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PubMed1989

Differential vasodilator effect of nitroglycerin on systemic capacitance and resistance vessels in anesthetized dogs, and the mechanism of its action--a study by measuring mean circulatory pressure and total peripheral resistance.

The aim of our studies was to examine if the baroreceptor reflex induced by intravenous injection of nitroglycerin (NG) nearly nullifies the vasodilator action of NG on the systemic capacitance vessels in dogs anesthetized with pentobarbital. We performed total spinal anesthesia (TSA) in open-chest dogs to eliminate the baroreceptor reflex. Dogs in which mean blood pressure (MBP) was maintained at about 100 mmHg by continuous intravenous infusion of epinephrine formed the TSA 100 group, and those in which MBP was maintained at about 70 mmHg formed the TSA 70 group. Dose-response curves relating 5-6 different doses (0.8 to 200 micrograms/kg) of intravenous NG, to changes in mean circulatory pressure (% delta MCP) and to changes in total peripheral resistance (% delta TPR), were constructed. These data were compared with those from untreated dogs. In addition, we also studied plasma catecholamine (CA) concentrations before and after the intravenous injection of NG. (1) There was no significant difference in the dose-response curves of NG for % delta TPR between the 3 groups. (2) There was no significant difference in the dose-response curves for % delta MCP between the 2 TSA groups. However, there was significant difference in the dose-response curves for % delta MCP between the TSA groups and the untreated dogs. The dose-response curves for % delta MCP in the TSA groups shifted upwards as compared with that of the untreated dogs. (3) In the TSA 100 group, there was no significant increase in the plasma CA concentrations with 100 micrograms/kg of NG. In the untreated group, intravenous injection of 12.5 micrograms/kg and 100 micrograms/kg of NG caused a dose-related fall in MBP and a dose-related rise in the plasma norepinephrine and epinephrine concentrations. Our results suggest that the vasodilator action of NG on the systemic capacitance vessels in the untreated dogs was counterbalanced partly by the vasoconstriction produced by the baroreceptor reflex, with its direct vasodilator effect masked when the hypotensive doses of NG were given acutely.

Anesthesia, Spinal↗
PubMed1981

Hemodynamic response to graded water immersion.

Hemodynamic response to graded immersion was studied in healthy male subjects in a thermoneutral bath in the sitting position. Pressures in the right heart and cardiac output were determined by means of a semifloating catheter with a thermistor probe. Pressures in the right atrium, pulmonary artery and in pulmonary wedge position increased with increasing depth of immersion, cardiac output was likewise augmented. Heart rate decreased from rest to hip immersion but remained constant from hip to head out water immersion. Plasma norepinephrine concentration remained constant throughout the experiment. The reported changes depend on the blood shift from capacitance vessels into the thoracic cavity. From this, preload increased and cardiac performance was improved. However, in patients with disturbed left ventricular function, immersion to the neck may be potentially hazardous due to augmented left ventricular filling pressure.

Adult↗
PubMed1984

Mechanism of action of nitrates. Role of changes in venous capacitance and in the left ventricular diastolic pressure-volume relation.

Nitroglycerin, when administered to patients with heart failure, causes a marked reduction in left ventricular filling pressure but often an increase in stroke volume and stroke work; based on the Frank-Starling principle, such a reduction in "preload" would be expected to result in a decrease in left ventricular end-diastolic volume and, therefore, a decline in stroke volume. Assessment of pressure-volume coordinates, however, has revealed that nitroglycerin produces a downward shift in the pressure-volume relationship. This apparent improvement in left ventricular compliance cannot be attributed to alterations in the elastic properties of the myocardium but rather appear to reflect a reduction in left ventricular external constraint. Recent animal and clinical investigations in our laboratory suggest that nitroglycerin causes venous dilatation (particularly in the mesenteric bed), thereby decreasing venous pressure at any given vascular volume. This decrease in cardiac filling pressure results in a decrease in heart size and, therefore, a reduction in pericardial pressure. Left ventricular transmural (intracavitary minus pericardial) pressure is little changed, however, so that end-diastolic volume and stroke volume are maintained.

