences of cardiovascular structural changes.

An increase in left ventricular (LV) wall thickness will lead to decreased LV distensibility during both LV passive filling and left atrial contraction. Reduced LV distensibility will change the filling pattern of the left ventricle, and a proportionally smaller part of the stroke volume will be delivered during the passive filling of the preceding diastole and a larger part during late diastole by a more powerful left atrial contraction. With a more pronounced increase in LV wall thickness a reduced distensibility of venous capacitance vessels (functional or structural) will probably help to preserve LV pump function by influencing LV filling and use of the Frank-Starling mechanism. LV wall stress (peak and end-systolic) is high and LV intrinsic contractility is normal or supernormal in early primary hypertension, as judged from the relationship between end-systolic wall stress and different indices of LV function (fractional shortening, mean velocity of circumferential fiber shortening, ejection fraction). Great differences in peak systolic wall stress may be recorded among groups with comparable values for LV end-systolic wall stress, which may be explained by very different degrees of cardiovascular structural changes, with higher values for peak systolic wall stress seen in hypertension caused by high output than those values seen in hypertension caused by high total peripheral resistance. Signs of supernormal LV systolic function are common in high output hypertension, which is also at least partly due to an increase in LV end-diastolic volume and use of the Frank-Starling mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)