Pressure-diameter Relationship Research Articles

Aortic pressure-diameter relation in patients with non-insulin dependent diabetes mellitus: new insights.

Type II (non-insulin-dependent) diabetes mellitus is associated with macrovascular disease. Therefore, we investigated the aortic elastic properties by a new method in patients with diabetes and control patients matched with them. Patients with Type II diabetes (n = 20) and control patients without diabetes (n = 21) were enrolled in the study. All patients had coronary artery disease. Instantaneous aortic diameter was measured by an intravascular catheter developed in our institution. Instantaneous aortic pressure was measured simultaneously at the same aortic level with a catheter-tip micromanometer. Thus, aortic pressure-diameter loops were obtained and slope and intercept were calculated. Aortic distensibility, stiffness constant and energy loss were also calculated. The mean age and the heart rate were similar in the two groups. The pulsatile changes in aortic diameter were greater in the control group (0.94 +/- 0.4 vs 1.28 +/- 0.4 mm, p < 0.01). The stiffness of the aortic wall was greater in diabetic patients as indicated from the following variables: the distensibility was less in patients with diabetes (1.16 +/- 0.6 vs 1.95 +/- 0.9 cm2 x dyne(-1) x 10(-6), p <0.01); the slope was greater (113.4 +/- 120.1 vs 51.61 +/- 3.3 mmHg/mm, p < 0.01) and the intercept was less in diabetic patients (-2301.9 +/- 2692.9 vs -1114.45 +/- 295.6 mmHg, p < 0.01); the stiffness constant was greater in patients with diabetes (1.66 +/- 1.8 vs 0.77 +/- 0.8 mm(-1), p < 0.03). Aortic energy loss was, however, similar between the groups. In patients with non-insulin dependent diabetes aortic elastic properties, evaluated by pressure-diameter relation, are impaired. This could play an important part in the development of vascular complications related to diabetes.

End-systolic pressure-diameter relation of the left ventricle during transient and sustained elevations of blood pressure.

To assess the effect of transient and sustained variations in cardiac load on the values of the end-systolic pressure-diameter relation (ESPDR) of the left ventricle. We studied 13 dogs under general anesthesia and autonomic blockade. Variations of cardiac loads were done by elevation of blood pressure by mechanical constriction of the aorta. Two protocols were used in each animal: gradual peaking and decreasing pressure variation, the "transient arterial hypertension protocol" (TAH), and a quick and 10 min sustained elevation, the "sustained arterial hypertension protocol"(SAH). Then, we compared the ESDR in these two situations. Acute elevation of arterial pressure, being it "transitory" or "sustained", did not alter the heart frequency and increased similarly the preload and after load. However, they acted differently in end systolic pressure-diameter relation. It was greater in the SAH than TAH protocol, 21.0+/-7.3 mm Hg/mm vs. 9.2+/-1. 2 mm Hg/mm (p<0.05). The left ventricular ESPDR values determined during sustained pressure elevations were higher than those found during transient pressure elevations. The time-dependent activation of myocardial contractility associated with the Frank-Starling mechanism is the major factor in inotropic stimulation during sustained elevations of blood pressure, determining an increase in the ESPDR values.

Mechanical dissociation of bronchi from parenchyma in the immature piglet lung

Previous studies of isolated piglet lungs suggested that local distending forces around bronchi might be relatively weak before postnatal growth and maturation. The present study used tantalum bronchograms to compare pressure-diameter relationships of bronchi in situ and after excision from the parenchyma in immature (3- to 7-day-old) and mature (3-mo-old) piglets. The mature group reproduced behavior that is well established in mature lungs from other species; i.e., bronchial diameters maintained a constant relationship to the parenchyma as the lungs were deflated from maximum to minimum volume. In sharp contrast, diameters failed to change until the immature lungs were deflated to <5 cmH(2)O transpulmonary pressure. Total percent change in bronchial diameter was then only 24% in the immature lungs compared with 47% in the mature lungs (P < 0.002). Total elastances of mature generation 3-8 bronchi did not change when they were excised from the parenchyma. However, in the same generations of immature bronchi, total elastances were lower after than before (1.06 vs. 1.60 cmH(2)O/%, P < 0.05) excision from the parenchyma. Elastances of the excised immature and mature bronchi were then the same (1.06 vs. 1.03 cmH(2)O/%, not significant). Because elastic moduli of the lung parenchyma are also similar in the two age groups, it was concluded that local features of airway-parenchyma coupling limited the generation of local parenchymal recoil around bronchi in the immature lungs.