Animals↗
PubMed1989

Endothelin sensitivity and receptor binding in the aorta of spontaneously hypertensive rats.

Endothelin is a very potent vasoconstrictor peptide secreted by endothelial cells. The aim of this study was to determine whether sensitivity to endothelin was greater in isolated aortic rings of spontaneously hypertensive rats (SHR) than in those of normotensive Wistar-Kyoto rats (WKY) and, if so, whether this was due to an increased binding affinity. Adult SHR were more sensitive to endothelin than age-matched WKY, but the maximal tension developed in response to endothelin was significantly lower in SHR than in WKY. The binding affinity of 125I-endothelin was similar in SHR [apparent dissociation constant (Kd) = 76 +/- 11 pmol/l, n = 5] and WKY (Kd = 60 +/- 10 pmol/l, n = 5). However, the density of endothelin binding sites in aortic smooth muscle cells in culture was significantly higher in WKY (2976 +/- 374 receptors per cell) than in SHR (1278 +/- 299 receptors per cell, P less than 0.01). The hyper-responsiveness of a large capacitance vessel in SHR seems relatively specific for endothelin, since the effects of norepinephrine were not significantly different between adult SHR and WKY. This hyper-responsiveness cannot be explained by an alteration in the affinity of endothelin for its receptor. However, a down-regulation of the number of binding sites could explain the lower maximal response to endothelin in SHR.

Animals↗
PubMed1986

Venous reactivity and pregnancy abnormalities.

An impedance plethysmograph recording was obtained on at least two occasions from 162 women between their 24 and 36th week of pregnancy; 29 while in labor and 21 at the time of their 6-week postpartum visit. There was a significant increase in venous capacitance and a decline in venous capacitance index during apparently normal pregnancy. Those with pregnancy complications (hypertension, premature labor and fetal growth retardation) appeared to have significantly abnormal venous reactivity. It is proposed that equal consideration be given to abnormal venous activity in the mechanisms and therapy of pregnancy-related cardiovascular abnormalities.

Female↗
PubMed1999

Synchrotron microangiography reveals configurational changes and to-and-fro flow in intramyocardial vessels.

In 8 dogs, in situ microangiography using synchrotron radiation visualized penetrating transmural arteries (PTAs) with a diameter of >60 micrometers and allowed quantitation of vessel diameters of >140 micrometers. Myocardial contraction reduced the vascular short-axial diameters to 87 +/- 17% (n = 62, P < 0.001, paired t-test) of the end-diastolic values and increased the longitudinal dimension to 129 +/- 5% (n = 45, P < 0.001). The diameter reduction in the subendocardial PTA segments was significantly more marked than that in the subepicardial PTA segments (60 +/- 12 vs. 88 +/- 12%, n=13, P < 0.001, paired t-test). Intracoronary administration of dobutamine (0.1 micrograms. kg-1. min-1) increased, and in contrast, partial clamping of the coronary artery (ischemia) decreased, the configurational changes. To-and-fro blood flow was clearly observed in PTAs with visual identification of capacitive backflow, resistive forward flow during ischemia on coronary arteriography, and even under baseline conditions in coronary venography. Thus this method advances our understanding of mechanical influences on the coronary circulation.

Animals↗
PubMed2005

The role of mitochondria for Ca2+ refilling of the endoplasmic reticulum.

