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PubMedDate not supplied

Clotrimazole inhibits smooth muscle cell proliferation and has a vasodilator effect on resistance arteries.

Clotrimazole (CLT) is a drug known to interfere with cellular calcium homeostasis, which in turn is reported to intervene in cell proliferation and in the reactivity of small blood vessels. Experiments were designed to test the influence of CLT on the proliferative and vasorelaxant effect of bradykinin (BK) and on calcium homeostasis in smooth muscle cells (SMC). To this purpose two model systems were employed: (i) cultured human smooth muscle cells (HSMC), and (ii) isolated resistance arteries maintained in an organ bath. The effect of various concentrations of CLT (2-15 microM) on BK-induced proliferation of HSMC was quantitated by spectrometry following [3H]-thymidine incorporation, and intracellular calcium [Ca+]i was determined by spectrofluorimetry using Fura 2-AM assay. In other experiments the roles of BK receptor (AB2) and of thapsigargin were assessed. The reactivity of the resistance arteries was measured by the myograph technique, and the effects of BK, CLT, and NO synthase blocker, L-NAME were evaluated. The results showed that 10 microM CLT: (i) inhibits the BK-induced proliferation of HSMC by 45-50%: (ii) prevents the rise of [Ca2+]i induced by BK (120.8 +/- 12.4 nM vs. 235.8 +/- 34.1 nM), an cffect similar to that of "classic" L-type calcium channels blockers: (iii) reduces the release of Ca2+ entry induced by thapsigargin suggesting a possible inhibition of the capacitative Ca2+ entry. Organ bath assays showed that CLT enhanced the BK-induced relaxation of the resistance arteries by an endothelium NO-independent pathway. Together, these data suggest that the mechanism of action of CLT on SMC implies mainly a modification of intracellular calcium homeostasis, with a minor contribution of BK B2 receptors. These new distinctive features of CLT effects suggest the potential use of this drug in the therapy of cardiovascular diseases associated with SMC increased proliferation and impeded relaxation in small arteries, such as atherosclerosis and restenosis.

Arteriosclerosis↗
PubMed2003

Anandamide initiates Ca(2+) signaling via CB2 receptor linked to phospholipase C in calf pulmonary endothelial cells.

The endocannabinoid anandamide has been reported to affect neuronal cells, immune cells and smooth muscle cells via either CB1 or CB2 receptors. In endothelial cells, the receptors involved in activating signal transduction are still unclear, despite the fact that anandamide is produced in this cell type. The present study was designed to explore in detail the effect of this endocannabinoid on Ca2+ signaling in single cells of a calf pulmonary endothelial cell line. Anandamide initiated a transient Ca2+ elevation that was prevented by the CB2 receptor antagonist SR144528, but not by the CB1 antagonist SR141716A. These data were confirmed by molecular identification of the bovine CB2 receptor in these endothelial cells by partial sequencing. The phospholipase C inhibitor 1-[6-[[(17beta)-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5dione and the inositol 1,4,5-trisphosphate receptor antagonist 2-aminoethoxydiphenylborate prevented Ca2+ signaling in response to anandamide. Using an improved cameleon probe targeted to the endoplasmic reticulum (ER), fura-2 and ratiometric-pericam, which is targeted to the mitochondria, anandamide was found to induce Ca2+ depletion of the ER accompanied by the activation of capacitative Ca2+ entry (CCE) and a transient elevation of mitochondrial Ca2+. These data demonstrate that anandamide stimulates the endothelial cells used in this study via CB2 receptor-mediated activation of phospholipase C, formation of inositol 1,4,5-trisphosphate, Ca2+ release from the ER and subsequent activation of CCE. Moreover, the cytosolic Ca2+ elevation was accompanied by a transient Ca2+ increase in the mitochondria. Thus, in addition to its actions on smooth muscle cells, anandamide also acts as a powerful stimulus for endothelial cells.

