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PubMed2003

Myogenic responses and compliance of mesenteric and splenic vasculature in the rat.

In the rat, the spleen is a major site of fluid efflux out of the blood. By contrast, the mesenteric vasculature serves as a blood reservoir. We proposed that the compliance and myogenic responses of these vascular beds would reflect their different functional demands. Mesenteric and splenic arterioles ( approximately 150-200 microm) and venules (<250 microm) from rats anesthetized with pentobarbital sodium were mounted in a pressurized myograph. Mesenteric arterial diameter decreased from 146 +/- 6 to 133 +/- 6 microm on raising intraluminal pressures from 80 to 120 mmHg. This response was enhanced in the presence of N(omega)-nitro-l-arginine methyl ester (l-NAME; 139 +/- 6 to 112 +/- 7 microm). There was no such myogenic response in the splenic arterioles, except in the presence of l-NAME (194 +/- 4 to 164 +/- 4.2 microm). We propose that, whereas mesenteric arterioles exhibit myogenic responses, this is normally masked by NO-mediated dilation in the splenic vessels. The mesenteric venules were highly distensible (active, 184 +/- 15 to 320 +/- 30.9 microm; passive in Ca(2+)-free media, 209 +/- 31 to 344 +/- 27 microm; 4-8 mmHg) compared with the splenic vessels (active, 169 +/- 11 to 184 +/- 16 microm; passive, 187 +/- 12 to 207 +/- 17 microm). We conclude that, in response to an increase in perfusion pressure, mesenteric arterial diameter would decrease to limit the changes in flow and microvascular pressure. In addition, mesenteric venous capacitance would increase. By contrast, splenic arterial diameter would increase, while there would be little change in venous diameter. This would enhance the increase in intrasplenic microvascular pressure and increase fluid extravasation.

Animals↗
PubMed1996

Subconstrictor doses of neuropeptide Y potentiate alpha 1-adrenergic venoconstriction in vivo.

The 36-amino acid human neuropeptide Y is a vasoactive compound released after stimulation of the sympathetic nervous system. In addition to its direct and long-lasting vasopressor effects, it may potentiate the constrictor action of catecholamines and other vasoconstrictors at doses that do not per se exert vascular effects. Using the hand vein compliance technique, we have previously shown that neuropeptide Y also constricts superficial hand veins and that its effects may last for several hours. In this study, we investigated the local effect of neuropeptide Y on alpha 1-adrenergic venoconstriction in nine healthy volunteers at dose rates that did not affect venous compliance. On separate days, cumulative dose-response curves to phenylephrine alone and with coadministration of 1 or 30 pmol neuropeptide Y per minute were constructed, and the responses were fitted to a four-parameter logistic equation. Neuropeptide Y dose dependently shifted the phenylephrine curves toward lower dose rates without affecting maximal effects. ED50 values for phenylephrine alone and with 1 or 30 pmol/min neuropeptide Y were 4.0, 4.9 (P = NS versus control), and 1.2 (P < .005) nmol/min, respectively. Comparison with neuropeptide Y dose-response curves revealed that the interaction was synergistic. These are the first data in humans to show that small dose rates of neuropeptide Y may potentiate alpha-adrenergic effects in vivo. Because this interaction occurs at estimated local concentrations nearly achieved in humans, these studies suggest that neuropeptide Y might modulate the filling of this capacitance system in vivo.

Adrenergic alpha-Agonists↗
PubMed1996

Age and reproductive status affect basal venous tone in the rat.

OBJECTIVE: Changes in venous tone alter vessel diameter and capacitance of veins. These alterations may be induced by the steroid hormonal milieu. Therefore, our question was whether venous tone differs between estrous cycle, pregnancy and old rats. STUDY DESIGN: Mesenteric veins from young, pregnant and old Sprague-Dawley rats were dissected and cannulated in a venograph system with a continous readout of pressure-dependent lumen diameter. RESULTS: During estrous cycle venous tone was increased in metestrous (P < 0.05), whereas it was decreased in all old rats (P < 0.05). There was higher venous tone in pregnant animals compared to controls (P < 0.05). CONCLUSIONS: Venous tone exhibits marked differences during rat estrous cycle. It is increased during pregnancy and decreased in old rats.