Assessment of aortic line of elasticity using polynomial regression analysis.

The aim of this study was to assess the sigmoid line of elasticity in the human aorta. The pressure-diameter relation was measured in the descending aorta in 120 subjects. In an additional group of 6 subjects, transient vena caval occlusion produced 5 sets of pressure-diameter data. We found that the best fit curve of the pooled pressure-diameter data was a third-order polynomial. A polynomial equation was used to calculate the sigmoid line of elasticity in the entire population and after the administration of diltiazem (15 patients) or enalaprilat (10 patients). The sigmoid line of elasticity was significantly different with respect to age (P<0.001), history of hypertension (P<0.004), and hypercholesterolemia (P<0.02). The difference between the transition point and the peak systolic pressure was increased in normal subjects compared with patients (P<0.0001). The sigmoid line shifted leftward and upward with diltiazem, but it remained unchanged with enalaprilat. During an average of 3 years of follow-up, 19 of 88 patients developed stroke (n=4), unstable angina (n=8), acute myocardial infarction (n=4), or acute pulmonary edema (n=3). This approach provides a quantitative evaluation of the aortic line of elasticity, which can differentiate the intrinsic from the extrinsic aortic elastic properties. Furthermore, it is a powerful and independent risk factor for cardiovascular events.

Definition of arterial compliance

To the editor : In the March 1999 issue of The American Journal of Physiology , Hardt et al. ([1][1]) presented an elegant experimental study on the validation of intravascular ultrasound (IVUS) in assessing changes in the pressure-diameter relationship in the aorta of dogs. They compared

Static versus Dynamic Distensibility of the Carotid Artery in Humans

In clinical studies, the elastic behavior of central arteries is usually assessed by measuring dynamic distensibility. In this study, we aimed to investigate how dynamic and static distensibility of the common carotid artery (D_dyn and D_stat, respectively) are related in 28 healthy volunteers of 20–71 years. The carotid diameter and its change with the pressure pulse were measured using an ultrasound echo-tracking device. Arterial blood pressure was measured by Finapres and carotid pressure was determined by applanation tonometry. D_dyn was determined at rest using the pressure pulse, while D_stat was determined during pressor responses induced by handgrip or cold pressor test. Data are given as mean ± 1 SD. In younger subjects (<35 years), D_stat did not differ from D_dyn (7.0 ± 3.4 vs. 6.5 ± 2.1·10^–3·mm Hg^–1, respectively), whereas in older subjects (>35 years), D_stat was significantly higher than D_dyn (3.8 ± 1.4 vs. 2.1 ± 0.9· 10^–3·mm Hg^–1, p < 0.001). For all subjects, D_stat and D_dyn decreased with increasing age and mean arterial pressure (MAP). Using stepwise multiple regression analysis, the strongest predictor of D_stat proved to be MAP, while that of D_dyn was age. D_stat was found to be linearly related to the hysteresis loop area of the pressure-diameter relation (r = 0.94), i.e. to vessel wall viscosity. It is concluded that, with increasing age, static distensibility overestimates the distension capacity of large arteries.

Aortic stiffness as a risk factor for recurrent acute coronary events in patients with ischaemic heart disease

Aortic elasticity is an important determinant of left ventricular performance and coronary blood flow. Moreover, it has been shown that aortic elastic properties deteriorate in patients with coronary artery disease. However, the predictive role of aortic elasticity in the occurrence of coronary events, has not been addressed so far. Therefore, we set out to test prospectively the hypothesis that invasive as well as non-invasive measures of aortic elastic properties, assessed at rest from pressure-diameter relationships, could predict the development of recurrent coronary events. Clinical variables and measures of aortic function were assessed in 54 normotensive patients with coronary artery disease. The aortic pressure-diameter relationship was derived invasively with a high-fidelity Y shaped catheter (developed in our Institution) for aortic diameter measurements, simultaneously with a Millar catheter for aortic pressure measurements. Aortic root distensibility was assessed by non-invasive techniques. During an average of 3 years follow-up, 12 of 54 patients either developed unstable angina (n=8) or acute myocardial infarction (n=4). By multivariate Cox model analysis, aortic stiffness was the strongest predictor of progression to any end-point (relative risk: 3.24, CI: 1.79 to 5.83;P=0.000). When aortic stiffness was not considered, aortic distensibility was the only independent predictor for acute coronary syndromes (relative risk: 0.37 CI: 0.21 to 0.65;P=0.000). In patients with coronary artery disease, aortic elastic properties are powerful and independent risk factors for recurrent acute coronary events.

