Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Vascular Capacitance”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 739 records · Page 41Linked to original sources
PubMed1994

In vivo effects of endothelin-2, endothelin-3 and ETA receptor blockade on arterial, venous and capillary functions in cat skeletal muscle.

This study describes, in quantitative terms, the effects of endothelin-2 and endothelin-3 on vascular tone (resistance) in large-bore arterial resistance vessels (> 25 microns), small arterioles (< 25 microns) and the veins, as well as on capillary pressure and fluid exchange in cat gastrocnemius muscle in vivo. Infusion of endothelin-2 or endothelin-3 (200-1600 ng kg-1 min-1, i.a.) elicited an initial transient dilation, followed by a dose-dependent, slowly developing constrictor response, being maintained after cessation of the infusion. At the dose of 400 ng kg-1 min-1 (n = 9), infused i.a. during 20 min, endothelin-2 caused an average increase in total regional vascular resistance of 80%, and endothelin-3 of 35%, and the site of constrictor action of both peptides was preferentially located to the small arterioles. Endothelin-2 also constricted veins and, hence, evoked a pronounced capacitance response, whereas endothelin-3 was devoid of any venoconstrictor effect. This difference, via effects on the pre-/post-capillary resistance ratio, led to a more pronounced fall of capillary pressure in response to endothelin-3 than to endothelin-2. The new specific competitive ETA receptor antagonist, FR 139317, abolished the vasoconstrictor response to both endothelin-2 and endothelin-3 in vivo, whereas the preceding vasodilator responses were unaffected. These results, taken together with those of our previous analogous study of the effects of endothelin-1, indicated that all three endothelins were approximately equally as effective in eliciting the transient dilator response in skeletal muscle in vivo, whereas the order of vasoconstrictor activity was endothelin-1 > endothelin-2 > endothelin-3. Due to an especially pronounced venoconstrictor activity of endothelin-1, this peptide, in contrast to endothelin-2 and -3, evoked a rise in capillary pressure, with a consequent net transcapillary fluid filtration and muscle tissue oedema formation. The results further indicated that the vasoconstrictor responses to all endothelins in skeletal muscle were mediated by the ETA receptor, whereas the initial transient vasodilator responses seemed to be mediated by the ETB receptor.

Animals↗
PubMed1992

First- and third-order models for determining arterial compliance.

BACKGROUND: Engineering models of the arterial vasculature have been used to describe vascular properties of resistance and compliance. These approaches have used either Fourier frequency analysis, based on transmission line equations, or time domain analysis of the circuit equations describing modified Windkessel models of the vasculature. DESIGN: A third-order, four-element modified Windkessel model can reproduce arterial pressure waveforms, including both exponential and oscillatory pressure decays observed during the diastolic portion of the cardiac cycle. METHOD: A method to determine both capacitive and oscillatory compliance of the arterial vasculature was developed, and the effect of these compliance properties on the blood pressure waveform was examined.

Arteries↗
PubMed1986

[Organic nitrates and prostaglandins in the cardiovascular system].

The beneficial effect of organic nitrates in acute myocardial ischemia is commonly explained by their hemodynamic actions, especially the dilatation of venous capacitance vessels. Recent studies have shown an inhibition of platelet function by organic nitrates ex vivo but not in vitro. Antiplatelet activities of organic nitrates might represent an additional mechanism, independent of vascular actions which might eventually involve stimulation of prostacyclin formation by the vessel wall. In vitro experiments on isolated coronary artery preparations have demonstrated stimulation of PGI2 as well as inhibition of platelet thromboxane synthesis by a number of organic nitrates. Optimal stimulation requires the presence of a free nitro group in the molecule at a particular steric position and can be suppressed by a number of inhibitors, including corticosteroids, indomethacin and methylene blue. Administration of the organic nitrate teopranitol to healthy volunteers is associated with depressed platelet secretion ex vivo which is not seen with the compound in vitro. It is concluded that further clinical elucidation of the PGI2-related mechanism in the action of organic nitrates in patients appears to be both necessary and useful.

