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American Journal of Physiology. Heart... May 2007
Topics: Animals; Antihypertensive Agents; Blood Pressure; Hypertension; Muscle Contraction; Muscle, Smooth, Vascular; Rats; Sodium-Potassium-Chloride Symporters; Solute Carrier Family 12, Member 2; Vasoconstriction
PubMed: 17308011
DOI: 10.1152/ajpheart.00157.2007 -
Biomechanics and Modeling in... Feb 2024The capacity of small cerebral arteries (SCAs) to adapt to pressure fluctuations has a fundamental physiological role and appears to be relevant in different...
The capacity of small cerebral arteries (SCAs) to adapt to pressure fluctuations has a fundamental physiological role and appears to be relevant in different pathological conditions. Here, we present a new computational model for quantifying the link, and its contributors, between luminal pressure and vascular tone generation in SCAs. This is assembled by combining a chemical sub-model, representing pressure-induced smooth muscle cell (SMC) signalling, with a mechanical sub-model for the tone generation and its transduction at tissue level. The devised model can accurately reproduce the impact of luminal pressure on different cytoplasmic components involved in myogenic signalling, both in the control case and when combined with some specific pharmacological interventions. Furthermore, the model is also able to capture and predict experimentally recorded pressure-outer diameter relationships obtained for vessels under control conditions, both in a Ca -free bath and under drug inhibition. The modularity of the proposed framework allows the integration of new components for the study of a broad range of processes involved in the vascular function.
Topics: Muscle, Smooth, Vascular; Vasoconstriction; Cerebral Arteries; Cytosol
PubMed: 37925376
DOI: 10.1007/s10237-023-01774-7 -
British Journal of Pharmacology Oct 2010Purinergic signalling plays an important role in vascular tone regulation in humans. We have identified uridine adenosine tetraphosphate (Up(4)A) as a novel and highly...
BACKGROUND AND PURPOSE
Purinergic signalling plays an important role in vascular tone regulation in humans. We have identified uridine adenosine tetraphosphate (Up(4)A) as a novel and highly potent endothelial-derived contracting factor. Up(4)A induces strong vasoconstrictive effects in the renal vascular system mainly by P2X(1) receptor activation. However, other purinoceptors are also involved and were analysed here.
EXPERIMENTAL APPROACH
The rat isolated perfused kidney was used to characterize vasoactive actions of Up(4)A.
KEY RESULTS
After desensitization of the P2X(1) receptor by α,β-methylene ATP (α,β-meATP), Up(4)A showed dose-dependent P2Y(2)-mediated vasoconstriction. Continuous perfusion with Up(4)A evoked a biphasic vasoconstrictor effect: there was a strong and rapidly desensitizing vasoconstriction, inhibited by P2X(1) receptor desensitization. In addition, there is a long-lasting P2Y(2)-mediated vasoconstriction. This vasoconstriction could be blocked by suramin, but not by PPADS or reactive blue 2. In preparations of the rat isolated perfused kidney model with an elevated vascular tone, bolus application of Up(4)A showed a dose-dependent vasoconstriction that was followed by a dose-dependent vasodilation. The vasoconstriction was in part sensitive to P2X(1) receptor desensitization by α,β-meATP, and the remaining P2Y(2)-mediated vasoconstriction was only inhibited by suramin. The Up(4)A-induced vasodilation depended on activation of nitric oxide synthases, and was mediated by P2Y(1) and P2Y(2) receptor activation.
CONCLUSIONS AND IMPLICATIONS
Up(4)A activated P2X(1) and P2Y(2) receptors to act as a vasoconstrictor, whereas endothelium-dependent vasodilation was induced by P2Y(1/2) receptor activation. Up(4)A might be of relevance in the physiology and pathophysiology of vascular tone regulation.