Endoplasmic reticulum (ER) Ca2+ refilling is an active process to ensure an appropriate ER Ca2+ content under basal conditions and to maintain or restore ER Ca2+ concentration during/after cell stimulation. The mechanisms to achieve successful ER Ca2+ refilling are multiple and built on a concerted action of processes that provide a suitable reservoir for Ca2+ sequestration into the ER. Despite mitochondria having been found to play an essential role in the maintenance of capacitative Ca2+ entry by buffering subplasmalemmal Ca2+, their contribution to ER Ca2+ refilling was not subjected to detailed analysis so far. Thus, this study was designed to elucidate the involvement of mitochondria in Ca2+ store refilling during and after cell stimulation. ER Ca2+ refilling was found to be accomplished even during continuous inositol 1,4,5-trisphosphate (IP3)-triggered ER Ca2+ release by an agonist. Basically, ER Ca2+ refilling depended on the presence of extracellular Ca2+ as the source and sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) activity. Interestingly, in the presence of an IP3-generating agonist, ER Ca2+ refilling was prevented by the inhibition of trans-mitochondrial Ca2+ flux by CGP 37157 (7-chloro-5-(2-chlorophenyl)-1,5-dihydro-4,1-benzothiazepin-2(3H)-one) that precludes the mitochondrial Na+/Ca2+ exchanger as well as by mitochondrial depolarization using a mixture of oligomycin and antimycin A. In contrast, after the removal of the agonist, ER refilling was found to be largely independent of trans-mitochondrial Ca2+ flux. Under these conditions, ER Ca2+ refilling took place even without an associated Ca2+ elevation in the deeper cytosol, thus, indicating that superficial ER domains mimic mitochondrial Ca2+ buffering and efficiently sequester subplasmalemmal Ca2+ and consequently facilitate capacitative Ca2+ entry. Hence, these data point to different contribution of mitochondria in the process of ER Ca2+ refilling based on the presence or absence of IP3, which represents the turning point for the dependence or autonomy of ER Ca2+ refilling from trans-mitochondrial Ca2+ flux.

Calcium↗
PubMed2006

Contribution of both Ca2+ entry and Ca2+ sensitization to the alpha1-adrenergic vasoconstriction of rat penile small arteries.

Sympathetic adrenergic nerves maintain the flaccid state of the penis through the tonic release of norepinephrine that contracts trabecular and arterial smooth muscle. Simultaneous measurements of intracellular Ca(2+) concentration ([Ca(2+)](i)) and tension and experiments with alpha-toxin-permeabilized arteries were performed in branches of the rat dorsal penile artery to investigate the intracellular Ca(2+) signaling pathways underlying alpha(1)-adrenergic vasoconstriction. Phenylephrine increased both [Ca(2+)](i) and tension, these increases being abolished by extracellular Ca(2+) removal and reduced by about 50% by the L-type Ca(2+) channel blocker nifedipine (0.3 microM). Non-L-type Ca(2+) entry through store-operated channels was studied by inhibiting the sarcoplasmic reticulum Ca(2+)-ATPase with cyclopiazonic acid (CPA). CPA (30 microM) induced variable phasic contractions that were abolished by extracellular Ca(2+) removal and by the store-operated channels antagonist 2-aminoethoxydiphenyl borate (2-APB, 50 microM) and largely inhibited by nifedipine (0.3 microM). CPA induced a sustained increase in [Ca(2+)](i) that was reduced in a Ca(2+)-free medium. Under conditions of L-type channels blockade, Ca(2+) readmission after store depletion with CPA evoked a sustained and marked elevation in [Ca(2+)](i) not coupled to contraction. 2-APB (50 microM) inhibited the rise in [Ca(2+)](i) evoked by CPA and the nifedipine-insensitive increases in both [Ca(2+)](i) and contraction elicited by phenylephrine. In alpha-toxin-permeabilized penile arteries, activation of G proteins with guanosine 5'-O-(3-thiotriphosphate) and of the alpha(1)-adrenoceptor with phenylephrine both enhanced the myofilament sensitivity to Ca(2+). This Ca(2+) sensitization was reduced by selective inhibitors of PKC, tyrosine kinase (TK), and Rho kinase (RhoK) by 43%, 67%, and 82%, respectively. As a whole, the present data suggest the alpha(1)-adrenergic vasoconstriction in penile small arteries involves Ca(2+) entry through both L-type and 2-APB-sensitive receptor-operated channels, as well as Ca(2+) sensitization mechanisms mediated by PKC, TK, and RhoK. A capacitative Ca(2+) entry coupled to noncontractile functions of the smooth muscle cell is also demonstrated.

Adrenergic alpha-1 Receptor Agonists↗
PubMed1990

[The autonomic innervation of the nasal capacitance and resistance vessels in the cat].