Adenosine Triphosphate↗
PubMed1984

The dose-response characteristics of the acute non-diuretic peripheral vascular effects of frusemide in normal subjects.

The peripheral venous and arterial effects of frusemide, plasma renin activity and plasma frusemide concentrations were examined during the 15 min period following the i.v. administration of 0, 5, 10, 20, 40 and 80 mg of frusemide in a group of nine salt depleted volunteers. The responses to 80 mg frusemide given orally during the 1 1 h period after administration were also examined. Increases in venous capacitance 5 min after administration of 5 and 10 mg frusemide were observed (P less than 0.05) but no significant increases were apparent after the higher doses. At 10 min, the increases in venous capacitance showed a flat dose response effect with significant increases throughout the dose range (5-80 mg). Decreases in forearm blood flow occurred at 5 and 10 min after frusemide administration at all the doses studied (P less than 0.05) while blood pressure responses at 10 min showed increasing effect with increasing dose. An oral dose of 80 mg frusemide produced a rise in venous capacitance 15 min after administration and a decrease in forearm blood flow during the period 15-60 min without any alteration in heart rate or blood pressure.

Adolescent↗
PubMed1994

The correlation of cardiac mass with arterial haemodynamics of resistive and capacitive load in rats with normotension and established hypertension.

In hypertensive animals and humans, cardiac hypertrophy may occur as a consequence of an external load on the heart. Several studies have suggested that the non-pulsatile components of arterial haemodynamics, such as arterial pressure and vascular resistance, do not adequately represent the ventricular afterload and are not well correlated with the degree of cardiac hypertrophy (CH). The present study was undertaken to analyse the correlation between the degree of CH and various haemodynamic parameters in the spontaneously hypertensive rat (SHR) with established hypertension. A total of 36 SHRs (6-8 months) with a tail-cuff pressure above 190 mm Hg were used. Control data were obtained from 32 age-matched normotensive Wistar Kyoto rats (WKY). Animals were anaesthetized with pentobarbitone sodium (40 mg/kg i.p.) and artificially ventilated with a respirator. A Millar catheter with a high-fidelity pressure sensor was used to record the aortic pressure and an electromagnetic flow transducer to monitor the aortic flow. The pressure and flow signals were subjected to Fourier transformation for the analysis of the arterial impedance spectrum. The left ventricular weight-to-body weight ratio (LVW/BW) was taken as a measure of the degree of CH. The measured haemodynamic parameters in these anaesthetized, open-chest SHRs were systolic pressure (SP) (mean +/- SE) 172 +/- 4 mm Hg, diastolic pressure (DP), 120 +/- 3 mm Hg, pulse pressure (PP) 52 +/- 2 mm Hg, peripheral resistance (Rp) 344,032 +/- 8,012 dyne.s.cm-5, characteristic impedance (Zc) 6,442 +/- 313 dyne.s.cm-5, the impedance modulus at the first harmonic (Z1) 26,611 +/- 1,061 dyne.s.cm-5, mean arterial compliance (Cm) 0.87 +/- 0.04 microliter/mm Hg and LVW/BW 3.092 +/- 0.026 mg/g.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

[Effect of vasocative substances on resistance and capacitance vessels under high altitude conditions].

In cats, i.a. administration of adrenaline (10 microgram), serotonin (30 microgram), and acetylcholine (10 microgram) on the 3rd, 15th, and 30th days of animals stay at 3200 m altitude induced different vasomotor responses in precapillary and postcapillary portions of intestine vascular net during different periods of high altitude adaptation. Changes of reactivity in different receptor structures of smooth muscles, the initial tonus of the small intestine resistance vessels associated with the whole adaptive rearrangement of the organism functional state in the high altitude extreme conditions, are the possible mechanisms of detected changes.