Topics: Adenosine Triphosphate; Animals; Dinucleoside Phosphates; Dose-Response Relationship, Drug; Endothelium, Vascular; Kidney; Male; Nitric Oxide Synthase; Purinergic P2X Receptor Agonists; Purinergic P2X Receptor Antagonists; Purinergic P2Y Receptor Agonists; Purinergic P2Y Receptor Antagonists; Pyridoxal Phosphate; Rats; Rats, Inbred WKY; Receptors, Purinergic; Suramin; Triazines; Vasoconstriction; Vasodilation
PubMed: 20880394
DOI: 10.1111/j.1476-5381.2010.00914.x -
The Journals of Gerontology. Series A,... May 2015The endothelin-1 vasoconstrictor pathway contributes to age-related elevations in resting peripheral vascular tone primarily through activation of the endothelin subtype...
The endothelin-1 vasoconstrictor pathway contributes to age-related elevations in resting peripheral vascular tone primarily through activation of the endothelin subtype A (ET(A)) receptor. However, the regulatory influence of ET(A)-mediated vasoconstriction during exercise in the elderly is unknown. Thus, in 17 healthy volunteers (n = 8 young, 24±2 years; n = 9 old, 70±2 years), we examined leg blood flow, mean arterial pressure, leg arterial-venous oxygen (O2) difference, and leg O2 consumption (VO2) at rest and during knee-extensor exercise before and after intra-arterial administration of the ET(A) antagonist BQ-123. During exercise, BQ-123 administration increased leg blood flow to a greater degree in the old (+29±5 mL/min/W) compared with the young (+16±3 mL/min/W). The increase in leg blood flow with BQ-123 was accompanied by an increase in leg VO2 in both groups, suggesting a reduced efficiency following ET(A) receptor blockade. Together, these findings have identified an age-related increase in ET(A)-mediated vasoconstrictor activity that persists during exercise, suggesting an important role of this pathway in the regulation of exercising skeletal muscle blood flow and maintenance of arterial blood pressure in the elderly.
Topics: Aged; Aging; Arterial Pressure; Endothelin Receptor Antagonists; Exercise; Female; Healthy Volunteers; Humans; Leg; Lipids; Male; Oxygen Consumption; Peptides, Cyclic; Vasoconstriction; Young Adult
PubMed: 24821105
DOI: 10.1093/gerona/glu065 -
PloS One 2019We recently provided highly suggestive preliminary evidence that the renal interstitium contracts reactively in vivo. We demonstrated that renal medullary direct...
We recently provided highly suggestive preliminary evidence that the renal interstitium contracts reactively in vivo. We demonstrated that renal medullary direct interstitial volume expansion (rmDIVE = 100 μl bolus infusion of 0.9% saline (SS)/30 s) brought about a biphasic renal interstitial hydrostatic pressure (RIHP) response which was abolished when dibutyryl-cAMP was concomitant and interstitially infused. To assess more deeply the feasibility of the concept that the renal interstitium contracts in vivo, two experimental series (S1, S2) were performed in hydropenic rats subjected to acute left renal-denervation, hormonal clamping, and control of renal arterial pressure. In S1, RIHP and renal outer medullary blood flow (RoMBF) were continuously measured before and after a sudden micro-bolus (5μl) injection, into the renal medullary interstitium, of SS containing α-trinositol (α-TNS, anti-inflammatory drug) to either two doses 2 or 4 mM (SS + 2 α-TNS and SS + 4 α-TNS groups). No overall differences between groups in either ΔRIHP or %ΔRoMBF time courses were found; however, in the SS + 2 α-TNS group the data were less scattered and the ΔRIHP time course tended to peak faster and then persisted there, so that, this α-TNS dose was selected for S2. In S2, RIHP and RoMBF were similarly measured in rats randomly assigned to three groups: the CTR group (sham time-control), SS group (SS alone), and SS + α-TNS group. The micro-bolus injection of SS alone (SS group) was unable to increase ΔRIHP. The group with no micro-bolus injection (CTR group) experienced a decrease in ΔRIHP. The micro-bolus injection of SS + 2 α-TNS was accompanied by a differential increase in ΔRIHP (vs. CTR and SS groups). These responses were not associated with differential changes among groups in %ΔRoMBF or hemodilution parameters. These results provide additional evidence that the renal interstitium contracts in vivo.