In the present study reflex manners in capacitance and resistance vessels of the nasal mucosa have been observed respectively and simultaneously by stimulating the a) Cervical sympathetic nerve trunk, b) Vagal nerve, c) Vidian nerve, d) sympathectomized Vidian nerve electrically. Capacitance change in the nasal mucosa was measured by plethysmographic balloons inserted into the nasal cavity. Resistance change was measured as the pressure change in the terminal branch of the maxillary artery by using the constant flow perfusion method. a) Stimulation of the cervical sympathetic nerve trunk evoked a decrease change in the volume of the nasal mucosa and an increase change in the resistance of the maxillary artery. b) Stimulation of the Vagal nerve evoked an increase change in the volume of the nasal mucosa and a decrease change in the resistance of the maxillary artery. c) Stimulation of the Vidian nerve there were observed an increase change in the volume of the nasal mucosa and a decrease change in the resistance of the maxillary artery at the low stimulation intensity, from 0.2 to 0.8 volts. Further increasing the stimulation intensity, from 1.0 to 6.0 volts a decrease change in the volume of the nasal mucosa was observed. In spite of the reverse change in the capacitance vessel, pressure in the maxillary artery still maintained low pressure level. d) Stimulation of the sympathectomized Vidian nerve evoked an increase change in the volume of the nasal mucosa and a decrease change in the maxillary artery. Manner of these reflex was very similar to that of the Vagal nerve stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Role of the carotid sinus in response of integrated venous system to pulsatile and nonpulsatile perfusion.

Effects of pulsatile and nonpulsatile perfusion on capacity system were investigated in 33 open-chest mongrel dogs with extracorporeal circulation. In 28 dogs with intact carotid sinus nerves, after changing from nonpulsatile to pulsatile systemic perfusion the mean arterial pressure decreased by 14 +/- 1.5 mm Hg, peripheral resistance by 423 +/- 15 dyne.cm-5.sec, and venous blood volume by 3.3 +/- 0.4 ml/kg. After changing from pulsatile perfusion to nonpulsatile systemic perfusion the mean arterial pressure increased by 15 +/- 2.2 mm Hg, the peripheral resistance by 431 +/- 15 dyne.cm-5.sec, and venous volume by 3.9 +/- 0.5 ml/kg. The same effects were observed in five dogs with bilateral isolated carotid pulsatile perfusion or nonpulsatile perfusion and systemic nonpulsatile perfusion. These effects were abolished after denervation of pressor receptors and pharmacologic blockade of alpha and beta receptors. It is proposed that with nonpulsatile perfusion carotid sinus-mediated vasoconstriction occurs in the downstream part of the capacitive system, where more pronounced wall musculature with increased number of adrenergic receptors is present. The throttle effect caused by this "resistance" part of venous circulation leads to increase of pressure in the upstream section of the capacitive system, compensates for the constrictive effect of the sympathetic tone, and leads finally to an increased volume of the capacity system. We conclude that venous response to different perfusion modalities is critically dependent on intact carotid sinus nerves and adrenergic receptors in the veins.

Animals↗
PubMed2002

Comparative effects of clonidine and dihydroergotamine on venomotor tone and orthostatic tolerance in patients with severe hypoadrenergic orthostatic hypotension.