Animals↗
PubMed1985

[Changes in the functions of the blood vessels of skeletal muscles during acute hypothermia].

In acure experiments on cats, changes of resistance, capacitance and filtration-absorption functions of the m. gastrocnemius' vessels in acute cooling (from 37 degrees C to 29-27 degrees C) involved first a raise of the perfusion pressure in the vessels and its drop in further cooling to 25 degrees C. The pre- to post-capillary ratio remained unchanged. Integral stretching ability of the venous bed was increasing along with the cooling. The capillary filtration coefficient was considerably increased. The capillary hydrostatic pressure increased in cooling to 27 degrees C and then decreased in further cooling to 25 degrees C.

Animals↗
PubMed2002

Canine mesenteric artery and vein convey no difference in the content of major contractile proteins.

BACKGROUND: Mesenteric arteries and veins are composed of tonic smooth muscles and serve distinct functions in the peripheral circulation. However, the basis for the functional disparity of the resistive and capacitative parts of the mesenteric circulation is poorly understood. We studied potential differences in the expression levels of six contractile proteins in secondary and tertiary branches of the inferior mesenteric artery and vein along with differences in the vessel wall morphology. RESULTS: Bright field and electron microscopy showed that both vessel walls had the same major structural elements. The arterial walls, however, had greater number, and more tightly assembled, smooth muscle cell layers compared to vein walls. The content of actin, myosin heavy chain, myosin light chain, and calponin was similar in the two blood vessels. The artery expressed higher amount of the actin-binding protein caldesmon than the vein (41.86 +/- 2.33 and 30.13 +/- 3.37 microg/mg respectively, n = 12). Although the total tropomyosin content was almost identical in both blood vessels, the alpha isoform dominated in the artery, while the beta isoform prevailed in the vein. CONCLUSIONS: Canine mesenteric artery and vein differ in vessel wall morphology but do not convey differences in the expression levels of actin, myosin light chain, myosin heavy chain and calponin. The two vascular networks express distinct amounts of caldesmon and tropomyosin, which might contribute to the fine tuning of the contractile machinery in a manner consistent with the physiological functions of the two vascular networks.

Actins↗
PubMed2001

Upregulated TRP and enhanced capacitative Ca(2+) entry in human pulmonary artery myocytes during proliferation.

A rise in cytosolic Ca(2+) concentration ([Ca(2+)](cyt)) due to Ca(2+) release from intracellular Ca(2+) stores and Ca(2+) influx through plasmalemmal Ca(2+) channels plays a critical role in mitogen-mediated cell growth. Depletion of intracellular Ca(2+) stores triggers capacitative Ca(2+) entry (CCE), a mechanism involved in maintaining Ca(2+) influx and refilling intracellular Ca(2+) stores. Transient receptor potential (TRP) genes have been demonstrated to encode the store-operated Ca(2+) channels that are activated by Ca(2+) store depletion. In this study, we examined whether CCE, activity of store-operated Ca(2+) channels, and human TRP1 (hTRP1) expression are essential in human pulmonary arterial smooth muscle cell (PASMC) proliferation. Chelation of extracellular Ca(2+) and depletion of intracellularly stored Ca(2+) inhibited PASMC growth in media containing serum and growth factors. Resting [Ca(2+)](cyt) as well as the increases in [Ca(2+)](cyt) due to Ca(2+) release and CCE were all significantly greater in proliferating PASMC than in growth-arrested cells. Consistently, whole cell inward currents activated by depletion of intracellular Ca(2+) stores and the mRNA level of hTRP1 were much greater in proliferating PASMC than in growth-arrested cells. These results suggest that elevated [Ca(2+)](cyt) and intracellularly stored [Ca(2+)] play an important role in pulmonary vascular smooth muscle cell growth. CCE, potentially via hTRP1-encoded Ca(2+)-permeable channels, may be an important mechanism required to maintain the elevated [Ca(2+)](cyt) and stored [Ca(2+)] in human PASMC during proliferation.