Prevention of early myocardial depression in hyperdynamic endotoxemia in dogs.

In our study the pathomechanism of sepsis-induced early myocardial depression was investigated. We determined the effects of the inducible nitric oxide synthase inhibitor and free radical scavenger mercaptoethylguanidine (MEG) on the myocardial contractility, the endothelial and inducible nitric oxide synthase (eNOS and iNOS) activities, and the activation and tissue accumulation of polymorphonuclear leukocytes in hyperdynamic endotoxemia in dogs. Group 1 served as endotoxemic control. Mean arterial pressure and cardiac output were measured, myocardial contractility was estimated from the end-systolic pressure-diameter relationship. The eNOS, iNOS and myeloperoxidase activities were determined on myocardial biopsy samples, and the free radical-producing capacity of granulocytes was measured from separated cells. The effect of MEG on the in vitro free radical production of isolated granulocytes was measured by chemiluminometry. Endotoxin induced a hyperdynamic circulatory reaction and significant myocardial depression. The myocardial eNOS activity was significantly increased 4 h after induction of endotoxemia and remained elevated, the iNOS activity was increased only 8 h after endotoxemia induction. The free radical-producing capacity and the myocardial accumulation of the granulocytes were significantly increased. In group 2, MEG treatment selectively inhibited the iNOS activity, prolonged the hyperdynamic circulatory reaction, prevented myocardial depression and decreased the activation and tissue accumulation of granulocytes. The compound dose-dependently decreased the in vitro activation of previously resting granulocytes. Our study demonstrates that iNOS do not contribute to the early cardiac failure in endotoxemia. MEG selectively inhibits iNOS in vivo, but its beneficial effects are rather related to the decreases in leukocyte and free radical-mediated myocardial dysfunction during early endotoxemia.

Endothelin Mediates a Component of the Enhanced Myogenic Responsiveness Of Arterioles From Hypertensive Rats

To determine if the enhanced pressure-induced constriction of arterioles isolated from hypertensive rats is mediated by the endothelium. We utilized isolated, cannulated first-order arterioles (80 to 110 microns, i.d.) from the rat cremaster muscle of spontaneously hypertensive (SHR) and normotensive (WKY) rats. Arteriolar diameter was measured in response to changes in intraluminal pressures as well as various pharmacological agents in the presence and absence of an intact endothelial cell lining. All arterioles developed intrinsic tone (approximately 74% of passive). Pressure-diameter relationships over a pressure range of 30 to 170 cm H2O demonstrated that the myogenic response of arterioles derived from both WKY and SHR was not dependent upon an intact endothelium. However, at higher pressures (> 170 cm H2O) the ability of the denuded arteriole from the SHR to maintain a constricted diameter was completely abolished. Treatment of arterioles from the SHR having intact endothelium with diclofenac (10(-5) M; 30 min) to inhibit the effect of cyclooxygenase had no effect on the high pressure constriction. In contrast, application of BQ-123 (10(-7) M; 30 min), an ET-A receptor blocker used to inhibit vascular smooth muscle responses to endothelin, completely abolished the arteriolar constriction at higher pressures. Therefore, in the hypertensive, arteriolar vasomotor responses to changes in intraluminal pressure is due to at least two mechanisms; one that is intrinsic to vascular smooth muscle (i.e., myogenic) and a second that involves an endothelial cell release of endothelin.

A hemodynamic analysis of coronary capillary blood flow based on anatomic and distensibility data.

An understanding of cardiac health and disease requires knowledge of the various factors that control coronary capillary blood flow. An analysis of coronary capillary blood flow based on a complete set of actual data on the capillary anatomy and elasticity does not exist. Previously, a complete set of data on the branching pattern and the vascular geometry of the pig coronary capillary network were obtained in our laboratory. In the present study, we obtained distensibility data on the coronary capillary blood vessels on the epicardial surface in the form of a pressure-diameter relationship using intravital microscopy. A mathematical model of the coronary capillary blood flow was then constructed on the basis of measured anatomic and elasticity data of the coronary capillary network, rheology of blood, physical laws governing blood flow, and appropriate boundary conditions. The constructed model was used to examine the heterogeneity of the spatial distribution of coronary blood flow, which is an important issue in coronary physiology. One interesting result of the model is that the dispersions of pressure and flow are significantly reduced in the presence of capillary cross-connections, and the resistance to flow is reduced as well. Finally, we found that the compliance of the epicardial surface capillary vessels is so small that its effect on the blood pressure drop is negligible in the diastolic state. However, the compliance of the intramyocardial capillaries remains unknown, and the interaction of the muscle contraction and blood vessel elasticity in systole remains to be studied.