PURPOSE: Clonidine, an alpha(2)-adrenergic agonist, raises blood pressure in patients with autonomic failure, in whom failure of reflex neurogenic venoconstriction leads to severe orthostatic hypotension. Because animal studies suggest that postjunctional alpha(2)-adrenoreceptors are located mainly on venous capacitance rather than arterial resistance vessels, we tested the hypothesis that venoconstriction is the main mechanism by which clonidine raises blood pressure in patients with autonomic failure. SUBJECTS AND METHODS: We measured forearm venous and arterial tone using plethysmography in 4 patients with autonomic failure before and after acute administration of clonidine (0.4 mg orally) or dihydroergotamine (0.15 mg intravenously), a known venoconstrictor agent. We also recorded supine intraarterial pressure at rest and during graded orthostatic stress with lower body negative pressure. RESULTS: Clonidine and dihydroergotamine caused similar increases in supine (mean +/- SD) arterial pressure (+23 +/- 11 mm Hg vs. and +27 +/- 5 mm Hg) and forearm vascular resistance (+36% +/- 13% vs. +28% +/- 9%). However, the drugs had different effects on forearm venous tone, which increased by 38% +/- 9% with dihydroergotamine (P = 0.01 vs. control) but was unaffected by clonidine (change = 0% +/- 14%). A single dose of clonidine was less effective than a single dose of dihydroergotamine in maintaining arterial pressure during graded orthostatic stress. CONCLUSION: In contrast with what has been hypothesized, clonidine appears to function mainly as an arterial constrictor in patients with hypoadrenergic orthostatic hypotension. Further studies are needed to determine if venoconstrictor agents are of greater therapeutic benefit in this condition than are pure arterial vasoconstrictors.

Adrenergic alpha-Agonists↗
PubMed2000

Splanchnic-mesenteric capacitance bed in the postural tachycardia syndrome (POTS).

BACKGROUND: Gastroenterologic symptoms are common in the postural tachycardia syndrome (POTS), and postprandial worsening of orthostatic symptoms often occurs. We, therefore, investigated splanchnic-mesenteric vasoregulation in POTS. SUBJECTS AND METHODS: Eleven patients with POTS (one man, 10 women, 29.4 +/- 7.7 (S.D.) years) and 10 controls (two men, eight women, 27.9 +/- 5.6 years) participated in this study. The protocol included 5 min of 70 degrees head-up tilt (HUT) before and after a liquid meal, as well as 1.5 min of hyperventilation. Blood pressure (BP), heart rate (HR), endtidal CO2, and cardiovascular indices derived from thoracic electrical bioimpedance were continuously monitored. Superior mesenteric artery (SMA) blood flow was measured by real time Doppler ultrasound and analyzed off-line. Cross-sectional area of SMA (SMA-area) and time-averaged velocity (SMA-TAV) were measured; SMA blood flow (SMA-BF) and vascular resistance (SMA-VR) were derived. RESULTS: The following significant results were found: at supine rest, the POTS group had higher HR, BP, SMA-TAV and SMA-BF and a lower SMA-VR than the control group. HUT resulted in a reduction of pulse pressure, CO2 level, SMA-area, SMA-TAV and SMA-VF and increment of HR and SMA-VR in both groups. The POTS group underwent greater increment of HR and greater reduction of CO2 than controls. Hyperventilation induced increment of HR and cardiac index (CI) and reduction of SMA-VR in controls; no significant change occurred in POTS. The test meal induced increments of HR, CI, SMA-area, SMA-TAV and SMA-VF and reduction of SMA-VR in patients and controls for both supine rest and HUT. CONCLUSION: The main novel observations of increased resting SMA-BF, SMA-TAV supine, and reduced SMA-VR when compared with controls support the notion that there is excessive splanchnic capacity (pooling) at rest in POTS.

Adult↗
PubMed2005

Acute and chronic effects of relaxin on vasoactivity, myogenic reactivity and compliance of the rat mesenteric arterial and venous vasculature.

We investigated the effect of relaxin on vasodilation, myogenic reactivity, and compliance of small mesenteric arteries and veins. In acute experiments, small (second order) mesenteric arteries and veins from female rats were mounted in a pressure myograph, perfused intraluminally with relaxin, and exposed to incremental increases in intraluminal pressure (20-120 mm Hg for arteries, 2-12 mm Hg for veins). We expressed myogenic reactivity as the ratio of active to passive diameter at each pressure step. In chronic experiments, relaxin was administered to rats (4 microg/h) for 3 days prior to isolating the vessels and measuring myogenic reactivity. Arteries were more sensitive than were veins to the acute vasodilatory activity of relaxin (EC50: arteries=1.32+/-0.18x10(-8) M; veins=3.19+/-0.88x10(-8) M, P<0.05). Acute relaxin reduced myogenic reactivity of mesenteric arteries, but not veins. Chronic pretreatment with relaxin did alter the pressure/diameter relationship in Ca(2+)-containing medium, but this was due to increased passive compliance (control: 2.96+/-0.14 microm mm Hg(-1), n=5; relaxin: 3.72+/-0.16 microm mm Hg(-1), n=5) rather than to reduced myogenic reactivity. Chronic relaxin did not alter myogenic reactivity or compliance (control: 43.8+/-1.4 microm mm Hg(-1), n=5; relaxin: 46.1+/-2.3 microm mm Hg(-1), n=5) of veins. Thus, although relaxin reduces total peripheral resistance, it does not affect splanchnic venous capacitance or tone. In the face of elevated plasma relaxin levels, such as during pregnancy, cardiac preload may thus be maintained, concurrent with a reduction in cardiac afterload and blood pressure. We caution that, if an experimental treatment alters compliance, myogenic reactivity must be expressed as the ratio of active:passive diameter.