Blood Proteins↗
PubMed2001

Orthostasis fails to produce active limb venoconstriction in adolescents.

Orthostasis is characterized by translocation of blood from the upper body and thorax into dependent venous structures. Although active splanchnic venoconstriction is known to occur, active limb venoconstriction remains controversial. Based on prior work, we initially hypothesized that active venoconstriction does occur in the extremities during orthostasis in response to baroreflex activation. We investigated this hypothesis in the arms and legs of 11 healthy volunteers, aged 13-19 yr, using venous occlusion strain gauge plethysmography to obtain the forearm and calf blood flows and to compute the capacitance vessel volume-pressure compliance relation. Subjects were studied supine and at -10, +20, and +35 degrees to load the baroreflexes. With +20 degrees of tilt, blood flow decreased and limb arterial resistance increased significantly (P < 0.05) compared with supine. With +35 degrees of tilt, blood flow decreased, limb arterial resistance increased, and heart rate increased, indicating parasympathetic withdrawal and sympathetic activation with arterial vasoconstriction. The volume-pressure relation was unchanged by orthostatic maneuvers. The results suggest that active venoconstriction in the limbs is not important to mild orthostatic response.

Adolescent↗
PubMed1993

Dose-related cardiovascular effects of spironolactone.

The aim of this study was to assess the short-term hemodynamic effects of increasing doses of spironolactone (25, 50, and 75 mg/day) on oliguric patients (5 men, mean age 47 +/- 12 years) undergoing hemodialysis for chronic renal impairment. Parameters of interest included heart rate (HR), cardiac output, systemic vascular resistance (SVR), arterial pressure, right atrial pressure, and pulmonary capillary wedge pressure (PCWP). The study also evaluated how spironolactone modified the effects on arterial and right atrial pressures and PCWP of infusion of increasing doses of norepinephrine (20, 40, and 100 ng/kg/min) and angiotensin II (2, 4, and 10 ng/kg/min). Compared with placebo, the lowest dose of spironolactone (25 mg/day) produced statistically significant (p < 0.05) modifications in systemic arterial pressures without a compensatory increase in cardiac output. The modifications were more pronounced at 50 and 75 mg/day, and the latter had a significant dose-dependent effect. Moreover, doses of 50 and 75 mg/day produced significant (p < 0.05) decreases in right atrial pressure and PCWP. Spironolactone administration caused the curve expressing the relation between an infused norepinephrine or angiotensin II dose and the blood pressure response to shift significantly (p < 0.05 to < 0.01) to the right, and the pressor doses of norepinephrine or angiotensin II showed a significant (p < 0.05 to < 0.01) dose-related increase, suggesting that treatment with spironolactone inhibited cardiovascular reactivity. This effect was observed on both the capacitance (i.e., low-pressure) and resistance (i.e., high pressure) vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Implication of the systolic hump in systemic arterial pressure waves.

The systolic hump in the aortic blood pressure wave is defined as the aortic-resistance component proportional to the aortic blood flow superimposed on the windkessel component. An electrical analogue comprising a series resistance (aortic resistance) plus a resistance (peripheral resistance) and capacitance (aortic compliance) in parallel (i.e. windkessel component) is used for analysis. Curve fitting using the least-squares method is performed on calculated and measured blood pressure waves from dogs under haemodynamical conditions induced by infusion of three drugs (noradrenaline, isoproterenol and acetylcholine). The curve fitting RMS (root mean square) errors are < 3% for blood pressure waves and < 30% for blood flow waves, with good agreement between measured and calculated blood flow waveforms. Infusion of noradrenaline and acetylcholine is found to induce a significant decrease and increase in the aortic resistance, respectively. Although only a small fraction of the blood pressure wave, the systolic hump has a marked effect on the systolic pressure waveform.

Animals↗
PubMed1997

Concomitant and hormonally regulated expression of trp genes in bovine aortic endothelial cells.

