Microcirculation and Macrocirculation in Hypertension: A Dangerous Cross-Link?

Hypertension ◽  
2022 ◽  
Author(s):  
Stephane Laurent ◽  
Claudia Agabiti-Rosei ◽  
Rosa Maria Bruno ◽  
Damiano Rizzoni
Keyword(s):  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Vicious Circle ◽  
Large Artery ◽  
Resistance Arteries ◽  
Cross Link ◽  
Small Artery ◽  
Structural Abnormalities ◽  
Small Resistance

Microcirculation and macrocirculation are tightly interconnected into a dangerous cross-link in hypertension. Small artery damage includes functional (vasoconstriction, impaired vasodilatation) and structural abnormalities (mostly inward eutrophic remodeling). These abnormalities are major determinants of the increase in total peripheral resistance and mean blood pressure (BP) in primary hypertension, which in the long term induces large artery stiffening. In turn, large artery stiffening increases central systolic and pulse pressures, which are further augmented by wave reflection in response to the structural alterations in small resistance arteries. Finally, transmission of high BP and flow pulsatility to small resistance arteries further induces functional and structural abnormalities, thus leading to increased total peripheral resistance and mean BP, thus perpetuating the vicious circle. Hyperpulsatility, in addition to higher mean BP, exaggerates cardiac, brain, and kidney damages and leads to cardiovascular, cerebral, and renal complications. The dangerous cross-link between micro and macrocirculation can be reversed into a virtuous one by ACE (angiotensin-converting enzyme) inhibitors, sartans, and calcium channel blockers. These three pharmacological classes are more potent than β-blockers and diuretics for reducing arterial stiffness and small artery remodeling. The same ranking was observed for their effectiveness at reducing left ventricular hypertrophy, preserving glomerular filtration rate, and preventing dementia, suggesting that they can act beyond brachial BP reduction, by breaking the micro/macrocirculation vicious circle.

scholarly journals Polarized Proteins in Endothelium and Their Contribution to Function

2021 ◽  
pp. 1-27
Author(s):  
Abigail G. Wolpe ◽  
Claire A. Ruddiman ◽  
Phillip J. Hall ◽  
Brant E. Isakson
Keyword(s):  
Endothelial Cells ◽  
Endothelial Function ◽  
Planar Cell Polarity ◽  
Protein Localization ◽  
Peripheral Resistance ◽  
Specific Protein ◽  
Resistance Arteries ◽  
Extracellular Stimuli ◽  
Small Resistance ◽  
Signaling Domains

Protein localization in endothelial cells is tightly regulated to create distinct signaling domains within their tight spatial restrictions including luminal membranes, abluminal membranes, and interendothelial junctions, as well as caveolae and calcium signaling domains. Protein localization in endothelial cells is also determined in part by the vascular bed, with differences between arteries and veins and between large and small arteries. Specific protein polarity and localization is essential for endothelial cells in responding to various extracellular stimuli. In this review, we examine protein localization in the endothelium of resistance arteries, with occasional references to other vessels for contrast, and how that polarization contributes to endothelial function and ultimately whole organism physiology. We highlight the protein localization on the luminal surface, discussing important physiological receptors and the glycocalyx. The protein polarization to the abluminal membrane is especially unique in small resistance arteries with the presence of the myoendothelial junction, a signaling microdomain that regulates vasodilation, feedback to smooth muscle cells, and ultimately total peripheral resistance. We also discuss the interendothelial junction, where tight junctions, adherens junctions, and gap junctions all convene and regulate endothelial function. Finally, we address planar cell polarity, or axial polarity, and how this is regulated by mechanosensory signals like blood flow.

scholarly journals Left ventricular and proximal aorta coupling in magnetic resonance imaging: aging together?

2019 ◽  
Vol 317 (2) ◽  
pp. H300-H307 ◽  
Author(s):  
Alban Redheuil ◽  
Nadjia Kachenoura ◽  
Emilie Bollache ◽  
Wen-Chung Yu ◽  
Anders Opdahl ◽  
...  
Keyword(s):  
Total Peripheral Resistance ◽  
Characteristic Impedance ◽  
Myocardial Strain ◽  
Peripheral Resistance ◽  
Wall Stress ◽  
Aortic Distensibility ◽  
Left Ventricular ◽  
Ascending Aorta ◽  
Left Ventricular Geometry ◽  
Age Related