Aging↗
PubMed2002

Propofol prevents endothelial dysfunction induced by glucose overload.

Surgical operations often induce acute hyperglycemia, which is known to affect endothelial functions. In this study, we examined the effects of propofol, a commonly used general anaesthetic, on bovine aortic endothelial cell (BAEC) dysfunction induced by glucose overload. 2 D-glucose overload (23 mM) induced an accumulation of superoxide anion (O2-), assessed by MCLA chemiluminescence, to a similar extent as that generated by 233 microU ml(-1) xanthine oxidase (XO) and 100 micro M xanthine. Propofol inhibited this accumulation with an IC50 of 0.21 micro M, whereas much higher concentrations of propofol were required to scavenge O2- generated by 250 microU ml(-1) XO and 100 microM xanthine (IC50: 13.5 micro M). 3 D-glucose overload attenuated ATP-induced NO production which was detected using diaminofluorescence-2 (DAF-2). The inhibition was reversed by propofol with an EC50 of 0.60 microM. In contrast, inhibitions caused by xanthine/XO were not altered by propofol (1 microM). 4 D-glucose overload suppressed ATP-induced Ca2+ oscillations and capacitative Ca2+ entry (CCE), which were both restored by superoxide dismutase, indicating that O2- was responsible. Propofol restored these attenuated Ca2+ oscillations and CCE with EC50 of 0.31 and 1.0 microM, respectively. 5 D-glucose overload (23 mM) increased the intracellular glucose concentration 4 fold, compared with cells exposed to 5.75 mM glucose, and 1 micro M propofol reduced this increase to 2.8 fold. 6 We conclude from these results that anaesthetic concentrations of propofol prevent the impairment of Ca2+-dependent NO production in BAEC induced by glucose overload. This effect is mainly due to the reduction of O2- accumulation, and involves, at least in part, the inhibition of cellular glucose uptake.

Animals↗
PubMed1990

Arginine vasopressin increases apparent whole body capacity in anesthetized cats.

The effects of arginine vasopressin (AVP) on capacitance function were assessed in anesthetized cats by draining blood from the superior and inferior venae cavae into an external reservoir and then returning blood to the right atrium at a constant rate. Under these conditions, changes in reservoir volume were assumed to reflect reciprocal changes in whole body capacity. Intravenous infusions of AVP (1, 10, and 100 ng.kg-1.min-1) that elevated plasma AVP concentrations by approximately 30, 400, and 4,000 fmol/ml were associated with concentration-dependent increases in whole body capacity that ranged between 1.6 and 8 ml/kg. In contrast to AVP, intravenous infusions of angiotensin II (5, 10, and 50 ng.kg-1.min-1) had relatively little influence on capacity, whereas norepinephrine administration (300, 1,000, and 3,000 ng.kg-1.min-1) was associated with dose-dependent decreases in capacity of 4.5-10.3 ml/kg. Virtually the entire increase in whole body capacity to AVP can be accounted for by summation of the predicted contributions of an active reflex venodilatatory component and those of a passive component (arterial and cardiopulmonary compartments). Because systemic compliance (delta reservoir volume/delta venous pressure) was not changed by AVP administration, the contribution of a reflex venodilatatory component must be the result of increases in unstressed vascular volume (contained volume at 0 transmural pressure) as opposed to changes in compliance. These results may explain why AVP decreases cardiac output to a greater extent than either angiotensin II or sympathomimetics and, thus, why AVP is a weaker pressor agent in animals with intact autonomic function.

Anesthesia↗
PubMed2003

Hypoxia increases AP-1 binding activity by enhancing capacitative Ca2+ entry in human pulmonary artery endothelial cells.

