Changes in systemic vascular resistance and capacitance elicited by some systemic reflexes.
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Animals↗
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Neuroleptanalgesia: effects of Innovar on myocardial contractility, total peripheral vascular resistance, and capacitance.
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Animals↗
Action of AR-L 115 BS on myocardial oxygen consumption, cardiac performance and vascular resistance and capacitance.
2-[(2-Methoxy-4-methylsulfinyl)phenyl]-1H-imidazo[4,5-b]-pyridine (AR-L 115 BS) (0.1--1.0 mg/kg i.v.) exerted positive inotropic and chronotropic actions without inducing marked elevations of myocardial oxygen consumption in anaesthetized dogs. Doses between 0.5 and 5.0 mg/kg i.v. reduced peripheral resistance by a direct vasodilating activity and increased venous capacity. Stroke volume and cardiac output were only slightly influenced by the drug. Residual and end-diastolic left ventricular volumes were reduced and ejection fraction was increased.
Animals↗
Studies on capacitative calcium entry in vascular smooth muscle cells by measuring 45CA2+ influx.
Capacitative calcium entry was studied in the A7r5 vascular smooth muscle cell line by measuring 45Ca2+ influx. Entry was induced by depletion of the Ca2+ pools by either the receptor agonist [Arg]8 vasopressin (AVP) or the SR-Ca(2+)-ATPase inhibitor thapsigargin (TG). TG showed a higher efficacy for calcium influx than AVP. This is probably due to a larger Ca2+ release from the pools induced by TG compared to AVP and the irreversible inhibition of the SR-Ca(2+)-ATPase by TG causing influx to persist for a longer period of time. At maximally effective concentrations signals induced by AVP and TG were synergistic in the absence but not in the presence of the intracellular calcium chelator, 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA). Depolarisation with 55 mM KCl completely inhibited 45Ca2+ influx induced by TG but only slightly the one induced by AVP, both effects being less pronounced in the presence of BAPTA. [Ca2+]c signals induced by AVP and TG were both inhibited by depolarisation. In conclusion, although our results show differences between AVP- and TG- induced Ca2+ influx, they can be explained by their different mechanism of action and are in accordance with an activation of the same capacitative entry pathway by both agents.
Animals↗
Regulation of capacitative and non-capacitative Ca2+ entry in A7r5 vascular smooth muscle cells.
A capacitative Ca2+ entry (CCE) pathway, activated by depletion of intracellular Ca2+ stores, is thought to mediate much of the Ca2+ entry evoked by receptors that stimulate phospholipase C (PLC). However, in A7r5 vascular smooth muscle cells, vasopressin, which stimulates PLC, empties intracellular Ca2+ stores but simultaneously inhibits their ability to activate CCE. The diacylglycerol produced with the IP3 that empties the stores is metabolized to arachidonic and this leads to activation of nitric oxide (NO) synthase, production of NO and cyclic GMP, and consequent activation of protein kinase G. The latter inhibits CCE. In parallel, NO directly activates a non-capacitative Ca2+ entry (NCCE) pathway, which is entirely responsible for the Ca2+ entry that occurs in the presence of vasopressin. This reciprocal regulation of two Ca2+ entry pathways ensures that there is sequential activation of first NCCE in the presence of vasopressin, and then a transient activation of CCE when vasopressin is removed. We suggest that the two routes for Ca2+ entry may selectively direct Ca2+ to processes that mediate activation and then recovery of the cell.
Animals↗
Extracellular Mg2+ inhibits capacitative Ca2+ entry in vascular smooth muscle cells.