MEDICAL TREATMENT OF THE AORTA II

Because of its elastic properties, the aorta influences left ventricular function and coronary blood flow. The aortic pressure-diameter relationship provides direct estimations of the elastic properties of the aorta in humans. Current research is focused on examining strategies that might improve aortic function. Therapeutic interventions alter the elastic properties of the aorta, and improvement of the elastic properties of the aorta may be beneficial in modifying the natural history of the disease. Certain pharmacological agents that result in improved aortic function have been identified.

Aortic pressure-diameter relationship assessed by intravascular ultrasound: experimental validation in dogs.

Intravascular ultrasound (IVUS) has emerged as an important diagnostic method for evaluating vessel diameter and vessel wall motion. To evaluate the validity of IVUS in assessing changes in the pressure-diameter relationship we compared measurements of abdominal aortic diameters derived from IVUS with those simultaneously obtained at the same site using implanted sonomicrometers in five chronically instrumented conscious dogs and in seven acutely instrumented anesthetized dogs. Five hundred eighty beats were analyzed to obtain peak systolic and end-diastolic diameters and to calculate aortic compliance at different blood pressure levels induced either by an aortic pneumatic cuff or by intravenous injections of nitroglycerin or norepinephrine. IVUS agreed closely with sonomicrometer measurements at different blood pressure levels. However, IVUS slightly but significantly underestimated aortic diameters by 0.6 +/- 0.7 mm for systolic diameters (P < 0.001) and by 0.7 +/- 0.6 mm for diastolic diameters (P < 0.001) compared with the sonomicrometer measurements. We conclude that IVUS is a feasible and reliable method to measure dynamic changes in aortic dimensions and has the potential to provide ready access to assess aortic compliance in humans.

Endothelin Mediates a Component of the Enhanced Myogenic Responsiveness Of Arterioles From Hypertensive Rats

Objective: To determine if the enhanced pressure-induced constriction of arterioles isolated from hypertensive rats is mediated by the endothelium. Methods: We utilized isolated, cannulated first-order arterioles (80 to 110 µm, i.d.) from the rat cremaster muscle of spontaneously hypertensive (SHR) and normotensive (WKY) rats. Arteriolar diameter was measured in response to changes in intraluminal pressures as well as various pharmacological agents in the presence and absence of an intact endothelial cell lining. Results: All arterioles developed intrinsic tone (approximately 74% of passive). Pressure-diameter relationships over a pressure range of 30 to 170 cm H2O demonstrated that the myogenic response of arterioles derived from both WKY and SHR was not dependent upon an intact endothelium. However, at higher pressures (>170 cm H2O) the ability of the denuded arteriole from the SHR to maintain a constricted diameter was completely abolished. Treatment of arterioles from the SHR having intact endothelium with diclofenac (10−5 M; 30 min) to inhibit the effect of cyclooxygenase had no effect on the high pressure constriction. In contrast, application of BQ-123 (10−7 M; 30 min), an ET-A receptor blocker used to inhibit vascular smooth muscle responses to endothelin, completely abolished the arteriolar constriction at higher pressures. Conclusions: Therefore, in the hypertensive, arteriolar vasomotor responses to changes in intraluminal pressure is due to at least two mechanisms; one that is intrinsic to vascular smooth muscle (i.e., myogenic) and a second that involves an endothelial cell release of endothelin.

Pipette Aspiration Measurement of Local Elastic Modulus in Aortic Walls of WHHL Rabbits. Comparison with Global Elastic Modulus Measured from Pressure-Diameter Relationship.

Local and global mechanical properties of atherosclerotic aorta were measured in 6 Watanabe heritable hyperlipidemic (WHHL) rabbits. Descending thoracic aortas were obtained from animals aged 8 months. Local initial elastic modulus Elocal and global incremental elastic modulus Hθθ were measured with pipette aspiration technique and pressure diameter tests, respectively. Opening angles were measured as an index of residual strain. Elocal of atherosclerotic lesion (fatty streak) was 19.1±1.9 kPa (mean±SEM), which was significantly smaller than that of preserved area (38.9±7.5 kPa). Hθθ of the whole specimen was 1 260±140 kl'a at 100 mmHg, and was not statistically different from the value measured in age matched controls, Japanese White rabbits. Opening angle was significantly larger in WHHL rabbits than in their controls. These results suggest that, in the early stages of atherosclerosis. (1) the lesion is more compliant than normal aortic tissues ; (2) macroscopic mechanical properties are not sensitive to local mechanical change ; (3) residual strain increases with the development of the disease. It is important to assess local mechanical properties and residual strain when studying mechanical properties of atherosclerotic aortas.

