Effect of plasma from hypertensive subjects on Ca2+ transport in permeabilized human neutrophils

1988 ◽  
Vol 74 (1) ◽  
pp. 53-56 ◽  
Author(s):  
Walter Zidek ◽  
Agapios Sachinidis ◽  
Claus Spieker ◽  
Walter Storkebaum
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Gel Filtration ◽  
Human Neutrophils ◽  
Increase Blood Pressure ◽  
Selective Electrode ◽  
Control Value ◽  
Plasma Fraction ◽  
Plasma Fractions ◽  
Normotensive Subjects

1. The effects of plasma fractions from essential hypertensive subjects (n = 14) and normotensive subjects (n = 14) on Ca2+ transport in permeabilized human neutrophils was studied using an ion-selective electrode. 2. Plasma fractions were obtained by gel filtration and contained substances with a molecular mass in the range 1000–1500 daltons. This fraction isolated from essential hypertensive subjects has been shown to increase blood pressure after intravenous injection in the rat. 3. The rate of Ca2+ uptake by permeabilized neutrophils after addition of extracellular Ca2+ was significantly accelerated during incubation of the cells with the hypertensive fraction (1049.3 ±807.7% vs 242.5 ±320.9% of the control value, mean ± sd, P < 0.05). 4. It is concluded that the hypertensive plasma fraction increases Ca2+ accumulation in subcellular particles, so that under excitatory conditions Ca2+ release in arterial smooth muscle might be enhanced.

Effect of plasma from patients with essential hypertension on vascular resistance in the isolated perfused rat kidney

1991 ◽  
Vol 80 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Jürgen Bachmann ◽  
Hartmut Schlüter ◽  
Walter Storkebaum ◽  
Herbert Witzel ◽  
Franz Wessels ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Direct Action ◽  
Rat Kidney ◽  
Gel Filtration ◽  
Hypertensive Patients ◽  
Vasopressor Agent ◽  
Resistance Vessels ◽  
Plasma Fractions ◽  
Normotensive Subjects ◽  
Rat Kidneys

1. Isolated perfused rat kidneys were used to study the effects of plasma fractions obtained by gel filtration from essential hypertensive patients (n = 40) and from normotensive subjects (n = 36) on resistance vessels. Perfusion pressure was recorded at a constant flow. 2. Plasma fractions were obtained by gel filtration and contained substances with a molecular mass in the range 1000–1500 Da. The plasma fractions from hypertensive patients used in this study had been shown to increase blood pressure after intravenous injection in rats. 3. In the isolated rat kidneys, the hypertensive fractions increased perfusion pressure by 20 ± 17 mmHg (mean ± SD, range 5–58 mmHg, n = 40). The analogous fractions from normotensive subjects did not change perfusion pressure significantly. 4. In Ca2+-free medium containing 2 mmol/l ethyleneglycol bis-(aminoethyl ether)tetra-acetate, the change in perfusion pressure induced by active plasma fractions was reduced by 95.2 ± 6.3%. Addition of nifedipine to the perfusion medium reduced, but did not abolish, the pressure response of the kidneys. 5. In solutions containing phentolamine or saralasin, vasoconstriction was not reduced. 6. Thus in the active fractions from hypertensive plasma, a vasopressor agent with direct action on resistance vessels can be demonstrated. This substance probably acts by increasing Ca2+ influx in vascular smooth muscle cells.

Effect of vasoactive drugs on carotid diameter in humans

1997 ◽  
Vol 273 (4) ◽  
pp. H1629-H1636 ◽  
Author(s):  
Istvan Bonyhay ◽  
Gabor Jokkel ◽  
Kristof Karlocai ◽  
Robert Reneman ◽  
Mark Kollai
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Systolic Pressure ◽  
Smooth Muscle Contraction ◽  
Vasoactive Drugs ◽  
Drug Induced ◽  
Control Value ◽  
Sinus Wall ◽  
Induced Changes ◽  
Passive Stretch

We studied whether vasoactive drugs used to determine baroreflex sensitivity influence baroreceptor firing by affecting carotid sinus smooth muscle or simply by stretching the sinus wall through changes in pressure. In six young healthy subjects, the diameter of the carotid artery and its change with arterial pulse were measured with ultrasonography. Blood pressure was measured by Finapres. Phenylephrine and nitroglycerin doses were injected intravenously to raise and lower pressure by ∼15–25 mmHg. Carotid dimensions increased in all subjects during the phenylephrine-induced rise and decreased during the nitroglycerin-induced fall in pressure. Diastolic diameter changed more than systolic diameter; changes were significantly different from the control value (assessed by single-factor analysis of variance and Scheffé’s post hoc test). The systolic pressure-diameter relationship appeared to be nonlinear, with a steeper slope above than below baseline, and contributed significantly to the nonlinearity of the R-R interval-systolic pressure relationship. It is concluded that during drug-induced changes in blood pressure, baroreceptor activity in humans is influenced more by passive stretch than by local smooth muscle contraction.