Activating protein (AP)-1 transcription factors modulate expression of genes involved in cell proliferation and migration. Chronic hypoxia increases pulmonary artery smooth muscle cell proliferation by upregulating AP-1-responsive genes encoding for endothelium-derived vasoactive and mitogenic factors implicated in pulmonary hypertension development. The expression of AP-1 transcription factors is sensitive to changes in cytosolic free [Ca2+] ([Ca2+]cyt). Capacitative Ca2+ entry (CCE) via store-operated Ca2+ channels (SOC) is an important mechanism for raising [Ca2+]cyt in pulmonary artery endothelial cells (PAEC). Using combined molecular biological, fluorescence microscopy, and biophysical approaches, we examined the effect of chronic hypoxia (3% O2, 72 h) on AP-1 DNA binding activity, CCE, and transient receptor potential (TRP) gene expression in human (h) PAEC. EMSA showed that AP-1 binding to hPAEC nuclear protein extracts was significantly enhanced by hypoxia, the increase being dependent on store-operated Ca2+ influx and sensitive to La3+, an SOC inhibitor. Hypoxia also increased basal [Ca2+]cyt, the amount of CCE produced by store depletion with cyclopiazonic acid, and the amplitude of SOC-mediated currents (ISOC). The increases of CCE amplitude and ISOC current density by hypoxia were paralleled by enhanced TRPC4 mRNA and protein expression. Hypoxia-enhanced CCE and TRPC4 expression were also attenuated by La3+. These data suggest that hypoxia increases AP-1 binding activity by enhancing Ca2+ influx via La3+-sensitive TRP-encoded SOC channels in hPAEC. The Ca2+-mediated increase in AP-1 binding may play an important role in upregulating AP-1-responsive gene expression, in stimulating pulmonary vascular cell proliferation and, ultimately, in pulmonary vascular remodeling in patients with hypoxia-mediated pulmonary hypertension.

Calcium↗
PubMed1996

The tracheobronchial vasculature: a possible role in asthma.

The tracheobronchial microcirculation consists of a subepithelial capillary network and in some species deeper capacitance vessels and an adventitial network. Postcapillary venules are the main site of plasma extravasation in inflammatory conditions. There are surprising species differences. The subepithelial capillary network is dense in species such as sheep and dog but relatively scanty in rabbit and humans. Sheep have conspicuous capacitance vessels or blood sinuses, especially in the trachea and at points of bronchial branching with walls that lack smooth muscle. The rabbit also has a well-developed capacitance system but the blood sinuses have thick muscular walls. Although the capacitance system in humans has not been studied much it is probably present with muscular walls. It is absent in rats but present in guinea pigs. Thus, in some species the tracheobronchial vasculature may give the mucosa an erectile capacity, as in the nose of each species. Arteriovenous anastomoses (AVA) cannot be demonstrated physiologically in sheep but they seem to be present as thoroughfare vessels in rats and guinea pigs. Whether they exist in humans is not known. The absence of AVA might indicate a weak or absent thermoregulatory and air conditioning role for the lower airway vasculature. Extensive studies of neurogenic inflammation in rodents show that sensory neuropeptides can open gaps between the endothelial cells of postcapillary venules and the same change can be caused by a large number of inflammatory mediators. These opened gaps cause extravasation of plasma into the interstitium. Small increases in interstitial pressure lead to spaces opening between the epithelial cells and exudation of plasma into the airway lumen. The role of the airway microvasculature in asthma is controversial. Cold and hyperosmolar solutions cause vasodilatation as do the mediators released in the mucosal inflammation of asthma. However, quantitation of the thickening of the airway wall due to vascular engorgement, mucosal edema, or increased luminal liquid does not prove that these changes are a cause of airway obstruction. The contraction of airway smooth muscle superimposed on the mucosal inflammatory pathology might lead to a synergistic mechanism to increase airway resistance.

Airway Resistance↗
PubMed1992

Plasma endothelin-1 during central hypovolaemia in man.