The importance of aorta-ventricular coupling in cardiovascular disease is recognized but underestimated. The contribution of the age-related decline in ascending aortic function compared with characteristic impedance and total peripheral resistance on left ventricular function and remodeling is poorly studied. Our aim was to evaluate the relation of proximal aortic distensibility and impedance with left ventricular geometry and function in asymptomatic individuals. We prospectively studied 100 subjects (47 men, 53 women, age: 20–84 yr). Aortic strain, distensibility, arch pulse wave velocity, characteristic impedance ( Zc), total peripheral resistance, left ventricular (LV) volumes and mass, wall stress, and peak global circumferential myocardial strain and strain rates were determined by MRI. Central pressures were measured from tonometry. Ea/ Ev, an index of vascular-ventricular coupling, and LV wall stress were preserved across age- or aortic-stiffness-stratified groups. Static and pulsatile components of aortic load were differentially associated with age. Increased total vascular resistance was associated with decreased LV strain and increased concentric remodeling [ratio of LV mass to end-diastolic volume (M/V ratio)] in all individuals. In younger individuals (<45 yr), aortic distensibility was related to LV strain and concentric remodeling (M/V ratio), whereas Zc was related to LV strain and concentric remodeling (M/V ratio) in older individuals (>45 yr). Early age-related stiffening of the ascending aorta is a component of LV afterload subsequently associated with increased aortic impedance and alterations in LV geometry, namely concentric remodeling, decreased myocardial strain, and increased stroke work such that LV wall stress and arterial-ventricular coupling are preserved. NEW & NOTEWORTHY Local flow and deformation can both be assessed with high precision noninvasively in the ascending aorta using MRI. Combined with central pressure measurement, they provide distensibility and impedance and simultaneous reference assessment of left ventricular deformation and geometry, hence a comprehensive evaluation of arterial-ventricular coupling to study physiology and disease.

Marriage of resistance and conduit arteries breeds critical limb ischemia

2005 ◽  
Vol 288 (3) ◽  
pp. H1044-H1050 ◽  
Author(s):  
Paul Coats ◽  
Roger Wadsworth
Keyword(s):  
Blood Supply ◽  
Critical Limb Ischemia ◽  
Limb Ischemia ◽  
Sudden Increase ◽  
Large Artery ◽  
Resistance Arteries ◽  
Tissue Edema ◽  
Surgical Bypass ◽  
Small Resistance ◽  
And Function

Atherosclerosis in a major leg artery leads to impaired blood supply, which normally progresses to critical limb ischemia. Atherosclerosis produces substantial alterations of structure and endothelial function in the large conduit arteries. Pressure unloading and ischemia in the distal vasculature bring about alterations in microvascular function. Resistance arteries undergo significant wall thinning and changes in their contractile regulation. Optimization of large artery dimensions by the small arteries through flow-mediated vasodilation is impaired. Angiogenesis is stimulated, which can result in the formation of major collateral feeder vessels in addition to small nutritive blood vessels. However, angiogenesis can also contribute to instability of atherosclerotic plaques, which ultimately leads to further deterioration in blood supply. Surgical bypass grafting to restore blood supply to the distal leg generates a sudden increase of pressure in the weakened resistance vasculature, leading to uncontrolled changes in capillary hydrostatic pressure, extravasation of fluid, and tissue edema. This review aims to highlight the importance of the resistance vasculature in critical limb ischemia and the interdependence of pathophysiological changes in the large conduit and small resistance arteries. The major unresolved question is why the physiological mechanisms that regulate vascular structure and function ultimately break down, leading to circulatory failure within the distal limb.

Cardiac performance enhancement from dobutamine in patients refractory to hypervolemic therapy for cerebral vasospasm

1993 ◽  
Vol 79 (4) ◽  
pp. 494-499 ◽  
Author(s):  
Michael L. Levy ◽  
Craig H. Rabb ◽  
Vladimir Zelman ◽  
Steven L. Giannotta
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cardiac Index ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Beta Agonist ◽  
Volume Index ◽  
Stroke Work ◽  
Hyperdynamic Therapy

✓ The use of the beta-agonist dobutamine in combination with hypervolemic preload enhancement of cardiac performance was analyzed in 23 patients who failed to respond to traditional preload enhancement following aneurysmal subarachnoid hemorrhage. The patients ranged in age from 13 to 82 years, and three had a history of cardiac disease. Each patient underwent placement of a flow-directed balloon-tipped catheter and the following measurements were obtained during hyperdynamic therapy: pulmonary artery wedge pressure, central venous pressure, cardiac index, stroke volume index, total peripheral resistance, and left ventricular stroke work index (LVSWI). Mean baseline cardiac function was found to be within normal limits (LVSWI = 47.6 ± 4.2 gm/min/sq m and cardiac index = 3.30 ± 0.22 liter/min/sq m). After baseline measurements were recorded, 5% albumin was infused at 300 cc/hr and dobutamine was initiated at a rate of 5 to 10 µg/kg/hr. This hyperdynamic therapy with dobutamine in the presence of volume loading resulted in a 52% increase in cardiac index, a 15% increase in LVSWI, and a 21% decrease in total peripheral resistance. The clinical reversal of ischemic symptoms due to subarachnoid hemorrhage was evident in 18 (78%) of the 23 patients.

