Neural mechanism underlying basilar arterial constriction by intracisternal L-NNA in anesthetized dogs

1993 ◽  
Vol 265 (1) ◽  
pp. H103-H107 ◽  
Author(s):  
N. Toda ◽  
K. Ayajiki ◽  
T. Okamura
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cerebral Arteries ◽  
Neural Mechanism ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Anesthetized Dogs ◽  
Arterial Constriction ◽  
Synthase Inhibitor

Basilar arterial diameters were angiographically measured in anesthetized dogs in which systemic blood pressure and heart rate were also monitored. Injections of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, into the cisterna magna produced a significant, persistent decrease in arterial diameter, the effect being reversed by intracisternal injections of L-arginine. The vasoconstrictor effect of L-NNA was diminished in dogs treated with hexamethonium. On the other hand, treatment with phentolamine in a dose sufficient to lower blood pressure to a level similar to that attained with hexamethonium did not inhibit, but rather potentiated, the effect of intracisternal L-NNA. Nicotine injected into the vertebral artery significantly dilated the basilar artery. The effect was abolished by treatment with L-NNA applied intracisternally, the inhibition being reversed by the addition of L-arginine. Systemic blood pressure and heart rate were not altered by intracisternally applied L-NNA and L-arginine. These findings support the hypothesis that basilar arterial constriction caused by intracisternal L-NNA is associated with a suppression of NO synthesis in nitroxidergic nerves innervating the cerebroarterial wall rather than an elimination of basal release of NO from the endothelium. Functional importance of nitroxidergic vasodilator innervation in cerebral arteries in vivo is thus clarified.

Methylprednisolone on circulating eicosanoids and vasomotor tone after endotoxin

1986 ◽  
Vol 61 (1) ◽  
pp. 185-191 ◽  
Author(s):  
C. A. Hales ◽  
R. D. Brandstetter ◽  
C. F. Neely ◽  
M. B. Peterson ◽  
D. Kong ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Physiological Effect ◽  
High Dose ◽  
Systemic Blood ◽  
Eicosanoid Production ◽  
Circulating Levels

Acute pulmonary and systemic vasomotor changes induced by endotoxin in dogs have been related, at least in part, to the production of eicosanoids such as the vasoconstrictor thromboxane and the vasodilator prostacyclin. Steroids in high doses, in vitro, inhibit activation of phospholipase A2 and prevent fatty acid release from cell membranes to enter the arachidonic acid cascade. We, therefore, administered methylprednisolone (40 mg/kg) to dogs to see if eicosanoid production and the ensuing vasomotor changes could be prevented after administration of 150 micrograms/kg of endotoxin. The stable metabolites of thromboxane B2 (TxB2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) were measured by radioimmunoassay. Methylprednisolone by itself did not alter circulating eicosanoids but when given 2.5 h before endotoxin not only failed to inhibit endotoxin-induced eicosanoid production but actually resulted in higher circulating levels of 6-keto-PGF1 alpha (P less than 0.05) compared with animals receiving endotoxin alone. Indomethacin prevented the steroid-enhanced concentrations of 6-keto-PGF1 alpha after endotoxin and prevented the greater fall (P less than 0.05) in systemic blood pressure and systemic vascular resistance with steroid plus endotoxin than occurred with endotoxin alone. Administration of methylprednisolone immediately before endotoxin resulted in enhanced levels (P less than 0.05) of both TxB2 and 6-keto-PGF1 alpha but with a fall in systemic blood pressure and vascular resistance similar to the animals pretreated by 2.5 h. In contrast to the early steroid group in which all of the hypotensive effect was due to eicosanoids, in the latter group steroids had an additional nonspecific effect. Thus, in vivo, high-dose steroids did not prevent endotoxin-induced increases in eicosanoids but actually increased circulating levels of TxB2 and 6-keto-PGF1 alpha with a physiological effect favoring vasodilation.

Abstract 066: The Undescribed Protein Caskin2 Is a Novel Regulator of eNOS Phosphorylation and Systemic Blood Pressure

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Sarah B Mueller ◽  
Susan B Gurley ◽  
Christopher D Kontos
Keyword(s):  
Blood Pressure ◽  
Molecular Mechanisms ◽  
Systemic Blood Pressure ◽  
Regulatory Subunit ◽  
Systemic Blood ◽  
Homologous Expression ◽  
Ongoing Work ◽  
Inducing Factors