Acclimatization↗
PubMed2003

Inhibitory effects of carvedilol on calcium channels in vascular smooth muscle cells.

Carvedilol has hypotensive effects and inhibits agonist-induced cell proliferation of vascular smooth muscle and then prevents vascular remodeling. However, the basic mechanisms have not been clarified. We examined the effects of carvedilol on [Ca2+]i mobilization and voltage-dependent L-type Ca2+ current (ICa.L) in vascular smooth muscle cells, and compared them with metoprolol. [Ca2+]i was measured using fura-2 AM and patch clamp techniques in rat embryonic aortic smooth muscle cells (A7r5). In the presence of extracellular Ca2+, vasopressin and endothelin-1 increased [Ca2+]i due first to the Ca2+ release from store sites, and subsequently Ca2+ entry. Carvedilol did not inhibit the Ca2+ release, but significantly suppressed the sustained rise due to Ca2+ entry concentration-dependently. Nilfedipine and nicardipine (10 microM) partly inhibited the sustained rise, but carvedilol inhibited it more effectively than the Ca2+ channel blockers. Under voltage clamp conditions, carvedilol (0.2-10 microM) reversibly inhibited the ICa.L concentration-dependently without any changes in the current-voltage relationships of ICa.L. Carvedilol shifted the steady-state inactivation for ICa.L to more negative potentials and inhibited ICa.L in a voltage-dependent manner. In addition, carvedilol did not inhibit Ca2+ release from store sites induced by thapsigargin, but significantly inhibited the sustained rise due to capacitative Ca2+ entry unrelated to ICa.L. In contrast, metoprolol did not mimic these effects of carvedilol. These results provide evidence that carvedilol inhibits ICa.L and may also inhibit the channels for agonist (vasopressin and endothelin-1)-induced Ca2+ entry in vascular smooth muscle cells, which might contribute to the vasorelaxing and antiproliferative effects of carvedilol.

Adrenergic beta-Antagonists↗
PubMed1979

Cardiovascular 'reactivity' to graded splanchnic nerve stimulation in spontaneously hypertensive and normotensive control rats.

Cardiovascular 'reactivity' to graded splanchnic nerve stimulation was compared in adult spontaneously hypertensive rats (SHR) and normotensive controls (NCR), during abolished adrenal medullary secretion and neurogenic cardiac control and depressed reflex vascular adjustments. Arterial pressure, heart rate and cardiac output were measured, and total peripheral resistance (TPR) and stroke volume (SV) computed before, during and after nerve stimulation. The neurogenic resistance increases in the major gastrointestinal-renal-hepatic circuits expressed themselves as TPR elevations, which were much accentuated in SHR. This reflects an increased w/ri of SHR resistance vessels rather than any altered effector sensitivity, since the responses were particularly accentuated at high discharge rates when noradrenaline junction concentrations approach maximal levels. The splanchnic capacitance responses expressed themselves as SV increases, being the most relevant aspect of capacitance control. SV increased less in SHR, mainly reflecting the reduced diastolic compliance of the hypertrophied SHR left ventricle and the consequent rightward shift of its Frank-Starling curve. The results indicate that an elevated resistance may well be maintained by a normal sympathetic discharge in established SHR hypertension. There seems, however, to be an increasing need for accentuated discharge to the capacitance side to maintain proper cardiac filling of the hypertrophied left ventricle.

Animals↗
PubMed1986

Cardiovascular effects of nipradilol, a beta-adrenoceptor blocker with vasodilating properties.