Effects of dihydroergotamine on hemodynamic molsidomine actions in anesthetized dogs

1984 ◽  
Vol 62 (6) ◽  
pp. 634-639 ◽  
Author(s):  
Volker B. Fiedler ◽  
Helmut Göbel ◽  
Rolf-Eberhard Nitz
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Venous Capacitance ◽  
Heart Performance ◽  
Dose Dependent Fashion ◽  
Anesthetized Dogs

In pentobarbital-anesthetized mongrel dogs the intravenous actions of 0.50 mg/kg molsidomine on pulmonary artery and left ventricular (LV) end-diastolic pressures and internal heart dimensions (preload), left ventricular systolic and peripheral blood pressures, and total peripheral resistance (afterload), as well as on heart rate, dP/dt, stroke volume, and cardiac output (heart performance) were studied for 2 h. Hemodynamic molsidomine effects were influenced by increasing amounts of intravenously infused dihydroergotamine solution (DHE, 1–64 μg∙kg−1∙min−1). Molsidomine decreased preload, stroke volume, and cardiac output for over 2 h but decreased ventricular and peripheral pressures for 45 min. Systemic vascular resistance showed a tendency to decrease while heart rate and LV dP/dtmax were not altered. DHE infusion reversed molsidomine effects on the preload and afterload of the heart. The diminished stroke volume was elevated so that cardiac output also increased. Total peripheral resistance increased while heart rate fell in a dose-dependent fashion. The LV dP/dtmax remained unchanged until the highest dose of 64 μg∙kg−1∙min−1 DHE elevated the isovolumic myocardial contractility. These experiments indicate that DHE can reverse the intravenous molsidomine effects on hemodynamics. Most likely, this is mediated through peripheral vasoconstriction of venous capacitance vessels, thereby affecting moldisomine's action on postcapillary beds of the circulation.

Structural changes in small resistance arteries and left ventricular geometry in patients with primary and secondary hypertension

2002 ◽  
Vol 20 (7) ◽  
pp. 1439-1444 ◽  
Author(s):  
Maria Lorenza Muiesan ◽  
Damiano Rizzoni ◽  
Massimo Salvetti ◽  
Enzo Porteri ◽  
Cristina Monteduro ◽  
...  
Keyword(s):  
Structural Changes ◽  
Secondary Hypertension ◽  
Left Ventricular ◽  
Left Ventricular Geometry ◽  
Resistance Arteries ◽  
Ventricular Geometry ◽  
Small Resistance

Cytokines and vascular reactivity in resistance arteries

2005 ◽  
Vol 288 (3) ◽  
pp. H1016-H1021 ◽  
Author(s):  
Elisabet Vila ◽  
Mercedes Salaices
Keyword(s):  
Vascular Reactivity ◽  
Peripheral Resistance ◽  
Resistance Arteries ◽  
Vascular Effects ◽  
Arterial Blood ◽  
Vasoactive Mediators ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Small Resistance ◽  
Vascular Beds

Cytokine levels are elevated in many cardiovascular diseases and seem to be implicated in the associated disturbances in vascular reactivity reported in these diseases. Arterial blood pressure is maintained within a normal range by changes in peripheral resistance and cardiac output. Peripheral resistance is mainly determined by small resistance arteries and arterioles. This review focuses on the effects of cytokines, mainly TNF-α, IL-1β, and IL-6, on the reactivity of resistance arteries. The vascular effects of cytokines depend on the balance between the vasoactive mediators released under their influence in the different vascular beds. Cytokines may induce a vasodilatation and hyporesponsiveness to vasoconstrictors that may be relevant to the pathogenesis of septic shock. Cytokines may also induce vasoconstriction or increase the response to vasoconstrictor agents and impair endothelium-dependent vasodilatation. These effects may help predispose to vessel spasm, thrombosis, and atherogenesis and reinforce the link between inflammation and vascular disease.