Recent findings have suggested that the vertebrate trp family of channel proteins is the structural basis for Ca2+ influx through the capacitative calcium entry (CCE) pathway. We have discerned, in bovine aortic endothelial cells, the concomitant expression of four such vertebrate genes: trp-1 (two splice variants), trp-3, trp-4 and trp-5. Exogenous hormones rendered dynamic effects on the transcript levels of these genes. Most notably, beta-estradiol significantly down-regulated trp-4 while trans-retinoic acid dramatically up-regulated trp-5; yet these hormones rendered little change in CCE. These findings suggest that the extent of a given trp channel's participation in CCE is not reflected in alterations of its transcript level.

Amino Acid Sequence↗
PubMed2002

Differential exocytosis from human endothelial cells evoked by high intracellular Ca(2+) concentration.

Endothelial cells secrete a range of procoagulant, anticoagulant and inflammatory proteins by exocytosis to regulate blood clotting and local immune responses. The mechanisms regulating vesicular exocytosis were studied in human umbilical vein endothelial cells (HUVEC) with high-resolution membrane capacitance (C(m)) measurements. The total whole-cell C(m) and the amplitudes and times of discrete femtoFarad (fF)-sized C(m) steps due to exocytosis and endocytosis were monitored simultaneously. Intracellular calcium concentration [Ca(2+)](i) was elevated by intracellular photolysis of calcium-DM-nitrophen to evoke secretion and monitored with the low-affinity Ca(2+) indicator furaptra. Sustained elevation of [Ca(2+)](i) to > 20 microM evoked large, slow increases in C(m) of up to 5 pF in 1-2 min. Exocytotic and endocytotic steps of amplitude 0.5-110 fF were resolved, and accounted on average for ~33 % of the total C(m) change. A prominent component of C(m) steps of 2.5-9.0 fF was seen and could be attributed to exocytosis of von-Willebrand-factor-containing Weibel-Palade bodies (WPb), based on the near-identical distributions of capacitance step amplitudes, with calculated estimates of WPb capacitance from morphometry, and on the absence of 2.5-9.0 fF C(m) steps in cells deficient in WPb. WPb secretion was delayed on average by 23 s after [Ca(2+)](i) elevation, whereas total C(m) increased immediately due to the secretion of small, non-WPb granules. The results show that following a large increase of [Ca(2+)](i), corresponding to strong stimulation, small vesicular components are immediately available for secretion, whereas the large WPb undergo exocytosis only after a delay. The presence of events of magnitude 9-110 fF also provides evidence of compound secretion of WPb due to prior fusion of individual granules.

Calcium↗
PubMed2000

Hypoxia-induced alterations in Ca(2+) mobilization in brain microvascular endothelial cells.

To investigate the possible cellular mechanisms of the ischemia-induced impairments of cerebral microcirculation, we investigated the effects of hypoxia/reoxygenation on the intracellular Ca(2+) concentration ([Ca(2+)](i)) in bovine brain microvascular endothelial cells (BBEC). In the cells kept in normal air, ATP elicited Ca(2+) oscillations in a concentration-dependent manner. When the cells were exposed to hypoxia for 6 h and subsequent reoxygenation for 45 min, the basal level of [Ca(2+)](i) was increased from 32.4 to 63.3 nM, and ATP did not induce Ca(2+) oscillations. Hypoxia/reoxygenation also inhibited capacitative Ca(2+) entry (CCE), which was evoked by thapsigargin (Delta[Ca(2+)](i-CCE): control, 62.3 +/- 3.1 nM; hypoxia/reoxygenation, 17.0 +/- 1.8 nM). The impairments of Ca(2+) oscillations and CCE, but not basal [Ca(2+)](i), were restored by superoxide dismutase and the inhibitors of mitochondrial electron transport, rotenone and thenoyltrifluoroacetone (TTFA). By using a superoxide anion (O(2)(-))-sensitive luciferin derivative MCLA, we confirmed that the production of O(2)(-) was induced by hypoxia/reoxygenation and was prevented by rotenone and TTFA. These results indicate that hypoxia/reoxygenation generates O(2)(-) at mitochondria and impairs some Ca(2+) mobilizing properties in BBEC.