Topics: Animals; Hydrostatic Pressure; Kidney Medulla; Male; Rats; Rats, Wistar; Renal Circulation; Sodium Chloride; Vasoconstriction
PubMed: 31774858
DOI: 10.1371/journal.pone.0225640 -
Critical Care (London, England) Aug 2018Arterial hyperoxia may induce vasoconstriction and reduce cardiac output, which is particularly undesirable in patients who already have compromised perfusion of vital... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Arterial hyperoxia may induce vasoconstriction and reduce cardiac output, which is particularly undesirable in patients who already have compromised perfusion of vital organs. Due to the inaccessibility of vital organs in humans, vasoconstrictive effects of hyperoxia have primarily been studied in animal models. However, the results of these studies vary substantially. Here, we investigate the variation in magnitude of the hyperoxia effect among studies and explore possible sources of heterogeneity, such as vascular region and animal species.
METHOD
Pubmed and Embase were searched for eligible studies up to November 2017. In vivo and ex vivo animal studies reporting on vascular tone changes induced by local or systemic normobaric hyperoxia were included. Experiments with co-interventions (e.g. disease or endothelium removal) or studies focusing on lung, brain or fetal vasculature or the ductus arteriosus were not included. We extracted data pertaining to species, vascular region, blood vessel characteristics and method of hyperoxia induction. Overall effect sizes were estimated with a standardized mean difference (SMD) random effects model.
RESULTS
We identified a total of 60 studies, which reported data on 67 in vivo and 18 ex vivo experiments. In the in vivo studies, hyperoxia caused vasoconstriction with an SMD of - 1.42 (95% CI - 1.65 to - 1.19). Ex vivo, the overall effect size was SMD - 0.56 (95% CI - 1.09 to - 0.03). Between-study heterogeneity (I) was high for in vivo (72%, 95% CI 62 to 85%) and ex vivo studies (86%, 95% CI 78 to 98%). In vivo, in comparison to the overall effect size, hyperoxic vasoconstriction was less pronounced in the intestines and skin (P = 0.03) but enhanced in the cremaster muscle region (P < 0.001). Increased constriction was seen in vessels 15-25 μm in diameter. Hyperoxic constriction appeared to be directly proportional to oxygen concentration. For ex vivo studies, heterogeneity could not be explained with subgroup analysis.
CONCLUSION
The effect of hyperoxia on vascular tone is substantially higher in vivo than ex vivo. The magnitude of the constriction is most pronounced in vessels ~ 15-25 μm in diameter and is proportional to the level of hyperoxia. Relatively increased constriction was seen in muscle vasculature, while reduced constriction was seen in the skin and intestines.
Topics: Animals; Arteries; Cardiac Output; Cats; Cricetinae; Disease Models, Animal; Hyperoxia; Rabbits; Rats; Vasoconstriction
PubMed: 30075723
DOI: 10.1186/s13054-018-2123-9 -
Transfusion Dec 2013Cell-free hemoglobin (Hb) in the vasculature leads to vasoconstriction and injury. Proposed mechanisms have been based on nitric oxide (NO) scavenging by oxyhemoglobin...
BACKGROUND
Cell-free hemoglobin (Hb) in the vasculature leads to vasoconstriction and injury. Proposed mechanisms have been based on nitric oxide (NO) scavenging by oxyhemoglobin (oxyHb) or processes mediated by oxidative reactions of methemoglobin (metHb). To clarify this, we tested the vascular effect and fate of oxyHb or metHb infusions.