Analysis of Variance↗
PubMed1990

Hemodynamic effects of dexmedetomidine, an alpha 2-adrenergic agonist, in autonomically denervated dogs.

The hemodynamic effects of the alpha 2-adrenergic agonist, dexmedetomidine (DM), were studied in eight anesthetized, autonomically denervated dogs. Autonomic block decreased mean arterial pressure (MAP) and cardiac index (CI) by approximately 20% to 95 +/- 8 mm Hg and 4.1 +/- 0.1 L/min/m2, respectively (mean +/- SEM), and reduced norepinephrine (NE) and epinephrine plasma levels to almost undetectable levels. DM, administered intravenously (i.v.) either by bolus injection or by slow (20 min) infusion in doses between 1 and 30 micrograms/kg, had no effect on heart rate (HR), increased MAP significantly by 98%, decreased CI by 59%, and increased calculated systemic vascular resistance index (SVRI) significantly by 376%, maximally. The effect of the lowest dose was mediated mainly by arteriolar vasoconstriction, and that of higher doses was mediated by vasoconstriction and decreased CI. Left ventricular end-diastolic pressure (LVEDP) increased significantly from 6 +/- 2 to greater than 30 mm Hg. maximally. The effects were cumulative, and the first dose caused near maximal pressor effect; the resistance increase was as great with slow infusion as with bolus injection. Prazosin (1 mg/kg) did not affect the changes, but 0.3 mg/kg atipamezole, a selective alpha 2-antagonist, completely antagonized them. These observations demonstrate potent constriction of both arteriolar resistance and venous capacitance vasculature in dogs. The combination of decreased CI and increased filling pressure implies marked decrease in cardiac function which was, however, fully reversible by atipamezole.

Adrenergic beta-Agonists↗
PubMed2000

The effects of hindlimb unweighting on the capacitance of rat small mesenteric veins.

Microgravity is associated with an impaired cardiac output response to orthostatic stress. Mesenteric veins are critical in modulating cardiac filling through venoconstriction. The purpose of this study was to determine the effects of simulated microgravity on the capacitance of rat mesenteric small veins. We constructed pressure-diameter relationships from vessels of 21-day hindlimb-unweighted (HLU) rats and control rats by changing the internal pressure and measuring the external diameter. Pressure-diameter relationships were obtained both before and after stimulation with norepinephrine (NE). The pressure-diameter curves of HLU vessels were shifted to larger diameters than control vessels. NE (10(-4) M) constricted veins from control animals such that the pressure-diameter relationship was significantly shifted downward (i.e., to smaller diameters at equal pressure). NE had no effect on vessels from HLU animals. These results indicate that, after HLU, unstressed vascular volume may be increased and can no longer decrease in response to sympathetic stimulation. This may partially underlie the mechanism leading to the exaggerated fall in cardiac output and stroke volume seen in astronauts during an orthostatic stress after exposure to microgravity.

Animals↗
PubMed1991

Hemodynamic efficacy of E-1020 in comparison with dopamine on acute mitral regurgitation in anesthetized dogs.