Adenosine Triphosphate↗
PubMed2001

Electrical impedance of cultured endothelium under fluid flow.

The morphological and functional status of organs, tissues, and cells can be assessed by evaluating their electrical impedance. Fluid shear stress regulates the morphology and function of endothelial cells in vitro. In this study, an electrical biosensor was used to investigate the dynamics of flow-induced alterations in endothelial cell morphology in vitro. Quantitative, real-time changes in the electrical impedance of endothelial monolayers were evaluated using a modified electric cell-substrate impedance sensing (ECIS) system. This ECIS/Flow system allows for a continuous evaluation of the cell monolayer impedance upon exposure to physiological fluid shear stress forces. Bovine aortic endothelial cells grown to confluence on thin film gold electrodes were exposed to fluid shear stress of 10 dynes/cm2 for a single uninterrupted 5 h time period or for two consecutive 30 min time periods separated by a 2 h no-flow interval. At the onset of flow, the monolayer electrical resistance sharply increased reaching 1.2 to 1.3 times the baseline in about 15 min followed by a sustained decrease in resistance to 1.1 and 0.85 times the baseline value after 30 min and 5 h of flow, respectively. The capacitance decreased at the onset of flow, started to recover after 15 min and after slightly overshooting the baseline values, decreased again with a prolonged exposure to flow. Measured changes in capacitance were in the order of 5% of the baseline values. The observed changes in endothelial impedance were reversible upon flow removal with a recovery rate that varied with the duration of the preceding flow exposure. These results demonstrate that the impedance of endothelial monolayers changes dynamically with flow indicating morphological and/or functional changes in the cell layer. This in vitro model system (ECIS/Flow) may be a very useful tool in the quantitative evaluation of flow-induced dynamic changes in cultured cells when used in conjunction with biological or biochemical assays able to determine the nature and mechanisms of the observed changes.

Animals↗
PubMed1995

Relative potency and arteriovenous selectivity of nitrovasodilators on human blood vessels: an insight into the targeting of nitric oxide delivery.

The arteriovenous potency of sodium nitroprusside (SNP), linsidomine (SIN-1) and S-nitrosoglutathione (GSNO) was determined in human capacitance (veins) and resistance (arterioles) vessels in vitro and in vivo and compared with the venoselective nitrovasodilator nitroglycerin (GTN). Concentration-response curves were constructed to GTN, SNP, GSNO and SIN-1 (0.001-10 microM) in preconstricted human saphenous vein and to GTN, GSNO and SIN-1 (0.001-10 microM) in omental resistance vessels. In vivo the dilator responses of the dorsal hand vein and the forearm resistance bed were recorded during local infusions of GTN, SNP, GSNO and SIN-1 (1 pmol/min to 160 nmol/min). SNP and SIN-1 had similar arteriovenous profiles to that of GTN. SNP was equipotent with GTN in arterioles and veins but SIN-1 was 10-fold less potent than GTN in vitro and 100-fold less potent in vivo; the potency of SIN-1 was increased after incubation of saphenous vein with superoxide dismutase. GSNO was equipotent with GTN in arterioles but 10-fold less potent in veins in vitro and in vivo. These results demonstrate that most nitrovasodilators are venoselective irrespective of their mechanism of biotransformation to nitric oxide (NO) and suggests that NO itself might be venoselective in vivo. Endogenous carrier molecules, including glutathione, could alter the vascular profile of NO with physiological and therapeutic implications.

Arteries↗
PubMed1990

Parametric analysis of flow in the intramyocardial circulation.