In anesthetized dogs, an intravenous injection of nipradilol produced a long lasting fall in mean arterial blood pressure which was accompanied by transient decreases in peripheral vascular resistance and sustained decreases in heart rate, cardiac output and left ventricular (LV) dP/dt. LV end-diastolic pressure (LVEDP) was not changed while LV diameters and central venous pressure were slightly increased. Under propranolol pretreatment conditions, nipradilol no longer affected the heart rate, but the drug still induced a transient reduction in peripheral vascular resistance, and sustained decreases in arterial blood pressure and cardiac output. Furthermore, indicators of LV preload (LVEDP, LV end-diastolic diameter and central venous pressure) were significantly reduced, suggesting a direct dilating action of nipradilol on capacitance vessels. In intact conscious dogs, nipradilol caused a sustained reduction in LVEDP, while propranolol increased LVEDP. After administration of nipradilol, coronary blood flow in anesthetized dogs decreased in association with diminished myocardial oxygen consumption, and large coronary vessel resistance also decreased. Nipradilol competitively antagonized the isoproterenol-induced positive chronotropic response (DR10: 0.04 mg/Kg, i.v.) and the phenylephrine-induced vasopressor response (DR10: 3.95 mg/Kg, i.v.). In conclusion, nipradilol, in contrast to propranolol, possesses the properties to decrease arterial blood pressure, LV preload and large coronary vessel resistance through its dilating action on arterial and venous vessels. It is proposed that nipradilol may be beneficial for the treatment of hypertension and coronary heart disease.

Adrenergic beta-Antagonists↗
PubMed1985

Vascular selectivity of felodipine.

Felodipine, a new antihypertensive 'calcium antagonist', was tested in animal experiments which specifically demonstrated its vascular selectivity. In vitro inorganic and organic calcium antagonists were added cumulatively to the spontaneously active rat portal vein, and the paced papillary muscle of the rat, residing in the same organ bath. Felodipine was the first compound tested to display a 100-fold vascular selectivity in this test system. In the portal vein the spontaneous activity and noradrenaline (norepinephrine)-induced responses are reduced by the drug in therapeutic concentrations in an insurmountable way, indicating that felodipine prevents activation of the vascular effector cells or interferes with the contractile process, possibly due to an intracellular action on Ca2+-binding proteins. The negative myocardial effect of felodipine, attainable only in vitro, is characterised by surmountable antagonism of the inotropic response to added adrenergic agonists or Ca2+ and is compatible with calcium influx inhibition. In vivo, felodipine was given to conscious dogs with indwelling arterial and venous catheters. The animals were studied in the horizontal position and at 45 degrees tilt. Felodipine (1 mumol/kg) and minoxidil (4 mumol/kg) lowered mean arterial blood pressure by 20 to 25%, due to reduced peripheral resistance with a reflex rise in cardiac output. Following head-up tilt (2 min) there was no orthostatic hypotension, and stroke volume was well maintained. This strongly indicates that arterial resistance vessels, but not venous capacitance vessels or myocardium, were directly affected by felodipine.

Animals↗
PubMed1999

Characteristics of impaired endothelium-dependent relaxation of rat aorta after streptozotocin-induced diabetes.

AIM: To study whether impaired endothelium-dependent relaxation (EDR) in early diabetic mellitus in response to different receptor-mediated and nonreceptor-mediated vasodilators ran parallel and its possible mechanism. METHODS: Isometric tension recording in aortic rings from streptozotocin (Str)-induced diabetic and age-matched nondiabetic rats. RESULTS: EDR induced by receptor agonist acetylcholine (ACh), histamine (His) or bradykinin (BK) were all significantly reduced in diabetic rings compared with control rings, whereas nonreceptor agonist calcimycin-induced EDR was well reserved in diabetic rings [IC50 control: (0.13 +/- 0.07) mumol.L-1 diabetic: (0.14 +/- 0.06) mumol.L-1, P > 0.05, n = 7]. Cyclopiazonic acid (CPA) which also is a nonreceptor mediated endothelium-dependent vasorelaxant and cells' capacitative Ca2+ entry stimulant, failed to trigger EDR in diabetic rings. Pretreatment with N omega-nitro-L-arginine methylester (L-NAME, 0.3 mmol.L-1) not only abolished all of the EDR elicited by above mentioned vasodilators in either of diabetic or control rings, but also leveled responses triggered by each of the agonists between diabetic and control rings. Upon the maximal EDR induced by ACh (1 mol.L-1) or CPA (3 mumol.L-1) in phenylephrine (1 mumol.L-1) precontracted rings, calcimycin (1 mumol.L-1) further relaxed diabetic rings, but contracted control preparations. When endothelium was denuded, relaxation evoked by sodium nitroprusside and contractions triggered by CPA or His were all identical between diabetic and control rings. CONCLUSION: Receptor agonists but not nonreceptor agonists-induced EDR are commonly impaired in 4-wk Str-induced diabetic rat aorta, and this defective effect is attributable to the low formation of EDRF/NO which is related to impaired capacitative Ca2+ entry pathway in endothelium.