Endothelin-1 (ET-1) is a potent vasoconstricting peptide with effect on resistance as well as capacitance vessels. We followed ET-1 in arterial plasma together with heart rate (HR), central venous pressure (CVP), mean arterial pressure (MAP), and thoracic electrical impedance (TI) in seven men during central hypovolaemia induced by 50 degrees head-up tilt. During tilting plasma ET-1 increased from 1.1 +/- 0.2 to 1.4 +/- 0.3 pmol l-1 (mean +/- SE) concomitant with an increase in total peripheral resistance (TPR) (from 15 +/- 2 to 25 +/- 3 mmHg min l-1) (P < 0.01), and HR (from 67 +/- 2 to 94 +/- 5 beats min-1) (P < 0.01) while MAP remained unchanged. CVP decreased (from 1.8 +/- 0.9 to -1.6 +/- 1.0 mmHg) (P < 0.01) during tilting and remained unchanged during sustained tilt despite further reduction of central blood volume as recorded by TI. Presyncopal symptoms occurred after 28 +/- 6 min associated with decreases in HR (to 70 +/- 6 beats min-1), MAP (from 90 +/- 3 to 52 +/- 4 mmHg) and TPR (to 11 +/- 2 mmHg min l-1) (P < 0.01). At this time plasma ET-1 reached its highest level of 1.6 +/- 0.3 pmol l-1 (P < 0.01). Data show that head-up tilt is associated with increased plasma concentrations of ET-1 which may play a role in maintaining vascular tone in situations with a reduced central blood volume.

Adult↗
PubMedDate not supplied

Effects of arginine-vasopressin on regional blood volume distribution in supine humans.

In healthy humans, the increase in arterial blood pressure seen in patients with autonomic dysfunction in response to exogenous vasopressin (AVP) is abolished. We tested the hypothesis that redistribution of blood from the intra- to the extrathoracic vascular compartment might contribute to this buffer response. Regional distribution of 99mTc labeled autologous red cells was assessed in healthy supine volunteers (n = 7) during arginine-vasopressin administration (1 ng.kg-1 bolus i.v. followed by a 14-min infusion of 3 ng.kg-1 x min-1), along with arterial and central venous pressures, and heart rate. Exogenous vasopressin increased plasma vasopressin concentration from 4.0 +/- 1.4 SEM to 91 pg.ml-1 +/- 12. Thoracic counts increased slightly but significantly by 2.2% +/- 0.9, while global abdominal counts remained unchanged. Most surprisingly, counts in the liver markedly increased (+8.1% +/- 1.8, p = 0.02), but significantly decreased in the spleen (-3.1% +/- 1.4). Intestinal (-2.5% +/- 2.4) and limb counts did not change significantly. Consistent with the increase in thoracic counts central venous pressure increased from 3.6 mmHg +/- 1 to 4.7 +/- 1 (p = 0.02), while arterial pressure and heart rate did not change. All changes reversed towards baseline when vasopressin administration ceased. Thus, in humans with an intact autonomic system, vasopressin, at concentrations observed during hypotension, increases liver and, albeit to a small extent, also thoracic blood volume, but decreases splenic blood content. These results: 1) are incompatible with the hypothesis that AVP induces a shift of blood from intra- to extrathoracic capacitance vessels, and 2) show that AVP increases rather than decreases central blood volume.

Adult↗
PubMed1988

Vasodilatation by calcitonin gene-related peptide and by substance P: a comparison of their effects on resistance and capacitance vessels of human forearms.

A comparison has been made of the effects of the potent vasodilating peptide calcitonin gene-related peptide (CGRP) and substance P (SP) on resistance and capacitance vessels of normal subjects. Brachial artery infusion of 1.25 to 10 pmol/min CGRP and of 0.25 to 1.5 pmol/min SP produced maximal increases in forearm blood flow (177 +/- 75% and 198 +/- 50%, respectively), as measured by venous occlusion plethysmography. The vasodilation due to CGRP was prolonged, with a half-life of biological effect of approximately 18 min, while that due to SP was of short duration, with a half-life of biological effect of approximately 15 sec. There was rapid development of tachyphylaxis to the effects of arterial infusion of SP, but not of CGRP, during a prolonged infusion at one dose. CGRP did not alter the diameter of a superficial hand vein, either at rest or when the vein was constricted by a simultaneous infusion of norepinephrine or by the single deep breath reflex. In contrast, SP caused dilatation of veins preconstricted with norepinephrine, although the effect was only transient and dose-response curves could not be constructed. The venoconstrictor response to a single deep breath was abolished by SP. Simultaneous arterial infusion of both peptides produced at least additive, and possibly synergistic, effects on forearm blood flow. We propose that both CGRP and SP have a role in the regulation of vascular smooth muscle tone.

Adult↗
PubMed1999

Characterisation of explanted endothelial cells from mouse aorta: electrophysiology and Ca2+ signalling.

