In vivo simultaneous comparison of pressor and uterine responses to a single agonist (oxypressin) in estrous rats

1987 ◽  
Vol 65 (1) ◽  
pp. 6-11
Author(s):  
Diana Gazis ◽  
Geneviève Gonzalez ◽  
Milton Mendlowitz
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Dissociation Rate ◽  
Peptide Receptor ◽  
Uterine Contractions ◽  
Receptor Compartment ◽  
Muscle Types ◽  
Simultaneous Comparison

To try to compare receptor compartment kinetics, receptor binding, and binding–response coupling for two smooth muscle types in vivo, pressor and uterine responses to oxypressin, an equipotent analog of oxytocin and vasopressin, were studied simultaneously in urethane-anesthetized, pentolinium–indomethacin treated rats. Access of peptide to the pressor and uterine receptor compartments and peptide–receptor dissociation rate had a negligible effect on the two responses. During both injections and infusions, the blood pressure response seemed to be determined largely by plasma levels of oxypressin. The uterine response to oxypressin, however, was paradoxical. The heights of individual uterine contractions seemed to be determined throughout by plasma oxypressin concentrations. The interval between contractions also seemed to be determined by plasma peptide concentrations during injections. However, as plasma peptide increased and reached steady state during infusion, contraction interval behaved as if plasma peptide concentrations were decreasing. This effect was more marked at the beginning of infusion. The implication of these results is that binding determines the pressor response to oxypressin and binding–response coupling does not change. In contrast, although binding determines the uterine response to oxypressin during injection and binding–response coupling appears constant, some factor in addition to binding affects the contraction interval portion of the uterine response and modifies the apparent binding–response coupling of this parameter during infusion.

In vivo apparent peptide-receptor dissociation rate constants for arginine vasopressin analogs estimated from inhibition of rat pressor responses

1987 ◽  
Vol 65 (10) ◽  
pp. 2099-2103
Author(s):  
Diana Gazis
Keyword(s):  
Blood Pressure ◽  
Arginine Vasopressin ◽  
Rate Constants ◽  
Dissociation Rate ◽  
Arginine Vasotocin ◽  
Moderate Dose ◽  
Peptide Receptor ◽  
Pressor Responses ◽  
Dissociation Rate Constants

Apparent pressor receptor dissociation rate constants for arginine vasopressin, arginine vasotocin, oxytocin, oxypressin, and [1-deamino, 9-D-alanineamide]arginine vasopressin were estimated by the following method. Two minutes after injection of a moderate dose of agonist into urethane-anesthetized rats prepared for recording mean blood pressure, a large dose of inhibitor was injected. Under these conditions, in the first few moments after inhibitor injection, there should be no rebinding of the agonist after it dissociates, because vacant receptors should be immediately occupied by inhibitor. The rate of the blood pressure drop at the initiation of inhibition was calculated and used as an estimate of the dissociation rate of the agaonist. Apparent dissociation rate constants thus estimated were 1.1, 1.1, 6.9, 5.8, and 13.9 min−1 for arginine vasopressin, arginine vasotocin, oxytocin, oxypressin, and [1-deamino, 9-D-alanineamide]arginine vasopressin, respectively. These rate constants were inversely related to the pressor potencies (435, 250, 5, 3, and 0.7 U/mg, respectively) of these five compounds. Such a relationship is to be expected if decreased potency is in part due to a faster "off" rate from pressor receptors.

Adrenergic interactions in uterus and vascular smooth muscle in rats in vivo

1989 ◽  
Vol 67 (12) ◽  
pp. 1586-1590
Author(s):  
Diana Gazis ◽  
Genevieve Gonzalez ◽  
Milton Mendlowitz
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Initial Portion ◽  
Norepinephrine Infusion

Simultaneous blood pressure and uterine responses to norepinephrine infusions were recorded in urethane-anesthetized, pentolinium–indomethacin treated rats in natural estrus under conditions in which no blockers or blockers of α1-, α2-, and β-adrenergic receptors or of "reuptake" of norepinephrine were present. The contributions of α1- and α2-adrenergic receptors to the blood pressure response were similar during the initial portion of the response. At later times, however, α1-adrenergic receptors were responsible for the major portion of the response. The tachyphylaxis of the pressor response that occurs during norepinephrine infusion could be prevented by preventing norepinephrine "reuptake" with imipramine. In the uterus, the initial small α-adrenergic contractile response (seen only at the lowest infusion rate) was quickly overwhelmed by a β-adrenergic relaxing component. Administration of the β-adrenergic receptor blocker, propranolol, during norepinephrine infusion caused similar increases in blood pressure in control, yohimbine-, and prazosin-treated rats. Uterine contractions, in contrast, were only significantly elevated during β-adrenergic receptor blockade when yohimbine or imipramine had also been administered.Key words: uterus, vascular smooth muscle, adrenergic receptors, rats.