Acetylcholine↗
PubMedDate not supplied

[Hemodynamic and cerebral ventricular functions during head-down tilt at -15 degrees].

Sixteen men were exposed to head-down tilt at -15 degrees for 6 h. Cerebral circulation was examined by bipolar rheoencephalography, ventricular function by one-dimensional echoventriculometry, and blood pressure by Korotkoff's sounds. Group 1 consisting of 10 test subjects tolerated the antiorthostatic exposure well enough (they reported only blood rush to the head and moderate facial puffiness). They showed stable parameters of cerebral circulation, ventricle size, and mean blood pressure, which is indicative of adequate compensatory capabilities of their organisms. Group 2 consisting of 6 test subjects exhibited polymorphic clinical symptoms, including the syndrome of liquor hypertension (burst-like headache, autonomic dysfunction, etc). This was accompanied by decreased pulse pressure of cerebral vessels, primarily in the vertebrobasilar area, instability of the vessel tone against the background of marked dilatation of the capacitance vessels and brain ventricles.

Adult↗
PubMed2006

Growth factor- and heparin-dependent regulation of constitutive and agonist-mediated human endothelial barrier function.

We report functional differences in constitutive and agonist-mediated endothelial barrier function between cultured primary and Clonetics human umbilical vein endothelial cells (pHUVEC and cHUVEC) grown in soluble growth factors and heparin. Basal transendothelial resistance (TER) was much lower in pHUVEC than in cHUVEC grown in medium supplemented with growth factors, such as basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF), and human epithelial growth factor (EGF), and heparin. On the basis of a numerical model of TER, the increased basal TER in cHUVEC was due to effects on cell-matrix adhesion and membrane capacitance. Heparin and bFGF increased constitutive TER in cultured pHUVEC, and heparin mediated additional increases in constitutive TER in pHUVEC supplemented with bFGF. EGF attenuated bFGF-mediated increases in TER. On the basis of the numerical model, in contrast to cHUVEC, heparin and bFGF augmented TER through effects on cell-cell adhesion and membrane capacitance in pHUVEC. Thrombin mediated quantitatively greater amplitude and a more sustained decline in TER in cultured cHUVEC than pHUVEC. Thrombin-mediated barrier dysfunction was attenuated in pHUVEC conditioned in EGF in the presence or absence of heparin. Thrombin-mediated barrier dysfunction was also attenuated when monolayers were exposed to low concentrations of heparin and further attenuated in the presence of bFGF. cAMP stimulation mediated differential attenuation of thrombin-mediated barrier dysfunction between pHUVEC and cHUVEC. VEGF displayed differential effects in TER in serum-free medium. Taken together, these data demonstrate marked differential regulation of constitutive and agonist-mediated endothelial barrier function in response to mitogens and heparin stimulation.

Capillary Permeability↗
PubMed1975

[Changes in the resistance and capacity of the cerebral vascular bed under the influence of vasoactive substances].