We describe here the isolation and primary culture of endothelial cells from mouse aorta ("primary explant technique"). These cells provide an excellent model for functional studies in transgenic mice. The primary explant method delivers cells that grow out from small pieces of mouse aorta placed on Matrigel enriched with endothelial growth factors. Cells can be studied on the Matrigel after removing the pieces of aorta or after passages by using dispase and reseeding the cells on gelatine-coated cover-slips. Cells on Matrigel or from the first and second passages were characterised using the combined patch-clamp and fura-2 fluorescence methods. Cells had a mean membrane resting potential of -19+/-3 mV (n=21), a membrane capacitance of 49+/-5 pF (n=37) and a resting cytosolic free [Ca2+] ([Ca2+]i) of 103+/-8 nM (n=30). Adenosine 5'-triphosphate (ATP), acetylcholine and bradykinin, but not histamine, induced fast release of intracellular Ca2+ followed by a sustained rise in [Ca2+]i. Oscillations in [Ca2+]i were observed at lower agonist concentrations. In nearly all cells (93%, n=30), these agonists activated charybdotoxin-sensitive, Ca2+-activated K+ channels and induced hyperpolarisation. In 84% of the cells (n=32), an increase in [Ca2+]i also activated strongly outwards-rectifying Cl- channels. These activated slowly at positive potentials and inactivated rapidly at negative potentials. Increasing [Ca2+]i to 1 microM activated a non-selective cation channel in 86% of the cells (n=28). Each tested cell responded to a challenge with hypotonic solution by activating a Cl- current that was modestly outwards rectifying and inactivated at positive potentials. This current is similar to the well-described swelling-activated current through volume-regulated anion channels (VRAC) in endothelial cells. However, its activation is slower, its inactivation faster and the current density lower than in cultured endothelial cells. It is concluded that the primary explant technique provides a reliable cell model for studying mouse vascular endothelial cell function.

Acetylcholine↗
PubMed1980

Erythrocyte uptake by the dog's spleen during splenic venous pressure elevation.

The spleens of chloralose-urethane anaesthetized dogs were isolated, placed in a plethysmograph and perfused at constant arterial pressure from a cannulated femoral artery. Splenic venous pressure (PV) was elevated by between 2.5 and 20 cm H2O: it caused pressure-dependent increases in spleen volume of up to 98 +/- 12 ml/100 g spleen weight. The increase in spleen volume could be separated into an initial phase associated with passive distension of capacitance vessels (Phase-1) followed by a more continuous increase in spleen volume (Phase-2). We used techniques designed to distinguish these components of the volume response to PV elevation, and found Phase-2 rates of increase in spleen volume of 5--10 ml min-1 mm Hg-1 100 g-1 expressed in terms of PV elevation and terminal, drained and trimmed spleen weight. Splenic venous haematocrit determination showed selective sequestration of RBCs during the Phase-2 volume response to PV elevation which was related to the extent of the PV elevation. Both the Phase-2 volume response and the haematocrit changes were reduced by splenic nerve stimulation or i.a. infusions of adrenaline but were unaffected by i.a. infusions of bradykinin.

Animals↗
PubMed2006

Correlation between brachial-ankle pulse wave velocity and arterial compliance and cardiovascular risk factors in elderly patients with arteriosclerosis.