To evaluate the effects of a new phosphodiesterase inhibitor, E-1020 (1, 2-dihydro-6-methyl-2-oxo-5-(imidazo [1, 2-a] pyridin-6-yl)-3-pyridine carbonitrile hydrochloride monohydrate), on cardiovascular hemodynamics in acute heart failure, we compared its effects with those of dopamine on experimentally produced acute mitral regurgitation in dogs. After the production of mitral regurgitation by transmyocardial chordal sectioning and obtaining a stable state, dopamine (5 micrograms/kg/min) was infused until the peak positive dP/dt (peak (+) dP/dt) increased to about 50% of the predopamine value. After complete recovery, E-1020 (30 micrograms/kg) was infused over 5 min and the data were obtained 10 min later. Both drugs equally increased peak (+) dP/dt, decreased systemic vascular resistance, and increased cardiac output. Left ventricular (LV) end-diastolic pressure, LV end-diastolic segment length (EDL), and mean left atrial (LA) pressure decreased with both drugs. The changes in EDL and mean LA pressure were larger with E-1020 than with dopamine (p less than .01 and p less than .05). Although mean inferior vena caval blood flow volume (mIVCF) increased and mean inferior vena caval pressure decreased with both drugs, the increment of mIVCF was smaller with E-1020 (p less than .001). Thus, E-1020 had not only a positive inotropic effect but also a vasodilatory action both on resistance vessels and on capacitance vessels.

Acute Disease↗
PubMed1992

Dose-response study of the redistribution of intravascular volume by angiotensin II in man.

1. The response of systemic and regional haemodynamic indices to increasing infusion rates of angiotensin II (1, 3 or 10 ng min-1 kg-1) or placebo [5% (w/v) D-glucose] was studied in eight normal male subjects. 2. As compared with placebo, angiotensin II infusion caused an incremental rise in the serum angiotensin II level [14.5 +/- 7.7 (placebo) to 187.2 +/- 36.1 (10 ng of angiotensin II min-1 kg-1) pmol/l; mean +/- 95% confidence interval] associated with a stepwise increase in total peripheral resistance [880 +/- 42 (placebo) to 1284 +/- 58 (10 ng of angiotensin II min-1 kg-1) dyn s cm-5] and a progressive reduction in cardiac output [8.3 +/- 0.4 (placebo) to 7.0 +/- 0.4 (10 ng of angiotensin II min-1 kg-1) litres/min]. 3. A stepwise fall in renal blood flow was observed with increasing angiotensin II infusion rate [1302 +/- 65 (placebo) to 913 +/- 64 (10 ng of angiotensin II min-1 kg-1) ml/min]. In contrast, calf blood flow was unaffected by 1 ng or 3 ng of angiotensin II min-1 kg-1 and was significantly increased by 10 ng of angiotensin II min-1 kg-1 (P less than 0.01). 4. Calf venous capacitance was uninfluenced by 1 ng of angiotensin II min-1 kg-1, but was significantly increased by both 3 ng (P less than 0.005) and 10 ng (P less than 0.001) of angiotensin II min-1 kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Relationship between the venoconstrictor activity of dihydroergotamine and its pharmacokinetics during acute and chronic oral dosing.

In a double-blind, interindividual comparative study 30 healthy volunteers were randomly allocated to oral treatment with 5 or 10 mg of dihydroergotamine (DHE) or placebo once daily for 16 days. Regional basic venous blood volume (BBV), pressure dependent venous capacitance (CV) of the calf, resting heart rate and blood pressure were determined on Days 1 and 15 of treatment. Plasma concentrations of DHE were monitored on Days 2 and 16. Due to spontaneous vasodilation BBV varied considerably, showing that it is an inappropriate parameter for investigating the venoconstrictor activity of DHE. CV remained unchanged after the first dose of DHE but it had declined significantly on both dosage regimens at the end of the treatment phase. In contrast, the blood concentration profiles of DHE were comparable at the beginning and the end of the trial. The discrepancy can best be explained by the existence of an effect compartment, e.g. smooth vascular musculature, which slowly becomes filled with DHE and/or its active metabolites. The venoconstrictor activity of DHE exhibited a significant dose-response relationship.

Administration, Oral↗