Mineralocorticoid antagonist inhibits stress-induced blood pressure response after repeated daily warming

1994 ◽  
Vol 267 (6) ◽  
pp. E921-E926 ◽  
Author(s):  
D. T. Van den Berg ◽  
W. de Jong ◽  
E. R. de Kloet
Keyword(s):  
Blood Pressure ◽  
Restraint Stress ◽  
Blood Pressure Response ◽  
Direct Method ◽  
Pressor Response ◽  
Blood Pressure Measurement ◽  
Training Procedure ◽  
Intracerebroventricular Infusion ◽  
Mineralocorticoid Antagonist ◽  
Corticosterone Response

We report here that with a direct method for measurement of cardiovascular parameters in conscious rats, intracerebroventricular administration of the mineralocorticoid receptor (MR) antagonist RU-28318 (100 ng) reduces the blood pressure, heart rate, and the corticosterone response to a brief restraint stress, provided the rats were previously subjected to a daily 30-min exposure to 32 degrees C for 2 wk. The daily exposure to warming and restraint stress are applied identically to the training procedure required for indirect blood pressure measurement using the tail-cuff method. The basal arterial pressure is not affected by the MR antagonist. The effect of the MR antagonist on the stress-induced pressor response develops with a delay of several hours in the normotensive rats. The corticosterone response to daily warming and stress is also attenuated by the intracerebroventricular infusion of MR antagonist but with shorter onset and shorter duration. The findings suggest that conditioning to daily warming and stress imposes mineralocorticoid dependency of the pressor response, which involves MR functioning in brain.

In vitro and in vivo inhibition of renin by fatty acids.

1978 ◽  
Vol 234 (6) ◽  
pp. E593 ◽  
Author(s):  
T A Kotchen ◽  
W J Welch ◽  
R T Talwalkar
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Linoleic Acid ◽  
Angiotensin Ii ◽  
Neutral Lipids ◽  
Pressor Response ◽  
Arterial Blood ◽  
Arachidonic Acids

Circulating neutral lipids inhibit the in vitro renin reaction. To identify the inhibitor(s), free fatty acids were added to human renin and homologous substrate. Capric, lauric, palmitoleic, linoleic, and arachidonic acids each inhibited the rate of angiotensin I production in vitro (P less than 0.01). Inhibition by polysaturated fatty acids (linoleic and arachidonic) was less (P less than 0.01) after catalytic hydrogenation of the double bonds. To evaluate an in vivo effect of renin inhibition intra-arterial blood pressure responses to infusions of renin and angiotensin II (5.0 microgram) were measured in anephric rats (n = 6) before and after infusion of linoleic acid (10 mg iv). Mean increase of blood pressure to angiotensin II before (75 mmHg +/- 9) and after (90 +/- 12) linoleic acid did not differ (P greater than 0.05). However, the pressor response to renin after linoleic acid (18 +/- 3) was less (P less than 0.00)) than that before (102 +/- 13). In summary, several fatty acids inhibit the in vitro renin reaction, and in part inhibition is dependent on unsaturation. Linoleic acid also inhibits the in vivo pressor response to renin. These results suggest that fatty acids may modify the measurement of plasma renin activity and may also affect angiotensin production in vivo.

Muscle chemoreflex alters vascular conductance in nonischemic exercising skeletal muscle

1994 ◽  
Vol 77 (6) ◽  
pp. 2761-2766 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
P. S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Response To Exercise ◽  
Muscle Chemoreflex

Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.

scholarly journals Human neuropeptide Y potentiates α1-adrenergic blood pressure responses in vivo

1998 ◽  
Vol 275 (3) ◽  
pp. H760-H766 ◽  
Author(s):  
Leander V. Schuerch ◽  
Lilly M. Linder ◽  
Eric Grouzmann ◽  
Walter E. Haefeli
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Neuropeptide Y ◽  
Blood Pressure Response ◽  
Human Hand ◽  
Response Curves ◽  
Fourfold Increase ◽  
Dose Rates ◽  
Blood Pressure Responses

Human neuropeptide Y (hNPY) potentiates the postjunctional vasoconstrictor effects of α1-adrenoceptor agonists in animals and in human hand veins in vivo. We therefore hypothesized that such an interaction might also occur in the human arterial bed. With the present single-blind cross-over study in 12 healthy volunteers, the effect of subpressor doses of hNPY on the blood pressure response to α1-adrenoceptor stimulation was evaluated. Dose-response curves were constructed to intravenously infuse phenylephrine with and without coinfusion with two different doses of hNPY (1.4 and 14.3 pmol ⋅ kg−1 ⋅ min−1). Blood pressure, heart rate, and forearm blood flow were recorded, and plasma hNPY was determined. During infusion of the higher hNPY dose, which increased hNPY from 24.0 ± 12.0 to 495.1 ± 12.6 pmol/l, blood pressure curves were 2.4-fold shifted toward lower phenylephrine dose rates ( P < 0.001). Forearm vascular resistance showed a similar trend, whereas the counterregulatory decrease of heart rate was similar in both groups. In contrast, the lower hNPY dose rate producing a fourfold increase in hNPY concentrations did not modify the response to phenylephrine. This in vivo study in humans demonstrates that hNPY induced potentiating effects on α1-adrenergic constriction also in the systemic arterial circulation and suggests that circulating hNPY may participate in the control of vascular tone.