Effects of intracarotid injections of vasoactive agents on cerebrovascular resistance (CVR) and cerebral blood volume (CBV) were studied in hemodynamically isolated brain of cats. Perfusion pressure shifts at a constant blood volume perfusion reflected CVR changes, and changes of venous outflow - CBV alterations. Administration of adrenaline, serotonin, and angiotensine was followed mainly by an increase of CVR and a decrease of CBV. The CBR could be reduced by isopropilnoradrenaline, acetylcholine, histamine, and caffeine. CBV was decreased after isopropilnoradrenaline, acetycholine, histamine injections and increased by caffeine. The possible role of the active changes of cerebral capacitance vessels in the transcapillary fluid exchange is discussed. Capacitance vessels active responses are supposed to entail wrong results when using certain techniques for measurement of cerebral blood flow and metabolism.

Acetylcholine↗
PubMed2004

The obligatory link: role of gap junctional communication in endothelium-dependent smooth muscle hyperpolarization.

Although an endothelium-derived hyperpolarizing factor (EDHF) has often been hypothesized to underpin vascular relaxations that are independent of nitric oxide (NO) and prostanoids, bioassay techniques have failed to confirm the existence of a freely transferable EDHF in a consistent fashion. Indeed, observations that inhibitors of direct cell-cell coupling such as connexin-mimetic peptides (e.g. Gap 26 and 27) and glycyrrhetinic acid derivatives attenuate "EDHF-type" smooth muscle hyperpolarizations and relaxations suggest that an electrotonic spread of endothelial hyperpolarization via myoendothelial and homocellular smooth muscle gap junctions plays an obligatory role in such responses. The endothelial hyperpolarization that initiates relaxation results from the opening of K(Ca) channels and is sustained by capacitative Ca(2+) entry triggered by the depletion of intracellular Ca(2+) stores in the endoplasmic reticulum. EDHF-type relaxations are also associated with a prostanoid-independent synthesis of cAMP that increases the conductance of gap junction channels and enhances the transmission of endothelial hyperpolarization through the vascular wall in a permissive fashion. This review will discuss the roles of these interacting signalling pathways in the mediation of the EDHF phenomenon.

Amino Acid Sequence↗
PubMed1994

Effect of orthotopic cardiac transplantation on peripheral vascular function in congestive heart failure: influence of cyclosporine therapy.

The objective of this study was to examine peripheral vascular function before and after cardiac transplantation and to assess the effect of immunosuppressive therapy on peripheral vascular reactivity. Peripheral vascular function abnormalities present in congestive heart failure may be reversed with cardiac transplantation, but immunosuppressive therapy may alter these changes in the peripheral vasculature. Venous occlusion plethysmography was used to study peripheral vascular function in nine patients with severe congestive heart failure who underwent cardiac transplantation. Forearm blood flow and forearm vascular resistance were measured in patients with congestive heart failure in response to cold stimulation, maximal hyperemia, and hand grip exercise (1) before transplantation; (2) 24 to 36 hours posttransplantation before the commencement of cyclosporine; (3) 6 to 8 days posttransplantation in the presence of therapeutic cyclosporine levels; and (4) 6 weeks posttransplantation. Venous capacitance was also measured. After cardiac transplantation, mean arterial pressure increased and remained elevated. Forearm blood flow initially increased after transplantation but subsequently decreased with cyclosporine. Cold-induced reflex sympathetic activation decreased immediately after transplantation but was significantly enhanced with cyclosporine. The maximal vasodilatory response following ischemic cuff occlusion and with 5 minutes of isometric hand grip exercise increased significantly after transplantation and remained improved at 6 weeks. Thus after cardiac transplantation, peripheral vasodilator function improves and is not altered by cyclosporine. However, with cyclosporine therapy resting forearm vascular resistance increases and reflex sympathetic vasoconstriction is enhanced, suggesting that cyclosporine may potentiate adrenergic-mediated peripheral vasoconstriction and thus may contribute to posttransplant hypertension.

Analysis of Variance↗