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PubMed1985

Adrenergic nervous control of resistance and capacitance vessels. Studies on isolated blood vessels from the rat.

A systematic comparison of neurogenic responses from consecutive sections of the cardiovascular system has not yet been performed under the well-defined conditions that an in-vitro system can offer. The present investigation aimed at analysing the neuroeffector properties of different isolated vessels, mounted in a myograph, where isotonic and isometric responses to transmural nerve stimulation could be determined. The vessels investigated were the abdominal aorta and caval vein, the superior mesenteric artery and vein, and 200-micron arteries and corresponding veins from the mesenteric arcades, the latter representing true resistance and capacitance vessels, respectively. Further, the vascular adrenergic innervation was visualized by Hillarp-Falck's formaldehyde fluorescence technique as well as immunohistochemical methods. In all vessels the innervation was confined to the adventitio-medial border. The responses to single neurogenic impulses differed markedly between the vessels, being distinct and rapid in the small, slow in the intermediate vessels, and absent in the aorta and the caval vein. This was in contrast to the responses to direct electrical activation of the muscle, which were quite rapid in all vessels. The organisation of the neuromuscular transmission thus has a marked influence on the effector response. The maximal neurogenic responses parallelled the innervation density, being greatest in the small arteries and least in the abdominal aorta. The frequency for half-maximal response appeared to depend also on other factors, such as velocity of contraction and relaxation of the smooth muscle. Of the small vessels, the veins were relatively more activated by low frequencies. Stimulation with an irregular impulse pattern, derived from human sympathetic nerve discharge, had greater effects than the corresponding constant-frequency stimulation on the resistance arteries; the small veins responded equally to either pattern. This difference could be related to the observed frequency-response relations around the average frequency used. The effects of inhibition of neuronal amine uptake on neurogenic responses and on responses to exogenous noradrenaline differed considerably, particularly in the resistance arteries. Here the magnitude of the neurogenic responses were hardly affected by this inhibition, whereas responses to exogenous noradrenaline were strongly enhanced. On its own, blockade of prejunctional adrenergic alpha 2-receptors had little effect on either response, but blocking both alpha 2-receptors and reuptake clearly potentiated the neurogenic responses.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic Fibers↗

PubMed1985

Dose-related prolongation of the bleeding time by intravenous nitroglycerin.

The effects of intravenous nitroglycerin (NTG) upon the bleeding time, platelet aggregation response, and plasma 6-keto-PGF1 alpha concentration were measured in 17 patients about to undergo coronary bypass grafting. NTG produced a dose-related prolongation of the bleeding time that correlated with the accompanying decrease in systolic blood pressure. Platelet aggregation was not affected and measurements of 6-keto-PGF1 alpha failed to reveal detectable levels (less than 10 pg/ml) either before or after NTG infusion. This suggests that the prolonged bleeding time associated with NTG infusion may be due to vasodilation and increased venous capacitance, rather than altered vascular-platelet interaction.

Adult↗

PubMed2000

Pulmonary and systemic vascular tissue collagen, growth factor, and cytokine gene expression in the rabbit.

During development, the vascular wall composition of the pulmonary and systemic capacitance vessels and their intravascular pressure changes. Little is known, however, about the factors controlling vascular collagen gene expression in both circulations during growth and development. The purpose of this study was to compare the developmental changes in collagen, major growth factors, and cytokines gene expression, in order to ascertain whether a circulation specific pattern is present in the rabbit. Fetal, neonatal, and adult rabbit extrapulmonary and aortic tissues were obtained and the mRNA levels for collagen I and III, as well as major growth factors and cytokines, were measured by a semi-quantitative RT-PCR technique. Collagen I, but not collagen III, expression was developmentally regulated in pulmonary vascular and aorta tissues. Collagen I expression was greatest during the fetal and neonatal period (P < 0.01) and higher in the aorta as compared with the pulmonary artery at these ages (P < 0.05). Significant developmental changes in growth factor mRNA levels were observed for TGF-beta, IGF-2, and bFGF (P < 0.01). IGF-2 mRNA levels significantly declined in both arteries from neonatal to adult, but bFGF increased only in the pulmonary artery during this transition. With regards to inducible enzymes, COX-2 mRNA levels changed developmentally, whereas iNOS mRNA levels were similar for both vessels at all ages. When comparing the two vessels, COX-2 transcripts were relatively more abundant in the adult pulmonary artery tissue and fetal aorta, with similar levels in the newborn. We conclude that circulation specific developmental regulation of collagen gene expression is present in the rabbit in a pattern that is unrelated to the intravascular pressure.