The objective of this study was to investigate an association between major cardiovascular risk factors and each of brachial-ankle pulse wave velocity (baPWV), ankle-brachial index (ABI), capacitive arterial compliance (C1), and oscillatory arterial compliance (C2) in elderly patients with arteriosclerosis. We analyzed 160 elderly patients with arteriosclerosis. Vessel wall properties were assessed by baPWV and ABI using a VP-1000 Automatic Arteriosclerosis Measurement System, and C1 and C2 were measured using a DO-2020 Cardiovascular Profiling Instrument. In multiple regression analysis, baPWV was significantly correlated with systolic blood pressure (SBP), mean artery pressure, pulse pressure, diastolic blood pressure (DBP), age, and heart rate (r = 0.670, 0.627, 0.580, 0.523, 0.490, 0.200; p < 0.05), ABI was significantly correlated with pulse pressure, SBP and age (r = -0.250, -0.206, -0.168; p < 0.05), C1 was significantly correlated with pulse pressure, SBP, mean artery pressure, age, DBP and heart rate (r = -0.481, -0.469, -0.363, -0.356, -0.239, -0.188; p < 0.05), and C2 was significantly correlated with age, SBP, pulse pressure, DBP, fasting blood glucose, mean artery pressure and heart rate (r = -0.411, -0.395, -0.383, -0.277, -0.213, -0.183, -0.173; p < 0.05). There were no close correlations between baPWV, ABI, or C1 and fasting blood glucose, total cholesterol, triglycerides, or body mass index. Moreover, there were significant correlations between baPWV and C1 (r = -0.444, p < 0.001), and between baPWV and C2 (r = -0.257, p < 0.01). In conclusion, these findings underscore the efficacy of baPWV and ABI in identifying the vascular damage of the aged.

Age Factors↗
PubMed1981

Radionuclide assessment of peripheral intravascular capacity: a technique to measure intravascular volume changes in the capacitance circulation in man.

Changes in the capacitance vasculature influence venous return and cardiac performance, so an understanding of the effects of pathophysiologic states on the human capacitance vasculature is necessary to understand integrated cardiovascular function in man. Techniques available to assess the capacitance vasculature in man, however, have limitations. We performed radionuclide imaging of the calf or forearm in 51 patients whose erythrocytes had been labeled in vivo with technetium-99m, basing our approach on the principle that counts from the radiolabeled intravascular space are proportional to blood volume. Two-minute or 15 second count acquisitions were obtained from the calf in 42 patients. Counts obtained at rest demonstrated little variation. With veno-occlusion at 15 and 30 mm Hg, counts increased 8 +/- 1% (+/- SEM) (p less than 0.001) and 28 +/- 2% (p less than 0.001), respectively. After 0.4 mg of sublingual nitroglycerin, counts increased 9 +/- 1% (p less than 0.001). With leg elevation, counts decreased 34 +/- 4% (p less than 0.001). Response patterns were similar with 2-minute and 15-second acquisitions. In nine patients who underwent forearm imaging (2-minute acquisitions), counts increased 14 +/- 2% (p less than 0.001) and 26 +/- 4% (p less than 0.001) at 15- and 30-mm Hg veno-occlusion and 15 +/- 3% (p less than 0.001) after nitroglycerin. Volume displacements, recorded simultaneously with a fluid-filled plethysmograph about the contralateral forearm, correlated linearly in all nine patients. Thus, gamma camera imaging of the radiolabeled peripheral intravascular space provides a quantitative and reliable assessment of peripheral vascular capacity in man. The technique could be used in conjunction with gated cardiac imaging in order to assess the interactions of peripheral vascular capacity and ventricular performance.

Animals↗
PubMed2005

Action potential stimulation reveals an increased role for P/Q-calcium channel-dependent exocytosis in mouse adrenal tissue slices.

Chromaffin cells of the adrenal medulla receive cholinergic input from the splanchnic nerve. Upon sympathetic activity, chromaffin cells fire action potentials that open voltage-gated calcium channels and evoke the exocytic release of catecholamines. Catecholamines then regulate homeostatic processes such as cardiac output and vascular tone. Thus control of the Ca(2+) influx in chromaffin cells represents a target for the regulation of multiple physiological functions. Previous reports utilized square pulse depolarizations to quantify the proportional exocytic response as a function of Ca(2+) channel subtype. In this study, we use perforated patch voltage clamp and action potential waveforms to depolarize cells in situ. We analyze Ca(2+) current components under conditions that match the dynamic native cell behavior. This approach revealed a greater role for P/Q-type calcium channels in evoked exocytosis than previously reported. Thus, the P/Q-type channels represent a more important control point for the regulation of catecholamine-dependent processes than previously believed.

Action Potentials↗
PubMed1994

Beat-to-beat determination of peripheral resistance and arterial compliance during +Gz centrifugation.