A simple mathematical model of the intramyocardial circulation has been utilized to provide a better understanding of coronary blood flow. The model includes three myocardial layers, each characterized by a three-parameter windkessel with one capacitance and two resistances. The effects of the beating heart are taken into account by means of an intramyocardial pump and the possible collapse of the vessels by an elevated backpressure. The three basic parameters that govern the flow are a normalized time constant, tau, the total resistance, Rt, and a parameter, alpha, which specifies the resistance distribution in the intramyocardial circulation. Both the normal beating heart and prolonged diastole have been investigated analytically as well as numerically. It is shown that each of these parameters has its own special significance. Calculated pressure-flow relationships and zero-flow pressures for the case of prolonged diastole show a high sensitivity to tau and alpha.

Animals↗
PubMed2000

Voltage-dependent Ca2+ channels in resistance arteries from Dahl salt-sensitive rats.

To determine whether chronic salt-loading would alter voltage-dependent Ca2+ channels in resistance arteries of Dahl salt-sensitive rats, whole-cell voltage-clamp experiments were performed on single cells that were isolated from small mesenteric arteries. Dahl salt-sensitive rats were fed either an 8% NaCl diet (high-NaCl group) or a 0.3% NaCl diet (low-NaCl group) from the age of 6 or 7 weeks. After 4 to 5 weeks, systolic blood pressure was significantly higher in the high-NaCl group than in the low-NaCl group. In the high-NaCl group, the threshold potential for Ca2+ channel current was more negative and the current amplitude that was normalized by cell capacitance was higher at negative command potentials (-40 mV to -20 mV), as compared with the low-NaCl group. When the current was separated into fast transient current and slow sustained (L-type) current, the alteration in the high-NaCl group was attributable to the change in L-type current. The steady-state inactivation curve was not different between the high-NaCl and low-NaCl groups. In conclusion, L-type Ca2+ channels in resistance arteries of Dahl salt-sensitive rats became more available for opening near the resting potential after dietary salt-loading.

Animals↗
PubMed1985

Effects of coronary and extravascular pressure on intramyocardial and epicardial blood velocity.

In open-chest anesthetized dogs we measured phasic coronary blood velocity in an epicardial artery (left anterior descending), a small epicardial artery (within 0.5 cm before penetration into the myocardium), and an intramyocardial artery (septal) during changes in perfusion pressure and extravascular pressure. Circumflex artery diameter was also measured during pressure changes to directly assess vascular compliance. At low and normal arterial pressures (less than 125/86 mmHg) and during aortic insufficiency, the phasic character of blood flow velocity in the large epicardial arteries was markedly different from that in the small epicardial and septal arteries: there was retrograde systolic blood flow velocity in the septal artery and small epicardial artery, whereas antegrade blood flow velocity persisted in the left anterior descending artery. At pressures greater than 150/106 mmHg, the differences in the phasic character of blood flow velocity in the left anterior descending artery from that in the septal artery and small epicardial artery were small and decreased as aortic pressure increased. At pressures greater than 125 mmHg, the cross-sectional area change per millimeter of mercury was approximately three times less than at pressures between 30 and 75 mmHg, indicating decreased coronary compliance at the higher pressures. Increasing extravascular pressure in the septum (right ventricular hypertension) greatly increased retrograde systolic blood flow velocity in the septal artery (P less than 0.05). However, right ventricular bypass (0 right ventricular pressure) did not alter the phasic nature of blood flow velocity in the septal artery. From these results we confirmed that epicardial capacitance is inversely related to distending pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1974

The cardiovascular effects of morphine. The peripheral capacitance and resistance vessels in human subjects.