Aging↗

PubMed1975

[Vascular responses to tilting in paraplegic subject compared to normal (author's transl)].

1 Vascular tone is higher in paraplegics than in normals, both in capacitance and resistance vessels. This is possibly correlated with the increase in circulating catecholamines which has recently been reported. 2 Tilting at 30 degrees from horizontal induces a hydrostatic increase in transmural pressure in the affected vascular bed. This pressure change causes: an initial decrease in resistance, followed by a progressive increase which can be explained by the Bayliss reflex. The time sequence and amplitude of the responses are comparable for normal and paraplegic subjects; an increase in vascular tone of the capacitance vessels (increase in venous pressure, decrease in local blood volume). This response was constantly observed in paraplegic subjects and was absent or weak in normal subjects. 3 In conclusion, reflex changes in vascular tone due to upright posture persist after traumatic section of the spinal chord. Orthostatic hypotension and blood pooling in the lower limbs in paraplegic subjects is probably due primarly to a deficit of the pumping action of the leg muscles.

Adult↗

PubMed1987

Effects of droperidol on peripheral vasculature: use of cardiopulmonary bypass as a study model.

The effects of droperidol on the systemic vascular resistance (SVR) and the venous capacitance were studied during cardiopulmonary bypass (CPB) in 24 patients. CPB was performed with either pulsatile or non-pulsatile flow. During non-pulsatile flow, droperidol (0.15 mg X kg-1 and 0.30 mg X kg-1) decreased SVR and increased venous capacitance. These values were significantly different after the 2nd and the 7th min, respectively. During pulsatile flow, the initial SVR was lower. The decremental effect of 0.30 mg X kg-1 droperidol on SVR was proportional to the preinjection level of SVR (r = 0.64). The increase in venous capacitance related to droperidol was independent of the dose and of the type of flow in all patients. It can be concluded that the vasodilating action of droperidol during CPB on the arterial bed is transient, independent of dose, and related to the preinjection level of SVR. The effect of droperidol on venous capacitance is not as rapid but has a longer duration.

Blood Vessels↗

PubMed1982

Effect of ouabain on total vascular capacity in the dog.

Whereas the cardiac effects of digitalis glycosides have been extensively studied, less is known of the extracardiac effects of the drug, in particular the effects on vascular capacity. We investigated the effects of parenteral ouabain on vascular capacity in the dog with particular emphasis on transhepatic resistance and its interaction with splanchnic and total intravascular capacity. We studied 49 dogs on total cardiopulmonary bypass in which the splanchnic and extrasplanchnic circulations could be separately perfused and drained, and the portal vein could be vented to systemic venous pressure. The results indicate: (a) ouabain produces a net central displacement of blood at 30 min after administration of 150 +/- 70 ml (SEM), (b) this displacement occurs despite a substantial increase in transhepatic resistance, although the early rise in transhepatic resistance may delay the net displacement of blood, and (c) the decrease of overall vascular capacity is due to an effect of ouabain on the capacitance vessels of both the splanchnic and extrasplanchnic circulations. The peripheral vascular capacity effects of ouabain may therefore contribute to overall cardiac performance.

Animals↗

PubMed2000

Akt1/PKB upregulation leads to vascular smooth muscle cell hypertrophy and polyploidization.