BACKGROUND: Agonist-induced Ca2+ entry is thought to be mediated by capacitative Ca2+ entry other than L-type Ca2+ channels in vascular smooth muscle cells (VSMCs). The mechanism for capacitative Ca2+ entry has not been fully elucidated. Our objective was to examine the effect of external Mg2+ on capacitative Ca2+ entry in cultured rat aortic VSMCs. METHODS AND RESULTS: Three doses of external Mg2+ concentration (nominally 0, 1, and 5 mmol/L) were used. After exposure to 1 mumol/L, angiotensin II (Ang II) in Ca(2+)-free medium, addition of Ca2+ to the medium caused an increase in cytosolic free Ca2+ concentration ([Ca2+]i), indicating Ang II-induced Ca2+ influx. This Ca2+ influx was attenuated in cells preincubated with high external Mg2+ concentrations or with 1 mumol/L nifedipine. After VSMCs in Ca(2+)-free medium were exposed to 1 mumol/L thapsigargin, which inhibits the sarcoplasmic reticulum Ca(2+)-ATPase and depletes Ca2+ stores, addition of Ca2+ to the medium induced an increase in [Ca2+]i, indicating capacitative Ca2+ entry. This entry pathway was found to be independent of dihydropyridine-sensitive Ca2+ channels and inhibited by increased external Mg2+ concentration. External Mg2+ concentration did not influence Ca2+ efflux across the plasma membrane after stimulation with Ang II plus thapsigargin. CONCLUSIONS: Results suggest that in VSMCs, capacitative Ca2+ entry is reduced by external Mg2+. This mechanism may explain in part the inhibitory effect of external Mg2+ on Ca2+ handling.
Angiotensin II↗
Methods for assessing hepatic distending pressure and changes in hepatic capacitance in pigs.
The equilibrium pressure obtained during simultaneous occlusion of hepatic vascular inflow and outflow was taken as the reference estimate of hepatic vascular distending pressure (P(hd)). P(hd) at baseline was 1.1 +/- 0.2 (mean +/- SE) mmHg higher than hepatic vein pressure (P(hv)) and 0.7 +/- 0.3 mmHg lower than portal vein pressure (P(pv)). Norepinephrine (NE) infusion increased P(hd) by 1. 5 +/- 0.5 mmHg and P(pv) by 3.7 +/- 0.6 mmHg but did not significantly increase P(hv). Hepatic lobar vein pressure (P(hlv)) measured by a micromanometer tipped 2-Fr catheter closely resembled P(hd) both at baseline and during NE-infusion. Dynamic pressure-volume (PV) curves were constructed from continuous measurements of P(hv) and hepatic blood volume increases (estimated by sonomicrometry) during brief occlusions of hepatic vascular outflow and compared with static PV curves constructed from P(hd) determinations at five different hepatic volumes. Estimates of hepatic vascular compliance and changes in unstressed blood volume from the two methods were in close agreement with hepatic compliance averaging 32 +/- 2 ml. mmHg(-1). kg liver(-1). NE infusion reduced unstressed blood volume by 110 +/- 38 ml/kg liver but did not alter compliance. In conclusion, P(hlv) reflects hepatic distending pressure, and the construction of dynamic PV curves is a fast and valid method for assessing hepatic compliance and changes in unstressed blood volume.
Animals↗
[Activity of ondansetron on the systemic vascular resistance and venous capacitance during cardiopulmonary bypass].
OBJECTIVE: To study the effect of ondansetron administered during cardio-pulmonary bypass surgery, in terms of mean arterial pressure, systemic vascular resistance and venous system capacitance. PATIENTS AND METHOD: Twenty patients scheduled for non coronary cardiac surgery were randomly assigned to 2 groups. The study group received 4 mg ondansetron during the bypass and the control group received the same volume of physiological saline solution. The following parameters were recorded during the 10 minutes following administration of either substance: mean arterial pressure, calculated systemic vascular resistance, and the venous reservoir volume at the beginning and end of the study period. RESULTS: Increased mean arterial pressure and systemic vascular resistance were recorded in both groups from the time of injection, with the highest levels recorded at 10 minutes. There were no statistical differences between the 2 groups. No changes in venous system capacitance were observed in either group, as there were no significant changes in venous reservoir volume of the extracorporeal circulation pump. CONCLUSIONS: Ondansetron at the dose used has no effect on arterial or venous vessels. The increased resistance recorded in both groups can be attributed to the release of catecholamines during non pulsatile extracorporeal circulation with a non pulsatile flow.
Aged↗
Morphine decreases peripheral vascular resistance and increases capacitance in man.
The response of the human peripheral circulation to morphine in large doeses independent of cardiac and respiratory influences has not been delineated. In 28 patients during cardiopulmonary bypass, alterations of peripheral vascular resistance (PVR) and capacitance in response to rapid arterial injection of morphine, 0.5 mg/kg or 1 mg/kg alone, or preceeded by promethazine, 1 mg/kg, naloxone, 10 mug/kg, or naloxone, 20 mug/kg, were recorded over 15 min at a constant perfusion rate. Both doses of morphine decreased PVR by 46 percent at 2 min, with values returning to control at 9 min. When promethazine preceded morphine, the decrease in PVR after morphine was 25 percent. Naloxone did not alter the response. An increase in capacitance of 600 ml observed 5 min after morphine administration did not revert to control after 15 min, and was unaltered by prior administration of naloxone.