scholarly journals Inhibition of NOX1 mitigates blood pressure increases in elastin insufficiency

Function ◽  
2021 ◽  
Author(s):  
Angela Troia ◽  
Russell H Knutsen ◽  
Carmen M Halabi ◽  
Daniela Malide ◽  
Zu Xi Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Reactive Oxygen Species ◽  
Systolic Blood Pressure ◽  
Blood Pressure Response ◽  
Reactive Oxygen ◽  
Vascular Wall ◽  
Vascular Stiffness ◽  
Oxygen Species

Abstract Elastin insufficiency leads to the cardiovascular hallmarks of the contiguous gene deletion disorder, Williams-Beuren syndrome, including hypertension and vascular stiffness. Previous studies showed that Williams-Beuren syndrome deletions that extended to include the NCF1 gene were associated with lower blood pressure and reduced vascular stiffness. NCF1 encodes for p47phox, the regulatory component of the NOX1 NADPH oxidase complex, that generates reactive oxygen species in the vascular wall. Dihydroethidium and 8-hydroxyguanosine staining of mouse aortas confirmed that Eln heterozygotes (Eln+/-) had greater reactive oxygen species (ROS) levels than wild types (Eln+/+), a finding that was negated in vessels cultured without hemodynamic stressors. To analyze the Nox effect on elastin insufficiency, we utilized both genetic and chemical manipulations. Both Ncf1 haploinsufficiency (Ncf1+/-) and Nox1 insufficiency (Nox1-/y) decreased oxidative stress and systolic blood pressure in Eln+/- without modifying vascular structure. Chronic treatment with apocynin, a p47phox inhibitor, lowered systolic blood pressure in Eln+/-, but had no impact on Eln+/+ controls. In vivo dosing with phenylephrine produced an augmented blood pressure response in Eln+/- relative to Eln+/+, and genetic modifications or drug-based interventions that lower Nox1 expression reduce the hypercontractile response to phenylephrine in Eln+/- mice to Eln+/+ levels. These results indicate that the mechanical and structural differences caused by elastin insufficiency leading to oscillatory flow can perpetuate oxidative stress conditions which are linked to hypertension, and that by lowering the Nox1-mediated capacity for vascular ROS production, blood pressure differences can be normalized.

Attenuation of Electroconvulsive Therapy Induced Hypertension with Sublingual Nifedipine

1989 ◽  
Vol 17 (1) ◽  
pp. 31-33 ◽  
Author(s):  
D. G. Wells ◽  
G. G. Davies ◽  
F. Rosewarne
Keyword(s):  
Blood Pressure ◽  
Electroconvulsive Therapy ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Systolic Pressure ◽  
Response To Therapy ◽  
Induced Hypertension ◽  
Sublingual Nifedipine ◽  
History Of ◽  
Significant Attenuation

Five patients known to be previously hypertensive but not currently receiving anti-hypertensive medications were studied for a total of twenty-six administrations of electroconvulsive therapy Patients randomly received sublingual nifedipine 10 mg, 20 minutes prior to half of their treatments, and for the remaining treatments acted as their own controls. The use of nifedipine resulted in significant attenuation of the blood pressure response to therapy. Systolic pressure increase was 24 mmHg (SD 14) versus 62 mmHg (SD 24) (P< 0.01). There was no difference in heart rate between the two groups. It is concluded that nifedipine reduces the pressor response to electroconvulsive therapy in individuals with a history of hypertension.

PRESSOR RESPONSIVENESS FOLLOWING ACUTE ELEVATION OF SODIUM IN THE RAT

1957 ◽  
Vol 35 (1) ◽  
pp. 327-331 ◽  
Author(s):  
Sydney M. Friedman ◽  
W. A. Webber ◽  
J. D. Jamieson ◽  
Constance L. Friedman
Keyword(s):  
Blood Pressure ◽  
Sodium Acetate ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
High Plasma ◽  
Potassium Citrate ◽  
Plasma Sodium ◽  
Adult Rats ◽  
Sodium Potassium ◽  
Acute Elevation

In order to test the effects of various ions on pressor responsiveness, groups of adult rats were infused with solutions containing sufficient sodium, potassium, calcium, or magnesium to elevate the plasma concentration of these ions. The infusions were completed within 5 minutes and in no case was more than 0.5 ml. injected. The test solutions used were sodium acetate, potassium citrate, calcium chloride, and magnesium sulphate. Control solutions of ammonium acetate, ammonium sulphate, sodium chloride, and sucrose were also infused. In no case was the amount of salt infused sufficient to affect the blood pressure during the infusion. The blood pressure response to 1 γ of norepinephrine or to 20 mU. of pitressin was recorded before infusion and again at the end of the infusion. A significant effect was observed only with sodium acetate. This consisted of a profound suppression of the ordinary pressor response to both norepinephrine and pitressin. The effect was not due to the acetate ion and hence may be specifically referable to the high plasma sodium. These results support our previous conclusions that pressor responsiveness and sodium mobility are causally connected.

Sign in / Sign up

Export Citation Format

Share Document