STUDY DESIGN AND METHODS
Twenty beagles were challenged with 1-hour similar infusions of (200 μmol/L) metHb (n = 5), oxyHb (n = 5), albumin (n = 5), or saline (n = 5). Measurements were taken over 3 hours.
RESULTS
Infusions of the two pure Hb species resulted in increases in mean arterial blood pressure (MAP), systemic vascular resistance index, and NO consumption capacity of plasma (all p < 0.05) with the effects of oxyHb being greater than that from metHb (MAP; increase 0 to 3 hr; 27 ± 6% vs. 7 ± 2%, respectively; all p < 0.05). The significant vasoconstrictive response of metHb (vs. albumin and saline controls) was related to in vivo autoreduction of metHb to oxyHb, and the vasoactive Hb species that significantly correlated with MAP was always oxyHb, either from direct infusion or after in vivo reduction from metHb. Clearance of total Hb from plasma was faster after metHb than oxyHb infusion (p < 0.0001).
CONCLUSION
These findings indicate that greater NO consumption capacity makes oxyHb more vasoactive than metHb. Additionally, metHb is reduced to oxyHb after infusion and cleared faster or is less stable than oxyHb. Although we found no direct evidence that metHb itself is involved in acute vascular effects, in aggregate, these studies suggest that metHb is not inert and its mechanism of vasoconstriction is due to its delayed conversion to oxyHb by plasma-reducing agents.
Topics: Albumins; Animals; Blood Pressure; Dogs; Methemoglobin; Nitric Oxide; Oxyhemoglobins; Random Allocation; Vasoconstriction
PubMed: 23488474
DOI: 10.1111/trf.12162 -
Journal of Atherosclerosis and... Dec 2021The cardio-ankle vascular index (CAVI) consists of intrinsic and functional arterial stiffness mainly regulated by vasoactive compounds. A new stiffness index of the...
AIM
The cardio-ankle vascular index (CAVI) consists of intrinsic and functional arterial stiffness mainly regulated by vasoactive compounds. A new stiffness index of the aorta (aBeta) and iliac-femoral arteries (ifBeta) was determined by applying the CAVI theory to the whole aorta and iliac-femoral arteries. We investigated the changes in aBeta and ifBeta in response to decreased blood pressure (BP) induced by the Ca channel blocker nicardipine to elucidate the involvement of Ca in aBeta and ifBeta.
METHODS
Pressure waves at the origin of the aorta (oA), distal end of the abdominal aorta (dA), and left femoral artery (fA) as well as flow waves at the oA were simultaneously recorded before and after the infusion of nicardipine (50 µg/kg/min) for 2 min in 12 male rabbits under pentobarbital anesthesia. Beta was calculated using the following formula: Beta=2ρ / PP×ln (SBP / DBP)×PWV, where ρ, SBP, DBP, and PP denote blood density and systolic, diastolic, and pulse pressures, respectively. aBeta, ifBeta, and aortic-iliac-femoral Beta (aifBeta) were calculated using aPWV, ifPWV, and aifPWV, respectively.
RESULTS
SBP, mean arterial pressure (MAP), DBP, and total peripheral vascular resistance significantly decreased during the administration of nicardipine, whereas cardiac output significantly increased. aBeta and ifBeta significantly increased and decreased, respectively, whereas aifBeta did not change despite the decrease in BP. ifBeta and aBeta positively and negatively correlated with BP, respectively, whereas aifBeta did not correlate with SBP.
CONCLUSIONS
There were contradictory arterial responses to nicardipine between the elastic and muscular arteries. Unknown vasoconstriction mechanisms that are not involved in Ca influx may function in the aorta in response to decreased BP.
Topics: Animals; Aorta, Abdominal; Arterial Pressure; Calcium Channel Blockers; Cardio Ankle Vascular Index; Femoral Artery; Iliac Artery; Nicardipine; Pulse Wave Analysis; Rabbits; Vascular Resistance; Vascular Stiffness; Vasoconstriction
PubMed: 33746145
DOI: 10.5551/jat.60848 -
Journal of Acupuncture and Meridian... Oct 2014This study investigated thermal changes in the skin at locations where soft tissue defects existed and acupuncture needles stimulated by using bipolar electroacupuncture...