Blood Pressure↗
Intracellular alkalinization augments capacitative Ca2+ entry in vascular smooth muscle cells.
Agonist-induced Ca2+ influx of vascular smooth muscle cells is thought to be triggered by depletion of intracellular Ca2+ stores. This study investigated the effects of intracellular alkalinization on capacitative Ca2+ entry in A7r5 rat aortic smooth muscle cells. Intracellular alkalinization was induced by NH(4)Cl. Transplasmalemmal Ca2+ influx due to Ca2+ store depletion induced by thapsigargin, which was abolished by pretreatment of the cells with SKF-96365 but not affected by that with verapamil, was significantly increased by pretreatment with NH(4)Cl. Neither 5-hydroxytryptamine-induced inositol monophosphate accumulation nor intracellular Ca2+ release from its stores was affected by NH(4)Cl. These results suggest that intracellular alkalinization acts on the process(es) after depletion of Ca2+ stores and facilitates capacitative Ca2+ entry in vascular smooth muscle cells.
Ammonium Chloride↗
Effect of somatostatin on resistance and on capacitance rabbit isolated arteries.
The effects of somatostatin, a tetradecapeptide isolated from hypothalamus extracts, were studied on the vascular reactivity of aorta and mesenteric arteries isolated from rabbits. We also investigated whether or not Ca(2+) movements were implicated in these effects. Rabbit aorta and mesenteric (fifth branch) arteries were isolated, cleaned off, and mounted in an organ bath containing Godfraind solution or physiological saline solution (PSS), respectively. Somatostatin (10(-8)-10(-4) M) produced a concentration-dependent inhibition of the contractile responses induced by high K(+) (80 mM) or noradrenaline (10(-6) M in aorta or 10(-4) M in mesenteric arteries) in both arteries studied. The inhibitory effect of somatostatin was greater in mesenteric resistance vessels (IC(50) 3.1+/-2.3x10(-5) M, and 5.2+/-4.8x10(-8) M with KCl and noradrenaline, respectively). Contractile responses produced by the addition of Ca(2+) (1-5 mM) to Ca(2+)-free high K(+) solution were also concentration dependently inhibited by somatostatin in aorta. Furthermore, somatostatin decreased noradrenaline-induced contraction attributed to intracellular Ca(2+) release in aorta, and inhibited 45Ca(2+) uptake stimulated by high K(+) or by noradrenaline. However, it did not modify 45Ca(2+) uptake in resting mesenteric resistance arteries. Taken together, these results suggest that somatostatin exerts an inhibitory effect on vascular contractions induced by some stimulating agents in different arteries isolated from rabbits, being more potent in mesenteric arteries.
Animals↗
Effects of nifedipine on forearm vascular resistance and venous capacitance in normal subjects and in patients with congestive heart failure.
The effects of oral nifedipine on limb hemodynamics were studied in 7 normal subjects, 8 patients with congestive heart failure and 2 patients who underwent sympathectomy of unilateral limb. Forearm venous capacitance remained unchanged both in normal subjects and in patients with congestive heart failure. In normal subjects, systemic vascular resistance decreased without change in forearm vascular resistance. On the other hand, both systemic and forearm vascular resistance decreased simultaneously in patients with congestive heart failure. In 2 patients with normal left ventricular function undergoing sympathectomy, limb vascular resistance decreased in the denervated side and increased in the contralateral innervated side. These findings indicate that the effects of nifedipine on forearm vascular resistance are dependent upon the circulatory state of the patient at the time the drug is administered, while venous dynamics were not changed by nifedipine, and that the difference in the density of sympathetic innervation results in a reordering of territorial blood flow by modifying the vasodilatation due to the calcium antagonistic action of nifedipine.
Adult↗
Carotid sinus baroreceptor reflex control and epinephrine. Influence on capacitive and resistive properties of the total pulmonary vascular bed of the dog.