Disruptions in the function of the quiescent endothelial cells (ECs) that line mature vessels can both result in and contribute to the progression of numerous cardiovascular diseases including hypertension, atherosclerosis, and disorders of vascular permeability. Despite recent attention, the signaling pathways that are active in quiescent ECs remain poorly characterized relative to those that regulate EC activation. In an effort to provide mechanistic insight into these pathways, we have characterized the previously undescribed protein Caskin2, which we hypothesize is a novel regulator of EC quiescence. Caskin2 is expressed in ECs throughout the vasculature, including the aorta, coronary arteries, and renal glomeruli. In vitro, Caskin2 promotes a quiescent EC phenotype characterized by decreased proliferation and increased resistance to apoptosis-inducing factors. Caskin2 knockout mice are viable and fertile. However, preliminary radiotelemetry measurements indicate that Caskin2 knockout (KO) mice have mildly elevated systemic blood pressure (BP). Compared to wild type (WT) littermates (n=8), Caskin2 KO mice (n=7) had increased mean arterial pressure (119+/-1 vs. 113+/-1, p=0.012), systolic BP (138+/-2 vs. 132+/-2, p=0.023), and diastolic BP (99+/-1 vs. 93+/-1, p=0.014) at baseline. To explore the molecular mechanisms of Caskin2’s effects, we used mass spectrometry to identify interacting proteins. Among the 67 proteins identified were the Ser/Thr phosphatase protein phosphatase 1 (PP1) and eNOS. Using standard in vitro biochemical techniques, we demonstrated that Caskin2 acts as a PP1 regulatory subunit. Interestingly, homologous expression of Caskin2 in vitro resulted in a marked increase in phosphorylation of eNOS on S1177, which is known to promote eNOS activity, and a decrease in phosphorylation on T495, which is associated with eNOS inhibition. Finally, PP1 has been shown to dephosphorylate eNOS T495 in vitro, suggesting a molecular mechanism for our in vivo findings. Ongoing work aims to determine if the interaction of Caskin2 and PP1 is required for the Caskin2-induced increase in activating phosphorylation of eNOS and to characterize the physiological mechanisms responsible for Caskin2’s effects on BP in more detail.

scholarly journals Changes in Respiratory Rate, Blood Pressure and Heart Rate Variability in Rabbits during Orthostasis

2006 ◽  
Vol 75 (1) ◽  
pp. 3-12 ◽  
Author(s):  
J. Mokrý ◽  
T. Remeňová ◽  
K. Javorka
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Respiratory Rate ◽  
Supine Position ◽  
Spectral Power ◽  
Systemic Blood Pressure ◽  
Microcomputer System ◽  
Systemic Blood ◽  
Frequency Bands

The purpose of the study was to evaluate the changes of respiratory rate, systemic blood pressure and heart rate variability parameters (HRV) during orthostasis in anaesthetized rabbits. Furthermore, these changes were influenced by affecting the renin-angiotensin-aldosterone (RAA) system and autonomic nervous system (ANS) to study the mechanisms participating in activity of spectral frequency bands of HRV in rabbits. Ten adult rabbits (Chinchilla) were anaesthetized by ketamine and flunitrazepam. The systemic blood pressure, tidal volume and respiratory rate were measured. HRV was evaluated by microcomputer system VariaPulse TF3E. The R-R intervals were derived from the electrocardiogram signal from subcutaneous needle electrodes. The evaluation of HRV in very low (VLF; 0.01-0.05 Hz), low (LF; 0.05-0.15 Hz) and high frequency bands (HF; 0.15-2.0 Hz) was made and parameters of frequency and time analysis were calculated. The measurements were made in horizontal (supine) position, in orthostasis (the angle of 60 °) and again in supine position before and after enalapril (0.5 mg/kg b.w.), metipranolol (0.2 mg/kg b.w.), and after subsequent bilateral cervical vagotomy. The orthostasis in anaesthetized rabbits is accompanied by depression of respiratory rate reversed only by vagotomy. Furthermore, decrease of systemic blood pressure, unchanged heart rate and increased characteristics of heart rate variability were found, with predominant increase of spectral power in LF and VLF bands. This elevation can be eliminated only by complete blockade of ANS. Although the participation of ANS or RAA system in modification of individual HRV frequency bands is not as specific as in humans, we confirmed the participation of RAA system in determination of the VLF band.