Stereoselective and nonstereoselective inhibition exhibited by the enantiomers of verapamil

1990 ◽  
Vol 68 (3) ◽  
pp. 439-446 ◽  
Author(s):  
Michael T. Piascik ◽  
Roslynn Collins ◽  
Brent T. Butler
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Calcium Channels ◽  
Vascular Smooth Muscle ◽  
Calcium Channel ◽  
Adrenergic Receptor ◽  
Increase Blood Pressure ◽  
High Efficacy ◽  
Inhibitory Potency

The interaction of the isomers of verapamil with sites on the calcium channel and α1-adrenergic receptor has been examined. The inhibitory potency of these enantiomers differ with respect to the agonist. KCl- or clonidine-induced contractions of rabbit aortic rings were inhibited in a stereoselective manner by the enantiomers of verapamil with the (−)-isomer being more potent than the (+)-isomer. Similarly, (−)-verapamil was also more potent at displacing (−)-[N-methyl-3H]desmethoxyverapamil than was the (+)-isomer. In contrast, the inhibition of norepinephrine- or phenylephrine-induced aortic contractions was not stereoselective. Differences in enantiomer potency were also observed in vivo. The ability of clonidine to increase blood pressure in the anesthetized rat was blocked in a stereoselective manner by the verapamil enantiomers, while inhibition of the pressor actions of phenylephrine was not. In summary, for agents that rely heavily on calcium channel function (KCl, clonidine), stereoselective inhibition was observed. Stereoselective inhibition was not observed against high efficacy α1-agonists. This difference in stereochemistry argues that verapamil does not act at the same site when inhibiting clonidine or KCl action when compared with norepinephrine or phenylephrine.Key words: calcium channels, phenylalkylamines, α-receptors, vascular smooth muscle, stereochemistry.

scholarly journals Norepinephrine-associated left ventricular outflow tract obstruction and systolic anterior movement

2019 ◽  
Vol 12 (12) ◽  
pp. e225879 ◽  
Author(s):  
Warner Mbuila Mampuya ◽  
Jonathan Dumont ◽  
Francois Lamontagne
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Outflow Tract ◽  
Myocardial Hypertrophy ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Increase Blood Pressure ◽  
Ventricular Outflow Tract Obstruction ◽  
Left Ventricular Outflow ◽  
Systolic Anterior Movement

In the perioperative setting, norepinephrine is used to increase blood pressure, an effect mediated mostly via arterial and venous vasoconstriction. Thus, norepinephrine is, allegedly, less likely to cause or worsen left ventricular outflow tract obstruction (LVOTO) than other inotropes. We report a case of norepinephrine-associated dynamic LVOTO and systolic anterior movement in a predisposed patient. This report highlights that unrecognised dynamic LVOTO may worsen shock parameters in patients treated with norepinephrine who have underlying myocardial hypertrophy.

scholarly journals RGS5 Attenuates Baseline Activity of ERK1/2 and Promotes Growth Arrest of Vascular Smooth Muscle Cells

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1748
Author(s):  
Eda Demirel ◽  
Caroline Arnold ◽  
Jaspal Garg ◽  
Marius Andreas Jäger ◽  
Carsten Sticht ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Map Kinase ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Genetic Ablation ◽  
Variable Expression ◽  
Arterial Blood

The regulator of G-protein signaling 5 (RGS5) acts as an inhibitor of Gαq/11 and Gαi/o activity in vascular smooth muscle cells (VSMCs), which regulate arterial tone and blood pressure. While RGS5 has been described as a crucial determinant regulating the VSMC responses during various vascular remodeling processes, its regulatory features in resting VSMCs and its impact on their phenotype are still under debate and were subject of this study. While Rgs5 shows a variable expression in mouse arteries, neither global nor SMC-specific genetic ablation of Rgs5 affected the baseline blood pressure yet elevated the phosphorylation level of the MAP kinase ERK1/2. Comparable results were obtained with 3D cultured resting VSMCs. In contrast, overexpression of RGS5 in 2D-cultured proliferating VSMCs promoted their resting state as evidenced by microarray-based expression profiling and attenuated the activity of Akt- and MAP kinase-related signaling cascades. Moreover, RGS5 overexpression attenuated ERK1/2 phosphorylation, VSMC proliferation, and migration, which was mimicked by selectively inhibiting Gαi/o but not Gαq/11 activity. Collectively, the heterogeneous expression of Rgs5 suggests arterial blood vessel type-specific functions in mouse VSMCs. This comprises inhibition of acute agonist-induced Gαq/11/calcium release as well as the support of a resting VSMC phenotype with low ERK1/2 activity by suppressing the activity of Gαi/o.

Exercise and pyridostigmine prevents gastric emptying delay and increase blood pressure and cisplatin-induced baroreflex sensitivity in rats

Life Sciences ◽  
2021 ◽  
Vol 267 ◽  
pp. 118972
Author(s):  
Mariana Sousa Silva ◽  
Yasmim de Andrade Gomes ◽  
Mickael Laudrup de Sousa Cavalcante ◽  
Pedro Victor Nogueira Telles ◽  
Alda Cássia Alves da Silva ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Gastric Emptying ◽  
Baroreflex Sensitivity ◽  
Increase Blood Pressure

Does calcium chloride increase blood pressure and uterine blood flow during hemorrhagic hypotension in hypermagnesemic gravid ewes?

1991 ◽  
Vol 75 (3) ◽  
pp. A822-A822
Author(s):  
R D Vincent ◽  
D H Chestnut ◽  
S L Sipes ◽  
C S Thompson ◽  
S A Bleuer ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Calcium Chloride ◽  
Increase Blood Pressure ◽  
Uterine Blood Flow ◽  
Hemorrhagic Hypotension
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