Vascular smooth muscle cells (VSMCs) at capacitance arteries of hypertensive individuals and animals undergo marked age- and blood pressure-dependent polyploidization and hypertrophy. We show here that VSMCs at capacitance arteries of rat models of hypertension display high levels of Akt1/PKB protein and activity. Gene transfer of Akt1 to VSMCs isolated from a normotensive rat strain was sufficient to abrogate the activity of the mitotic spindle cell-cycle checkpoint, promoting polyploidization and hypertrophy. Furthermore, the hypertrophic agent angiotensin II induced VSMC polyploidization in an Akt1-dependent manner. These results demonstrate that Akt1 regulates ploidy levels in VSMCs and contributes to vascular smooth muscle polyploidization and hypertrophy during hypertension.

Angiotensin II↗

PubMed1999

Venous return in the fetal-placental cardiovascular system.

For a quantitative understanding of the venous Doppler sonograms, a model of the fetal cardiovascular system is proposed which stresses the significance of flow. The model comprises three major components: the heart which provides constant power and dynamic capacitance, the peripheral fetal and placental vascular beds with flow limiting conductances (1/resistance), and the resistance of the hepato-ductal system. As long as cardiac power is maintained, the conductances control the flow rate and, depending upon hepato-ductal and ventricular filling resistance, the umbilical venous as well as the central venous pressure. According to the model, the mean flow velocity of venous return is total organ flow rate divided by cross sectional areas in the cardiac input system, i.e. the central veins, both atria and both AV valves respectively. The velocity pattern of venous return is related to cardiac performance and hepato-ductal resistance as follows: The E wave in early diastole describes the filling (driven by the central-venous pressure) of the relaxed ventricle. The time constant equals the ratio of elasticity over resistance in the ventricular wall. The A wave mirrors the contractility of atrial myocardium which is related to central venous pressure. The ratio of the forward A wave in the tricuspid valve to the backward A wave in the caval veins depends on ventricular capacitance. The S wave is related to systolic valvular shift. The velocity pulsations in the ductus venosus are transmitted backwards from the heart. The continuous velocity component in the ductus venosus and the non-pulsatile velocity in the umbilical vein are due to hepato-ductal and placental vascular resistance.

Animals↗

PubMed2005

Limb vasodilatory capacity and venous capacitance of trained runners and untrained males.

Aerobically trained athletes possess enhanced vasodilatory capacity and venous capacitance in their exercising muscles. However, whether they also possess these characteristics in their non-specific exercising muscles is undetermined. This study examined vasodilatory capacity and venous capacitance of specific (legs) and non-specific exercising muscles (arms) of ten trained runners and ten active but untrained males aged 18-35 years. Venous occlusion plethysmography determined baseline and peak blood flow after 5 min of reactive hyperaemia. Forearm and leg venous capacitance were determined as the difference between baseline and 2 min of venous occlusion at 50 mmHg. During reactive hyperaemia, trained runners had higher leg (48.4+/-5.3 ml.100 ml tissue(-1).min(-1)) and arm (40.8+/-2.1 ml.100 ml tissue(-1).min(-1)) vasodilatory capacity compared to the untrained (leg: 37.3+/-2.5 ml.100 ml tissue(-1).min(-1); arm: 34.2+/-2.2 ml.100 ml tissue(-1).min(-1); P<0.05), and higher calf vascular conductance (0.51+/-0.06 ml.100 ml tissue(-1).min(-1).mmHg(-1) versus 0.35+/-0.03 ml.100 ml tissue(-1).min(-1).mmHg(-1); P<0.05). The trained also had higher venous capacitance in both arms (3.5+/-0.2 ml 100.ml(-1)) and legs (4.8+/-0.1 ml.100 ml(-1)) compared to the untrained (3.0+/-0.2 ml 100.ml(-1); 4.2+/-0.2 ml.100 ml(-1); P<0.05). These findings show that vasculature adaptations to running occur in both specific and non-specific exercising muscles.

Blood Flow Velocity↗

PubMed2000

Cks1 mediates vascular smooth muscle cell polyploidization.