To quantify the importance of the carotid sinus baroreceptor reflex and the interaction with epinephrine infusion on total pulmonary vascular capacity and resistance, I have simultaneously measured total pulmonary vascular compliance, changes in pulmonary blood volumes, and changes in resistances in seven sodium pentobarbital-anesthetized dogs. A preparation was used that bypasses the right and left hearts allowing for the simultaneous measurement of the pulmonary as well as the systemic vascular bed parameters. At intrasinus pressures of 50, 125, and 200 mm Hg, without epinephrine infusion, the pulmonary vascular resistance was 0.134, 0.121, and 0.109 mm Hg/(ml per min per kg) and the systemic vascular resistance was 1.21, 0.87, and 0.63 mm Hg/(ml per min per kg). Epinephrine infusion of 1 microgram/min per kg at each intrasinus pressure caused the resistances of both vascular beds to increase. Pulmonary vascular resistance increased to 0.157 mm Hg/(ml per min per kg) and showed no further changes with changes in ISP. However, systemic vascular resistance did decrease from 1.49 to 1.41 and 1.25 at intrasinus pressures of 50, 125, and 200 mm Hg. During control runs, pulmonary vascular capacity changed 1.06 ml/kg and systemic capacity changed 7.63 ml/kg for SP changes between 50 and 200 mm Hg. Both responses were greatly attenuated after epinephrine infusion and amounted to only 0.17 ml/kg for the pulmonary and vascular bed and 2.26 ml/kg for the systemic vascular bed. The differences in capacity changes between control and epinephrine runs for the two vascular beds were nearly equal to the change in capacities brought about by epinephrine when it was infused at a fixed intrasinus pressure of 125 mm Hg. The pulmonary vascular compliance during the control runs increased from 0.303 to 0.329 ml/mm Hg per kg when ISP was increased from 50 to 200 mm Hg. After epinephrine infusion, the pulmonary compliance was 0.273 ml/mm Hg per kg and showed no changes with intrasinus pressure. Similar results were obtained for the systemic vascular compliance which was 2.07 ml/mm Hg per kg at an ISP of 50 mm Hg and increased to 2.39 ml/mm Hg per kg to an ISP of 200 mm Hg during control runs. After epinephrine infusion, the systemic compliance was 1.89 ml/mm Hg per kg and again showed no changes with ISP. These data indicate that the baroreceptor reflex can exert control of pulmonary and systemic vascular resistance and capacitance and epinephrine can greatly attenuate the reflex control of both vascular beds.
Animals↗
Effect of intermedin/adrenomedullin-2 on venous tone in conscious rats.
We investigated the effect of intermedin/adrenomedullin-2 (3 and 10 nmol/kg, i.v.), a member of the calcitonin gene-related peptide family, relative to the vehicle (0.9% NaCl) on mean circulatory filling pressure (index of venous tone) in conscious rats: intact (unblocked) or ganglionic blocked through treatment with mecamylamine (10 mg/kg, i.v.) and noradrenaline (4 microg/kg/min, i.v.). In intact rats, both doses of intermedin/adrenomedullin-2 reduced mean arterial pressure (-14+/-3, -30+/-3 mmHg), but did not alter mean circulatory filling pressure; the high dose also increased heart rate. In ganglionic-blocked rats, both doses decreased mean arterial pressure (-22+/-3, -46+/-5 mmHg) and the high dose also decreased mean circulatory filling pressure (-2.81+/-0.82 mmHg), but neither dose affected heart rate. The vehicle did not have any effects in any of the groups. In addition, intermedin/adrenomedullin-2 did not have any effect on blood volume in both intact and ganglion-blocked rats. The results show that intermedin/adrenomedullin-2 is a dilator of arterial resistance and capacitance vessels.
Adrenomedullin↗
[Resistance and capacitance of sural veins during electrical stimulation of ventral regions of the medulla oblongata].
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Animals↗
Role of endothelin in regulation of resistance, fluid-exchange, and capacitance functions of the systemic circulation.