Baroreceptor influence on postural changes in blood pressure and carotid blood flow

1963 ◽  
Vol 205 (2) ◽  
pp. 360-364 ◽  
Author(s):  
Francis L. Abel ◽  
John H. Pierce ◽  
Warren G. Guntheroth
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Sinus ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Carotid Blood Flow ◽  
Postural Changes ◽  
Nembutal Anesthesia

The effects of 30° head-down and head-up tilting on mean systemic blood pressure, carotid blood flow, and heart rate were studied in 16 dogs under morphine and Nembutal anesthesia. The tilting procedure was further repeated after denervation of the carotid sinus and aortic arch baroreceptors and after administration of a dihydrogenated ergot alkaloid mixture (Hydergine). The results indicate that the drop in pressure in the head-down position is primarily due to baroreceptor activity and that the baroreceptors are necessary for compensatory vasoconstriction on head-up tilting. Carotid blood flow decreased in both tilted positions in the control animals; the possible relationship to cerebral blood flow is discussed.

Method for measuring brain tissue pressure

1975 ◽  
Vol 43 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Robert M. Clark ◽  
Norman F. Capra ◽  
James H. Halsey
Keyword(s):  
Blood Pressure ◽  
Brain Tissue ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Tissue Pressure ◽  
Content Type ◽  
Pressure Changes ◽  
Local Brain

✓ The authors report a method for measuring total local brain tissue pressure (BTP) using a miniature catheter transducer stereotaxically introduced into the white matter of the cat's cerebrum. Quantitative rapid phasic pressure changes were satisfactorily demonstrated. Due to some drift of baseline of the transducers and inability to perform in vivo calibration, reliable long-term quantitative pressure measurements sometimes could not be studied. The BTP from each cerebral hemisphere and the cisternal pressure (CP) were monitored during alterations of pCO2 and systemic blood pressure, and distilled H2O injection prior to and after right middle cerebral artery (MCA) ligation. The catheter transducers functioned well on chronic implantation for up to 6 weeks. Compared to the chronically implanted catheters, acutely implanted catheters responded identically except for drift. The response of intracranial pressure and CP to MCA occlusion, alterations in pCO2, and systemic blood pressure were similar. No BTP gradients appeared in response to MCA ligation, hypercapnia, hypertension, or progressive swelling of the resulting infarction.

scholarly journals PROGNOSTIC VALUE OF HEART RATE AND SYSTEMIC BLOOD PRESSURE IN PULMONARY ARTERIAL HYPERTENSION

2010 ◽  
Vol 55 (10) ◽  
pp. A154.E1443
Author(s):  
Malcolm M. Bersohn ◽  
Shelley Shapiro ◽  
Michelle P. Turner ◽  
Glenna Traiger ◽  
Adaani E. Frost
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Prognostic Value ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Pulmonary Arterial

P504 HEMODYNAMIC RESPONSE TO NON-SELECTIVE BETA BLOCKERS DESPITE LACK OF EFFECTS ON HEART RATE AND SYSTEMIC BLOOD PRESSURE

2014 ◽  
Vol 60 (1) ◽  
pp. S237
Author(s):  
S. Bota ◽  
M. Mandorfer ◽  
P. Schwabl ◽  
P. Salzl ◽  
A. Ferlitsch ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Beta Blockers ◽  
Systemic Blood Pressure ◽  
Hemodynamic Response ◽  
Systemic Blood

Renal hemodynamics during hyperthermia caused by exposure to high environmental temperature

1961 ◽  
Vol 201 (5) ◽  
pp. 791-794 ◽  
Author(s):  
G. S. Kanter
Keyword(s):  
Blood Pressure ◽  
Environmental Temperature ◽  
Renal Plasma Flow ◽  
Systemic Blood Pressure ◽  
Renal Hemodynamics ◽  
Initial Increase ◽  
Systemic Blood ◽  
Acid Clearance ◽  
Anesthetized Dogs ◽  
Per Se

The GFR (glomerular filtration rate) and RPF (renal plasma flow), following an initial increase, fell significantly after 3–4 hr exposure of anesthetized dogs to an air temperature of 49 C. This alteration occurred with either dehydration or hydration present. Creatinine clearance was used as a measure of GFR and p-aminohippuric acid clearance at low plasma levels was used as a measure of RPF. Rectal temperature averaged 43 C at the conclusion of the experiment. The hematocrit increased 14%. The alteration in renal hemodynamics was shown to be due to a mild fall in mean systemic blood pressure, and a concomitant early decrease in intrarenal resistance followed a further decrease in blood pressure, combined with a progressively increasing intrarenal resistance. It can be concluded that while the fall in blood pressure, increasing intrarenal resistance during the latter part of the exposure, and decreased GFR and RPF are resultants of hyperthermia, the massive loss of plasma volume and increase in hematocrit previously reported in hyperthermia produced with heating pads (largely conductive heating) need not occur. Such major changes may be ascribed to tissue damage rather than to hyperthermia, per se.

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