Vascular smooth muscle cells (VSMC) at capacitance arteries of hypertensive individuals and animals undergo dramatic polyploidization that contributes toward their hypertrophic phenotype. We report here the identification of a defective mitotic spindle cell cycle checkpoint in VSMC isolated from capacitance arteries of pre-hypertensive rats. These cells demonstrated a high predisposition to polyploidization in culture and failed to maintain cyclin B protein levels in response to colcemid, a mitotic inhibitor. Furthermore, this altered mitotic spindle checkpoint status was associated with the overexpression of Cks1, a Cdc2 adapter protein that promotes cyclin B degradation. Cks1 up-regulation, cyclin B down-regulation, and VSMC polyploidization were evidenced at the smooth muscle of capacitance arteries of genetically hypertensive and Goldblatt-operated rats. In addition, angiotensin II infusion dramatically increased Cks1 protein levels at capacitance arteries of normotensive rats, and angiotensin II treatment of isolated VSMC abrogated their ability to down-regulate Cks1 and maintain cyclin B protein expression in response to colcemid. Finally, transduction of VSMC from normotensive animals with a retrovirus that drives the expression of Cks1 was sufficient to alter their mitotic spindle cell cycle checkpoint status and promote unscheduled cyclin B metabolism, cell cycle re-entry, and polyploidization. These data demonstrate that Cks1 regulates cyclin B metabolism and ploidy in VSMC and may contribute to the understanding of the phenomena of VSMC polyploidization during hypertension.

Animals↗

PubMed1978

Beneficial effects of hydralazine in severe mitral regurgitation.

The severity of mitral regurgitation is, in part, determined by aortic impedance to left ventricular outflow. Sodium nitroprusside acutely decreases regurgitant flow, but the importance of its dual vasodilating effects, the lowering of peripheral vascular resistance and increasing of venous capacitance, is unclear. We studied the hemodynamic response to intravenous hydralazine, which selectively acts on the arteriolar resistance bed, in 10 patients with severe mitral regurgitation. Hydralazine produced a 50% increase in forward stroke volume (22 +/- 2 to 33 +/- 3 ml/m2, P less than 0.001) and a 33% reduction in regurgitant stroke volume (40 +/- 6 to 27 +/- 6 ml/m2, P less than 0.001), with a resultant fall in pulmonary capillary wedge v wave and mean pressures. Unlike nitroprusside, it did not alter left ventricular end-diastolic volume or pressure. Oral hydralazine maintained this hemodynamic improvement for at least 48 hours and, in three patients, provided more sustained clinical improvement. We conclude that hydralazine, by virtue of its selective lowering of aortic impedance, reduces the amount of mitral regurgitation and thus may be a useful mode of interim or chronic therapy in selected patients.

Adult↗

PubMed1990

In vitro vascular reactivity to endothelin: a comparison between young and old normotensive and hypertensive rats.

In this study we have investigated whether the vascular smooth muscle of a large capacitance artery of spontaneously hypertensive rats (SHR) is hyperresponsive to endothelin-1 and whether the arterial responsiveness to endothelin-1 is affected by aging. Isometric contractions of spirally cut aortic strips from SHR of 11, 22, 33 and 44 weeks of age and from age-matched WKY were measured in parallel. The vessels from SHR did not exhibit a greater responsiveness to endothelin-1 than those from WKY. No difference of responsiveness to the peptide was found among the arteries isolated from WKY of different ages. In contrast, a progressive decrease of responsiveness to endothelin-1 with aging was observed in SHR. This finding seems to be specific for endothelin-1, since the responsiveness to norepinephrine was unchanged. The significant decrease of aortic responsiveness in SHR with aging might be due to chronic hypertension and indicate desensitization to endothelin-1. The latter might be related to chronic in vivo hyperproduction of endothelin, either genetically determined or related to the hypertension-induced endothelial damage.