This article reviews data at the in vivo whole animal and human level. The importance of both flow and pressure recordings and of the methods used to record these variables is emphasized. Exogenous administration of endothelin-1 evokes a transient depressor response mediated by endothelial endothelinB receptors, but the predominate effect of endothelin-1 is a sustained increase in blood pressure resulting from increases in total peripheral resistance. Resistance in the superior mesenteric, renal, and hindquarter vascular beds of animals and forearm resistance in humans is increased. Both endothelinA and, to a lesser extent, endothelinB receptors on vascular smooth muscle mediate the increases in resistance. Endothelin-1 evokes decreases in the precapillary/postcapillary resistance ratio, resulting in increased capillary pressure and net transcapillary filtration. Endothelin-1 evokes increases in mean circulatory filling pressure in animals and in constriction of the human dorsal hand vein. This venoconstrictor activity is mediated primarily through endothelinA and to a lesser extent endothelinB receptors. Endogenously generated endothelin contributes to the hemodynamic effects of angiotensin and vasopressin in certain animal models of hypertension. Antagonists of endothelin evoke modest hemodynamic changes in healthy humans and in some healthy animals, and they decrease vascular resistance dramatically in several salt-sensitive rat models of hypertension and also in some hypertensive human subjects. Thus, endogenously generated ET appears to play a modest role in the healthy organism, but it likely plays a major role in many pathophysiological states as described in companion articles in this issue.
Animals↗
Effect of felodipine on arterial blood flow and venous function at rest in patients with mild essential hypertension.
Felodipine is a second-generation dihydropyridine calcium antagonist used to treat mild to moderate arterial hypertension. The authors used venous occlusion plethysmography to study the effect of this drug on lower limb arterial inflow and venous outflow in 10 at rest patients with mild essential hypertension. They also sought correlations between changes in district blood flow and blood pressure. Plethysmography was carried out at 8 AM and 4, 8, and 24 hours later at baseline (after washout), on the first day of treatment with a single daily administration of 10 mg felodipine ER, and after 7 and 30 days of treatment. The drug was given after the 8 AM evaluation. The authors determined rest flow, maximal venous incremental volume (MVIV) at 40 mmHg and 60 mmHg, and gradient of venous volume between 60 and 40 mmHg divided by the pressure difference (DV/DP) as index of venous distensibility. On the days of plethysmographic evaluation, arterial blood pressure and heart rate were measured continuously over 24 hours by the ABPM (Ambulatory Blood Pressure Monitoring). The results were analyzed by ANOVA. Rest flow, MVIV, and DV/DP were stable at the baseline evaluation. On days 1, 7, and 30 of treatment the rest flow after 4 and 8 hours was significantly greater than at 8 AM but had always returned to normal after 24 hours. No other plethysmographic parameters changed significantly; in particular venous outflow remained unchanged. Mean arterial, systolic, and diastolic blood pressure were significantly reduced, compared with baseline, following treatment on the first day and after 7 and 30 days' treatment. There was no effect on heart rate. The authors conclude that felodipine is useful for the treatment of mild essential hypertension, since it reduces arterial resistance without altering venous capacitance or distensibility.
Aged↗
Reflex responses of venous capacitance vessels in patients with hypertrophic cardiomyopathy.
1. The aim of this study was to determine if there is impaired reflex venoconstriction in patients with hypertrophic cardiomyopathy and whether this is related to a history of syncope or exercise hypotension. 2. Thirty percent of patients with hypertrophic cardiomyopathy have exercise-induced hypotension associated with a failure of arteriolar constriction. Impaired venoconstriction could exacerbate this situation. 3. We evaluated 43 patients with hypertrophic cardiomyopathy and 24 controls. Nuclear venous plethysmography was used to measure forearm venous capacitance during lower body negative pressure, splenic venous volume changes during bicycle exercise and blood pressure responses to treadmill exercise. We assessed any association between abnormal reflex venous control and a history of syncope and exercise hypotension. 4. The percentage reduction in unstressed forearm venous volume during lower body negative pressure was similar in patients and controls (8.9 +/- 7.1% versus 9.7 +/- 5.9%, P not significant). Patients with a history of syncope demonstrated a less marked percentage reduction in volume than those without (-2.1 +/- 6.9% versus -10.6 +/- 6.0%, P = 0.001). In three patients with a history of syncope there was a paradoxical increase in forearm venous volume during lower body negative pressure. During exercise there was a substantially smaller decrease in splenic venous volume in patients compared with controls (-20.1 +/- 14.0% and -42.6 +/- 12.6% respectively, P = 0.0001). Furthermore, there was an association between attenuated splenic venoconstriction or venodilation and exercise hypotension in patients (P = 0.005). 5. Abnormal reflex control of venous capacitance beds in patients with hypertrophic cardiomyopathy was associated with both syncope and exercise hypotension.
Adult↗