This study focused on the problem of describing changes in total peripheral resistance (TPR) and systemic arterial compliance (SAC) under time-varying +Gz acceleration stress. Nonsteady-state measures of peripheral resistance can only be derived when arterial compliance is taken into account. We have developed a successful analytical model to track simultaneous changes in peripheral resistance and systemic arterial compliance during non-stationary periods of increased gravitational load on a beat-to-beat basis. Using a 2-element windkessel model, aortic flow into an input node was defined as equal to the sum of a capacitative (Cao) and a resistive (Rarterial) flow leaving the node such that: Iao = Caod(Pao - Ppleural)/dt + (Pao - Pra)/Rarterial We made the assumption that Cao and Rarterial were constant over a cardiac cycle, and divided the pressure and flow signals for each beat of a record into two different intervals, integrating this equation over each, giving two equations in two unknowns. Cao and Rarterial were then obtained from the matrix solutions. To test the model, we used recordings from chronically instrumented baboons subjected to a 10 s rapid onset +Gz (head-to-foot) stress. Beat-to-beat calculations of peripheral resistance and systemic arterial compliance from our model were compared to values obtained from a previously reported 3-element wind-kessel model.

Animals↗
PubMed1995

An investigation into the direct and indirect venoconstrictor effects of endothelin-1 and big endothelin-1 in man.

1. Endothelin-1 is a potent endothelium-derived vasoconstrictor peptide that is generated through cleavage of its precursor big endothelin-1 by 'endothelin converting enzyme' (ECE) in resistance vessels, including those of the forearm vascular bed. In some animal tissues, but not in resistance vessels of healthy human subjects, endothelin-1 appears to potentiate the actions of the sympathetic nervous system. We examined whether ECE activity is present in human hand veins and whether endothelin-1 or big endothelin-1 potentiate sympathetically mediated venoconstriction. 2. Six healthy subjects received dorsal hand vein infusion of local, non-systemic doses of endothelin-1 (5 pmol min-1), big endothelin-1 (50 pmol min-1) and, as a control, sodium chloride (0.9%; w/v) for 90 min. Vein diameter was measured using the Aellig displacement technique. Sympathetically mediated venoconstriction was elicited using the single deep breath reflex. 3. Endothelin-1 caused a progressive decrease in hand vein diameter, by 49% at 90 min (95% confidence intervals [CI]: -68 to -30%; P = 0.0001). Vein diameter did not change significantly after 90 min infusion of big endothelin-1 (+3%; CI: -11 to +17%; P = 0.0007 vs endothelin-1; P = 0.40 vs baseline) or sodium chloride (+2%; CI: -12 to +16%; P = 0.0002 vs endothelin-1; P = 0.60 vs baseline). Venoconstriction to deep breath was not potentiated by endothelin-1. 4. These results suggest that, in contrast to the situation in forearm resistance vessels, there is little or no local ECE activity in human hand veins and that endothelin does not potentiate sympathetic responses in these cutaneous capacitance vessels.

Adult↗
PubMed1984

Effect of temperature and baroreceptor stimulation on reflex venomotor responses.

To investigate the interaction of thermal reflexes and baroreflexes in the control of the peripheral veins, we studied in supine humans the effects of lower body negative pressure (LBNP) and neck suction (NS) on forearm veins at ambient temperatures (Ta) of 18, 28, and 37 degrees C. Forearm venous volume (FVV)-venous pressure (FVP) relations (forearm venous capacitance) on six subjects showed an increase from 18 through 28 to 37 degrees C (P less than 0.001). Heart rate increased (P less than 0.001) and forearm venous capacitance decreased (P less than 0.001) in proportion to the level of LBNP applied from 20 to 50 Torr at all Ta. At 50 Torr LBNP, FVV at 30 cmH2O, FVP decreased from control values of 2.5, 3.8, and 4.4 to 1.6, 2.7, and 3.4 ml/100 ml at 18, 28, and 37 degrees C, respectively. We also studied venomotor responses using the occluded limb technique. Although LBNP caused venoconstriction, NS applied either alone or during LBNP produced no change in venomotor tone. Therefore we concluded that carotid baroreceptors play little role in reflex venomotor adjustments. Since changes in mean arterial and pulse pressures during LBNP did not account for the observed venomotor responses, we concluded that low-pressure baroreceptors initiate significant venoconstrictor reflexes over a wide range of Ta.

Adult↗