Aging↗

PubMed2000

Properties of a native cation channel activated by Ca2+ store depletion in vascular smooth muscle cells.

Depletion of intracellular Ca(2+) stores activates capacitative Ca(2+) influx in smooth muscle cells, but the native store-operated channels that mediate such influx remain unidentified. Recently we demonstrated that calcium influx factor produced by yeast and human platelets with depleted Ca(2+) stores activates small conductance cation channels in excised membrane patches from vascular smooth muscle cells (SMC). Here we characterize these channels in intact cells and present evidence that they belong to the class of store-operated channels, which are activated upon passive depletion of Ca(2+) stores. Application of thapsigargin (TG), an inhibitor of sarco-endoplasmic reticulum Ca(2+) ATPase, to individual SMC activated single 3-pS cation channels in cell-attached membrane patches. Channels remained active when inside-out membrane patches were excised from the cells. Excision of membrane patches from resting SMC did not by itself activate the channels. Loading SMC with BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid), which slowly depletes Ca(2+) stores without a rise in intracellular Ca(2+), activated the same 3-pS channels in cell-attached membrane patches as well as whole cell nonselective cation currents in SMC. TG- and BAPTA-activated 3-pS channels were cation-selective but poorly discriminated among Ca(2+), Sr(2+), Ba(2+), Na(+), K(+), and Cs(+). Open channel probability did not change at negative membrane potentials but increased significantly at high positive potentials. Activation of 3-pS channels did not depend on intracellular Ca(2+) concentration. Neither TG nor a variety of second messengers (including Ca(2+), InsP3, InsP4, GTPgammaS, cyclic AMP, cyclic GMP, ATP, and ADP) activated 3-pS channels in inside-out membrane patches. Thus, 3-pS nonselective cation channels are present and activated by TG or BAPTA-induced depletion of intracellular Ca(2+) stores in intact SMC. These native store-operated cation channels can account for capacitative Ca(2+) influx in SMC and can play an important role in regulation of vascular tone.

Animals↗

PubMedDate not supplied

Recent advances in the treatment of congestive heart failure.

Treatment of heart failure should include correction of the underlying cause. These causes include large left to right shunts, obstructive lesions, arrhythmias, primary myocardial disease etc. The main pharmacological therapy includes inotropic agents, vasodilators and diuretics. Inotropic agents increase myocardial contractility and include digoxin, intravenous dopamine, dobutamine and isoproterenol. Vasodilators improve cardiac pump performance by decreasing the vascular resistance and/or increasing the venous capacitance. Commonly used vasodilator agents include angiotensin converting enzyme inhibitors (captopril, enalapril etc.), hydralazine, prazosin hydrochloride etc. Diuretics inhibit salt and water reabsorption promoting their excretion. Furosemide, thiazide diuretics, aldactone, are commonly used diuretics. Electrolyte and acid-base imbalance can occur on chronic diuretic therapy. Cardiac transplantation is considered for patients where all medical management has failed.

Cardiovascular Agents↗

PubMed1995

Hypoxic contraction of isolated rabbit mesenteric veins. Contribution of endothelium and attenuation by volatile anesthetics.