Finite Element Modeling and Numerical Simulation of the Artery in Active State.

A layer-structured finite element model is introduced for an artery, which consists of passive and active elements and is applicable to a variety of boundary-value problems. Constitutive equations are formulated for each type of element in the finite element model. The passive element is expressed as an incompressible isotropic hyperelastic material. The active element develops an active stress in the circumferential direction. To validate the model, we carried out numerical simulations, i.e., the pressure-diameter relationships and stress distributions at mean transmural pressure in the passive and active states, and the opening angle change with activation. The results of numerical simulation showed significant changes in the mechanical behavior of the vessel with activation. It also showed that a large contraction occurred at a higher level of activation for a higher level of constant pressure, and that the tendency of opening angle change was consistent with the experimental one reported in the literature.

A Mathematical Model of Arteries in the Active State. Incorporation of Active Stress and Activation Parameter.

A mathematical model for various types of arteries in the active state is proposed with the incorporation of an activation parameter, an inelastic strain and stiffening of elasticity. The total stress is divided into a passive stress and an active stress. The passive stress is expressed by an incompressible isotropic strain energy density function. The active stress is expressed as a fiber stress of smooth muscles with the use of the activation parameter and an isometric force-length relationship. The inelastic strain corresponds to the deformation between the reference configuration and the unloaded configuration. Stiffening of elasticity is considered mainly for elastic-type arteries. The simulation results show that the model adequately describes the pressure-diameter relationships in the physiological range. The stress analyses of the arterial walls show that the circumferential stress changes to compressive stress in the active state with a strong contraction and a lower transmural pressure of the vessel.

Aortic function in patients during intra-aortic balloon pumping determined by the pressure-diameter relation

Objective: The physiologic basis for the hemodynamic and clinical improvement achieved by the use of intra-aortic balloon pumping in patients with cardiogenic shock has not been clarified in all its aspects. This study evaluated the possible contribution of pump-induced alterations of aortic mechanics to the overall benefit gained by the implementation of this therapeutic modality in patients with acute heart failure of ischemic origin. Methods: The aortic pressure-diameter relation was obtained by use of an intravascular catheter for aortic diameter measurements developed in our institution and previously validated, simultaneously with a catheter-tip micromanometer for aortic pressure measurements at the same aortic level. Aortic function indices were compared before and during intra-aortic balloon pumping in 12 patients with cardiogenic shock. Results: Intra-aortic balloon pumping increased cardiac index and aortic distensibility by 24% and 30%, respectively, and reduced myocardial oxygen demand by 31% ( P < .001 for all alterations). Energy loss caused by aortic wall viscosity increased by 207% ( P < .001). The aortic diameter augmentation index increased by 68% ( P < .001); the aortic pressure augmentation index decreased by 117% ( P < .001). Linear regression analysis showed that cardiac index and myocardial oxygen demand were related with the aortic stiffness constant both before and during intra-aortic balloon pumping. Conclusions: During intra-aortic balloon pumping, aortic distensibility was improved, and wave reflection from the arterial periphery was reduced. The relationship between cardiac index and myocardial oxygen demand and aortic stiffness suggests that improvement of the elastic properties of the aorta was an important mechanism by which intra-aortic balloon pumping improved circulatory function. (J Thorac Cardiovasc Surg 1998;116:1052-9)

High dietary salt alters arteriolar myogenic responsiveness in normotensive and hypertensive rats.