Haemodynamic Abnormalities in Hypertensive Patients: A Review of the Influence of Vasodilating Drugs

1986 ◽  
Vol 14 (6) ◽  
pp. 289-298
Author(s):  
U Abshagen ◽  
E von Möllendorff
Keyword(s):  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Progressive Increase ◽  
Left Ventricular ◽  
Arterial System ◽  
Organic Nitrates ◽  
Moderate Increase ◽  
Ventricular Performance ◽  
Venous Capacitance

Mean arterial pressure is determined primarily by cardiac output and total peripheral resistance, in addition to blood volume and compliance of the arterial system. The regulation of these determinants occurs via reflex neurogenic mechanisms and metabolic or humoral mechanisms. The haemodynamic situation in the early stages of arterial hypertension is characterized by a slight hypercirculatory state due to a moderate increase in heart rate and cardiac output, whereas the total peripheral resistance is increased only moderately, if at all. In later stages, however, a progressive increase in total peripheral resistance prevails, accompanied by a decrease in left ventricular performance due to the development of left ventricular hypertrophy, changes in ventricle geometry and coronary heart disease. A pharmacologically-induced decrease of total peripheral resistance by means of vasodilators, therefore, represents a logical approach to therapy, at least of advanced hypertension. Vasodilators can be classified into three categories: (1) those with preferential activity on the arterial resistance vessels, eg hydralazine, diazoxide, minoxidil; (2) those with preferential activity on venous capacitance vessels, eg organic nitrates; and (3) those with activities on both branches, eg sodium nitroprusside, urapidil, prazosin and other α-blockers. Brief reference is made to new and possibly more acceptable vasodilators – in particular carvedilol and prizidilol.

Effect of nocturnal atrial demand cardiac pacing on diurnal hemodynamic patterns

1992 ◽  
Vol 72 (5) ◽  
pp. 1798-1802 ◽  
Author(s):  
B. T. Engel ◽  
M. I. Talan ◽  
P. H. Chew
Keyword(s):  
Central Venous Pressure ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Control Period ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Central Venous ◽  
Arterial Blood ◽  
Early Evening

Heart rate (HR), stroke volume (SV), intra-arterial blood pressure, and central venous pressure were recorded on a beat-to-beat basis, 18 h/day (1800–1200 h the following day), for approximately 2 mo in four monkeys (Macaca mulatta). Cardiac output, left ventricular work, and total peripheral resistance were derived from these primary measurements. During the 1st mo we measured these parameters under control conditions, and during the 2nd mo the animals were studied while HR was paced by atrial demand pacing sufficient to prevent the normal nocturnal fall in HR (approximately 10 beats/min above the fastest hourly average rate recorded during the control condition). The main hypothesis of this study was that when HR is prevented from falling, SV, which normally does not fall overnight, would fall; this hypothesis was confirmed. In addition, we observed that, during the period of pacing, relative to the control period, SV was approximately 14% greater during the early evening and 4% lower during the early morning; total peripheral resistance was similar during the early evening but was 13% higher by morning. Throughout the night, systolic pressure was approximately 4% greater, diastolic pressure was 17% higher, central venous pressure was 43% greater, and left ventricular work was 27% higher. These findings show that when HR is prevented from falling overnight by atrial demand pacing, even to a relatively modest degree, there can be very significant sustained changes in cardiovascular function.

Abstract P256: Structural Alterations of Subcutaneous Small Resistance Arteries in Resistant Hypertension

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Carolina De Ciuceis ◽  
Claudia Rossini ◽  
Maria Lorenza Muiesan ◽  
Massimo Salvetti ◽  
Enzo Porteri ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Resistant Hypertension ◽  
Subcutaneous Tissue ◽  
Blood Pressure Monitoring ◽  
Response To Treatment ◽  
Large Artery ◽  
Resistance Arteries ◽  
Hypertensive Patients ◽  
Structural Alterations ◽  
Small Resistance

Background: It is was suggested that, in resistant hypertension, the presence of particularly pronounced microvascular alterations may contribute to explain the relative lack of response to treatment Patients and Methods: We investigated a population of 94 treated essential hypertensive patients. Secondary forms of hypertension were excluded, and in all patients a 24-hour blood pressure monitoring was performed in order to exclude a white coat effect. In all patients, we evaluated small resistance arteries morphology by a wire micromyographic approach. Subcutaneous tissue was obtained by local biopsy or during election surgery and subcutaneous small resistance arteries were dissected and mounted on a myograph; the media to lumen ratio (M/L) was then measured. We subdived our patents according to the presence or not of resistant hypertension (clinic blood pressure values above 140/90 mm Hg despite administration of three antihypertensive agent including a diuretic and 24-hour blood pressure values >130/80 mm Hg). Sixteen patients had true resistant hypertension, and were compared with the remaining 78 patients with non-resistant hypertension. Results: are summarized in the Table, The two groups were also different in terms of mean age (57±12 vs. 67±7 years, p=0.016 and pulse pressure/stroke volume, a rough index of large artery distensibility: 0.63±0.31 vs. 0.90±0.33, p=0.02). Conclusion: Hypertensive patients with true resistant hypertension have greater microvascular structural alterations compared with non-resistant hypertensive patients. This could partly explain the resistance to treatment and the high cardiovascular risk observed in these patients.

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