BACKGROUND: Acute systemic hypoxia induces mesenteric venoconstriction in intact rabbits in part because of an increase in chemoreflex-mediated sympathetic efferent nerve activity. Inhaled anesthetics attenuate this reflex response. The direct effects of hypoxia on mesenteric veins are unknown. The purpose of the current study was to examine the effects of hypoxia on isolated rabbit mesenteric capacitance veins and to determine the effects of halothane, isoflurane, and enflurane on the responses to hypoxia. METHODS: Isometric tension was measured before, during, and after 10 min of hypoxia in the rings of either quiescent or norepinephrine contracted veins, with or without endothelium. Effects of various pharmacologic agents and volatile anesthetics on the responses to hypoxia were examined. RESULTS: Hypoxia augmented contractions to norepinephrine and phenylephrine only in endothelium-intact veins. The hypoxic response was inhibited by phentolamine (alpha-adrenoceptor antagonist) and abolished in the absence of extracellular Ca2+. There were no effects of propranolol (beta-adrenoceptor antagonist), ryanodine (a sarcoplasmic reticulum Ca2+ depleter), indomethacin (cyclooxygenase inhibitor), or nordihydroguaiaretic acid (lipoxygenase inhibitor). L-NAME (an inhibitor of nitric oxide synthase) enhanced basal sensitivity of veins to norepinephrine but had no effect on the response to hypoxia. Nicardipine (a blocker of voltage-gated calcium channels) depressed the hypoxic contraction by 86 +/- 5%, phosphoramidon (an inhibitor of endothelin-converting enzyme) by 82 +/- 8%, and BQ-123 (a specific endothelin-1 receptor antagonist) by 47 +/- 10%. Volatile anesthetics (1.0 MAC) inhibited responses to hypoxia in the absence as well as presence of L-NAME. CONCLUSIONS: These results suggest that in mesenteric capacitance veins of rabbits an intrinsic vascular mechanism contributes to endothelium-dependent hypoxic augmentation of contraction to alpha-adrenergic agonists that involve activation of endothelin-1, an endothelium-derived constricting factor. Inhibition of hypoxic contraction by volatile anesthetics is not mediated by endothelium relaxing factor.

Acetylcholine↗

PubMed1982

Treatment of hypertension with ketanserin, a new selective 5-HT2 receptor antagonist.

The new selective 5-HT2 receptor blocking agent ketanserin was given in a dose of 10 mg intravenously to 12 patients with essential hypertension. It caused a distinct fall in supine systemic arterial, right atrial, pulmonary artery, and pulmonary capillary "wedge" pressures. Cardiac output, renal blood flow, and glomerular filtration rate showed no persistent changes. Thus 5-HT2 receptor blockade caused dilatation of both resistance and capacitance vessels and of the renal vascular bed. Heart rate and plasma concentrations of renin and noradrenaline rose after ketanserin. These data suggest that 5-HT may have a role in maintaining high blood pressure.

Adult↗

PubMed1995

Noninvasive pulse wave analysis for the early detection of vascular disease.

A noninvasive technique has been developed and validated for calculating capacitive and oscillatory systemic arterial compliance with the use of pulse wave analysis and a modified Windkessel model. Application of the technique to subjects with hypertension, postmenopausal women with symptomatic coronary artery disease, and appropriate control subjects has confirmed a reduction of oscillatory compliance in the disease states and an increase in capacitive and oscillatory compliances in response to vasodilator drugs. This method should be useful in screening subjects for early evidence of vascular disease and in monitoring the response to therapy.

Blood Pressure↗

PubMed1977

Effect of indomethacin on the responses of resistance and capacitance vessels to noradrenaline in working skeletal muscles in the dog (1) (2).

The effect of indomethacin upon the responses of resistance and capacitance vessels to noradrenaline (NA) in working skeletal muscles of the dog's hind leg was investigated. Responses of the resistance and the capacitance vessels of NA (0,1-0,5 microgram/kg injected into the femoral artery--i.f.a) were reflected as the changes in peripheral vascular resistance and in tissue volume respectively, and determined during and following exercise before and after indomethacin (1-1,5 mg/kg i.f.a.). Muscular exercise was induced by sciatic nerve stimulation of 6 min duration. The results show that indomethacin potentiates constrictor effects of NA in both pre-and postcapillary sections of the muscular vascular bed during and following exercise. An augmentation of NA effects is significantly greater in the capacitance than in the resistance vessels. Potentiated constrictor responses to NA are also maintained longer in the capacitance than in the resistance segment during the postexercise period. The results suggest that endogenous prostaglandings are involved in a local vascular response to exercise within both pre-and postcapillary segments of the muscular vascular bed. Their role in the capacitance vessels of the limb may be related to a local inhibiton of sympathetic activity, reduction of postcapillary resistance and facilitation of the venous outflow.

Animals↗