This study investigated thermal changes in the skin at locations where soft tissue defects existed and acupuncture needles stimulated by using bipolar electroacupuncture (EA) had been inserted. Under general anesthesia (GA), experimental defects were made at the dorsum site of five New Zealand rabbits. Bipolar EA was used for 20 minutes to stimulate the experimental defects, and the skin temperature was monitored at the sites where the acupuncture needles had been inserted and the soft tissue defects existed. The initial thermography of those defects had the same trend as that of the negative pole of EA stimulation at the first acupoint. Skin thermography during the first 3 minutes of bipolar EA indicated a centrifugal vasoconstriction and a vasodilatation at the negative and positive poles, respectively. After that, the thermal change in soft tissue undergoing EA stimulation was not modified by a different EA polarity. The local temperature at the defect and its surroundings under both positive and negative electric loads was increased by 0.2-0.3 °C for vasodilatation. This study indicates that EA influences sympathetic modulation of soft tissue defects and that selective sympathetic modulation caused by bipolar EA is responsible for the clinical perception.
Topics: Animals; Electroacupuncture; Needles; Neuroleptanalgesia; Rabbits; Skin; Skin Temperature; Vasoconstriction
PubMed: 25441948
DOI: 10.1016/j.jams.2014.01.002 -
BMC Neurology Oct 2023Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by sudden onset thunderclap headache and multiple segmental reversible cerebral vasoconstrictions...
A case report of reversible cerebral vasoconstriction syndrome with thunderclap headache significantly exacerbated in the supine position and alleviated in the standing position.
BACKGROUND
Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by sudden onset thunderclap headache and multiple segmental reversible cerebral vasoconstrictions that improve within 3 months. The postpartum period is a well-known precipitating factor for the onset of RCVS. Cerebral venous thrombosis (CVT) causes thunderclap headaches in the postpartum period. While headache in CVT is sometimes exacerbated in the supine position, the severity of the headache in RCVS is usually independent of body position. In this study, we report a case of RCVS with thunderclap headache exacerbated in the supine position, and headache attacks that resolved quickly in the standing position during the postpartum period.
CASE PRESENTATION
A 33-year-old woman presented with a sudden increase in blood pressure and thunderclap headache on the fifth postpartum day (day 1: the first sick day). The headache was severe and pulsatile, with onset in the supine position in bed, and peaked at approximately 10 s. It was accompanied by nausea and chills but there were no scintillating scotomas or ophthalmic symptoms. The headache resolved in the standing or sitting position but was exacerbated and became unbearable within a few seconds when the patient was in the supine position. Therefore, she was unable to lie supine at night. Computed tomography angiography (CTA) of the head on day 2 and magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) on day 3 showed no abnormalities. However, considering the possibility of RCVS, verapamil was initiated on day 3. The headache resolved the following day. MRA of the head on day 10 revealed diffuse and segmental stenoses in the bilateral middle and posterior cerebral arteries and basilar artery. Therefore, the patient was diagnosed with RCVS. The headache gradually resolved and disappeared completely on day 42. Cerebral vasoconstriction was also improved on MRA on day 43.
CONCLUSIONS
This postpartum RCVS case was notable for the exacerbation of headaches in the supine position. For the diagnosis of thunderclap headache in the postpartum period, RCVS should be considered in addition to CVT when the patient presents with a headache that is exacerbated in the supine position.
Topics: Female; Humans; Adult; Vasoconstriction; Standing Position; Supine Position; Cerebrovascular Disorders; Vasospasm, Intracranial; Headache Disorders, Primary; Headache
PubMed: 37789263
DOI: 10.1186/s12883-023-03381-6