To evaluate the effects of morphine on the peripheral venous and arterial beds, 69 normal subjects were evaluated before and after the intravenous administration of 15 mg morphine. Venous tone was determined by three independent techniques in 22 subjects. The venous pressure measured in a hand vein during temporary circulatory arrest (isolated hand vein technique) fell from 20.2+/-1.4 to 13.4+/-0.9 mm Hg (P < 0.01) 10 min after morphine, indicating that a significant venodilation had occurred. With the acute occlusion technique, morphine induced a reduction in forearm venous tone from 12.8+/-1.1 to 7.9+/-2.3 mm Hg/ml/100 ml (P < 0.01). Although forearm venous volume at a pressure of 30 mm Hg (VV[30]) was increased from 2.26+/-0.17 to 2.55+/-0.26 ml/100 ml, measured by the equilibration technique, the change was not significant (P > 0.1). Of note is that the initial reaction to morphine was a pronounced venoconstriction, demonstrated during the first 1-2 min after the drug. (Isolated hand vein pressure increased to 37.2+/-5.4 mm Hg, P < 0.01). This rapidly subsided, and by 5 min a venodilation was evident. Morphine did not attenuate the venoconstrictor response to a single deep breath, mental arithmetic, or the application of ice to the forehead when measured by either the isolated hand vein technique or the equilibration technique. To evaluate the effects of morphine on the peripheral resistance vessels in 47 normal subjects, forearm blood flow was measured plethysmographically before and 10-15 min after the intravenous administration of 15 mg of morphine. Although mean systemic arterial pressure was unchanged, forearm blood flow increased from 2.92+/-0.28 to 3.96+/-0.46 ml/min/100 ml (P < 0.01), and calculated vascular resistance fell from 42.4+/-5.2 to 31.6+/-3.2 mm Hg/ml/min/100 ml (P < 0.01). When subjects were tilted to the 45 degrees head-up position, morphine did not block the increase in total peripheral vascular resistance that occurs; however, it did significantly attenuate the forearm arteriolar constrictor response (before morphine, + 25.7+/-5.4; after morphine, + 13.7+/-5.3 mm Hg/ml/min/100 ml, P < 0.05). However, morphine did not block the post-Valsalva overshoot of blood pressure, nor did it block the increase in forearm vascular resistance produced by the application of ice to the forehead. Similarly, morphine did not block the arteriolar or venoconstrictor effects of intra-arterially administered norepinephrine. Morphine infused into the brachial artery in doses up to 200 mug/min produced no changes in ipsilateral forearm VV[30], forearm blood flow, or calculated forearm resistance. Intra-arterial promethazine, atropine, and propranolol did not block the forearm arteriolar dilator response to intravenous morphine; however, intra-arterial phentolamine abolished the response. These data suggest that in human subjects, morphine induces a peripheral venous and arteriolar dilation by a reflex reduction in sympathetic alpha adrenergic tone. Morphine does not appear to act as a peripheral alpha adrenergic blocking agent but seems to attenuate the sympathetic efferent discharge at a central nervous system level.

Adult↗
PubMed1993

Endothelium-derived nitric oxide reduces baseline venous tone in awake instrumented rats.

To determine whether nitric oxide, which is likely endothelium-derived relaxing factor (EDRF), modulates baseline venous tone, the effects of intravenous NG-monomethyl-L-arginine (L-NMMA) (3-25 mg/kg), an EDRF inhibitor, on mean circulatory filling pressure (MCFP) were determined in 10 awake instrumented rats. MCFP, the equilibrated systemic pressure occurring when the circulation is arrested by transient inflation of a balloon in the right atrium, is a measure of total venous capacitance. L-NMMA caused a dose-dependent increase in mean arterial pressure and a dose-dependent decrease in heart rate. MCFP rose from 6.6 +/- 0.2 to 7.6 +/- 0.2 mmHg at the highest L-NMMA dose. The effects of L-NMMA on MCFP were reversed with L-arginine. In an additional four rats, in which hexamethonium was administered to induce ganglionic blockade, L-NMMA (25 mg/kg) caused a similar increase in MCFP (4.1 +/- 0.6 to 5.0 +/- 0.7 mmHg, P = 0.22) during the ganglionic blocked state as during the control unblocked state. These findings suggest that nitric oxide, which is likely EDRF, reduces baseline venous tone.

Animals↗