We evaluated arteriolar myogenic responsiveness in normotensive, salt-loaded and hypertensive rats and investigated the potential influence of luminal blood flow or shear stress on myogenic responses under each of these conditions. Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) fed low-salt (0.45%, LS) or high-salt (7%, HS) diets were enclosed in a ventilated airtight box with the spinotrapezius muscle exteriorized for intravital microscopy. Dietary salt did not affect mean arterial pressure (MAP) in WKY, whereas MAP in SHR was significantly higher and augmented by dietary salt. In all groups, box pressurization caused similar increases in MAP that were completely transmitted to the arterioles. After these pressure increases, large arteriole diameters decreased by 0-30% and intermediate arteriole diameters decreased by 21-27%. Arteriolar myogenic responsiveness was not different between WKY-LS and SHR-LS. Large arterioles in WKY-HS displayed an attenuated pressure-diameter relationship compared with that in WKY-LS. Large arterioles in SHR-HS displayed an augmented pressure-diameter relationship compared with that in SHR-LS. There were no correlations between resting flow or wall shear rate and the magnitude of initial myogenic constriction in any group or vessel type. The capacity for sustained myogenic constriction was unrelated to secondary decreases in flow (14-41%) or increases in wall shear rate (21-88%) in each group. We conclude that 1) dietary salt impairs the myogenic responsiveness of large arterioles in normotensive rats and augments the myogenic responsiveness of large arterioles in hypertensive rats, 2) hypertension does not alter arteriolar myogenic responsiveness in this vascular bed, and 3) flow- or shear-dependent mechanisms do not attenuate myogenic responses in the intact arteriolar network of normal, salt-loaded, or hypertensive rats.

Unfavorable effects of passive smoking on aortic function in men.

The aorta acts as both a conduit and an elastic buffering chamber that modulates left ventricular function and coronary blood flow. Previous studies have shown that active smoking has unfavorable effects on aortic elasticity. To study the association between passive smoking and the elastic properties of the human aorta. Comparison of nonsmokers during passive smoking studies and smokers during active smoking or sham smoking studies. Academic medical center. 16 male nonsmokers were assigned to passive smoking studies, and 32 current, long-term, male smokers were randomly assigned to either active smoking (16 patients) or sham smoking (16 patients) studies. All participants underwent diagnostic catheterization. In the passive smoking group, environmental tobacco smoke was vented into an exposure chamber for 5 minutes (mean carbon monoxide level, 30 parts per million). Each participant in the active smoking group smoked one filtered cigarette (1.0 mg of nicotine) under standardized conditions within 5 minutes; each participant in the sham smoking group performed a similar pattern of inhalation with one unlit cigarette. Aortic elastic properties were studied by measuring the aortic pressure-diameter relation before and for 20 minutes after passive, active, or sham smoking. Instantaneous diameter of the thoracic aorta was measured with a high-fidelity ultrasonic dimension catheter. Instantaneous aortic pressure and diameter were measured at the same site. Both passive and active smoking were associated with changes in the aortic pressure-diameter relation (change in mean distensibility in the passive smoking group, from 2.02 to 1.59 x 10(-6) cm2 x dyne(-1) [for comparisons of time course between passive and sham smoking groups, P < 0.001]; change in mean distensibility in the active smoking group, from 2.08 to 1.51 x 10(-6) cm2 x dyne(-1) [for comparisons of time course between active and sham smoking groups, P < 0.001]). These changes represent decreases of 21% and 27%, respectively. No changes in aortic elasticity were seen in the sham smoking group. Both passive and active smoking are associated with an acute deterioration in the elastic properties of the aorta. This association between exposure to tobacco smoke and aortic elasticity indicates that aortic function deteriorates during passive or active smoking.

Nitric oxide modulation of coronary artery myogenic tone in spontaneously hypertensive and Wistar-Kyoto rats.

1. The endothelium contributes substantially to the modulation of myogenic tone in coronary arteries from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). This study has addressed the contributions of endothelium-derived nitric oxide and cyclo-oxygenase products to this modulation in small coronary arteries (approximately 200 microns internal diameter) from 20-week-old SHR and WKY under pressurized, no-flow conditions in an arteriograph. 2. Active pressure-diameter relationships were uninfluenced by the cyclo-oxygenase inhibitor indomethacin (10 mumol/l) in either rat strain. In the presence of indomethacin and the nitric oxide synthase inhibitor N omega-nitro-L-arginine (L-NNA, 0.1 mmol/l), coronary arteries from SHR and WKY generated significantly greater myogenic tone. This increase in tone was similar in both strains. 3. In endothelium-denuded arteries, indomethacin and L-NNA did not influence tone. 4. Therefore, these results demonstrate that endothelium-derived nitric oxide is basally released to attenuate SHR and WKY coronary artery myogenic tone, whereas endothelium-derived cyclo-oxygenase products have no net vasoactive influence. Additionally, these data suggest that basal nitric oxide-mediated relaxation is normal in SHR coronary arteries and is therefore unlikely to be a pathogenic mechanism in this animal model of hypertension.